Cognitive Neuroscience an Introduction
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This is an introduction to Cognitive neuroscience lecture delivered at IIIT Hyderabad Jan 2010
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Cognitive Neuroscience an Introduction
- 3. Cognitive Science Neuro Science Psycology Philosophy Computer Science Genomics
- 4. Neuro Science Cognitive Neuroscience
- 5. Knowledge can be acquired by…. Surfing Diving
- 11. Leonardo Da Vinci April 15, 1452 – May 2, 1519
- 12. Renaissance Andreas Vesalius (1514-1564 CE)
- 14. Sleeping and Waking Descartes 1662
- 15. Phrenology 1806
- 16. Lobar Localization Paul Broca 1868
- 17. Bioelectricity
- 18. Discovery of Neuron Ramony Cajal and Camillo Golgi 1906 Noble
- 19. Nerve Cell
- 20. Supporting cells
- 22. Ion movement across cell
- 24. Action Potential
- 27. Synapse
- 29. Chemical Synapse
- 32. Depolarization of Post Synaptic Neuron
- 33. Repolarization
- 34. Excitatory and Inhibitory Post Synaptic Potential
- 37. Anatomical planes Anterior Posterior Lateral Medial Anatomical Planes
- 39. Cerebrum
- 41. Functional Organization of NS
- 42. Motor System
- 43. Motor System
- 45. Sensory System Pain temp touch Position and vibration sense
- 46. Smell and Taste
- 47. Hearing
- 48. Vision
- 49. Consciousness
- 50. Sleeping
- 52. Memory
- 54. Intelligence
- 55. Thank You
Editor's Notes
- Overview Perhaps the major reason that neuroscience remains such an exciting field is the wealth of unanswered questions about the fundamental structure and functions of the human brain. To understand this remarkable organ (and the rest of the nervous system), the myriad cell types that constitute the nervous system must be identified, their interconnections traced, and the physiological role of the resulting circuits defined. Adding to these several challenges is the fact that a specialized anatomical vocabulary has arisen to describe the structure of the nervous system, as well as a specialized set of physiological terms to describe its functions. In light of these conceptual and semantic difficulties, comprehending the brain and the rest of the nervous system is greatly facilitated by a general picture of the organization of the nervous system, and by a review of the basic terms and anatomical conventions used in discussing its structure and function.
- Mankind has been linking mind to the brain the for a long time. Human skulls with holes deliberately made in them were found in sites more than 10.000 years old. Probably, those holes were made in order to grant a way out for the bad spirits that should be tormenting those brains [ 4 ]. The link between brain and mental functions was a natural one to achieve, because primitive people in all ages could easily observe that strong blows to the skull resulted in loss of consciousness and of memory, and even convulsions, which often led to significant alterations of perception and behavior. The best and most important documental proof about this knowledge comes from the famous Surgical Papyrus, discovered by archeologist Edwin Smith [ 6 ], and which was written around 1.600 BC in Egypt. It contains the first known descriptions of cranial sutures, the external brain surface, brain liquor (CSF) and intracranial pulsation. Its author describes further 30 clincal cases of head and spine trauma, noting how the several brain injuries were associated to changes in the function of other parts of the body, especially in the lower limbs, such as hemiplegic contractures, paralysis, miction and ejaculation and priapism, due to trauma inflicted to the spinal medula.
- In our culture, Alcmaeon of Croton (5th century B.C) was possibly the first one to put in the brain the site of sensations. According to him, the optic nerves, supposed to be hollow, carried the information to the brain, where each sensory modality had its own localization. Alcmaeon of Croton, one of the most emlinent natural philosophers of antiquity, was a native of Croton in Magna Graecia. His father's name was Pirithus, and he is said to have been a pupil of Pythagoras , and must therefore have lived in the latter half of the sixth century before Christ. (Diog. Laërt. viii. 83.) Nothing more is known of the events of his life. His most celebrated anatomical discovery has been noticed in the Dict. of Ant. p. 756, a; but whether his knowledge in this branch of science was derived from the dissection of animals or of human bodies, is a disputed question, which it is difficult to decide. Chalcidius, on whose authority the fact rests, merely says (Comment. in Plat. "Tim." p. 368, ed. Fabr.), " qui primus exsectionem aggredi est ausus," and the word cxsectio would apply equally well to either case. He is said also (Diog. Laërt. l. c.; Clemens Alexandr. Strom. i. p. 308) to have been the first person who wrote on natural philosophy (Phusikon logon), and to have invented fables (fabulas, Isid. Oriy. i. 39). He also wrote several other medical and philosophical works, of which nothing but the titles and a few fragments have been preserved by Stobaeus (Eclog. Phys.) Plutarch (De Phys. Philos. Decr.), and Galen . (Histor. Philosophy.) A further account of his philosophical opinions may be found in Menage's Notes to Diogenes Laërtius, viii. 83, p. 387; Le Clerc, Hist. de la Méd. ; Alfons. Ciacconius ap. Flbric, Biblioth. Graec. vol. xiii. p. 48, ed. vet.; Sprengel, Hist. de la Méd. vol. i. p. 239; C. G. Kühn, De Philosoph. ante Hippocr. Medicinae Cultor. Lips. 1781, 4to., reprinted in Ackermann's Opusc. ad Histor. Medic. Pertinentia, Norimb. 1797, 8vo., and in Kühn's Opusc. Acad. Med. et Philol. Lips. 1827-8, 2 vols. 8vo.; Isensec, Gesch. der Medicin. [W.A.G] Although Alcmaeon is termed a pupil of Pythagoras, there is great reason to doubt whether he was a Pythagorean at all; his name seems to have crept into the lists of supposititious Pythagoreans given us by later writers. (Brandis, Geschichte der Philosophie, vol. i. p. 507.) Aristotle ( Metaphys . 1 ) mentions him as nearly contemporary with Pythagoras, but distinguishes between the stoicheia of opposites, under which the Pythagoreans included all things, and the double principle of Alcmaeon, according to Aristotle, less extended, although he does not explain the precise difference. Other doctrines of Alcmaeon have been preserved to us. He said that the human soul was immortal and partook of the divine nature, because like the heavenly bodies it contained in itself a principle of motion. (Arist. de Anima, i. 2, p. 405; Cic. de Nat. Deor. i. 11.) The eclipse of the moon, which was also eternal, he supposed to arise from its shape, which he said was like a boat. All his doctrines which have come down to us, relate to physics or medicine; and seem to have arisen partly out of the speculations of the Ionian school, with which rather than the Pythagorean, Aristotle appears to connect Alcmaeon, partly front the traditionary lore of the earliest medical science. (Brandis, vol. i. p. 508.)
- Aristotle (384-322 B.C.) diverged from his contemporaries and acknowledged the heart as the organ of thinking, of perception and feelings, whereas the brain was important to keep the body’s temperature, acting as a radiator. According to him, nutrients would go up through the blood vessels and part of them, a kind of garbage, would be cooled in the brain, being changed into a liquid, in a way that could be compared with what happens to water in nature, when rain is formed Aristotle was not the first to erroneously generalize a very old notion among all kinds of antique civilizations, that the seat of emotions was the heart. Even today we are still influenced by this, such as when we refer to a heart as the symbol of love, or when we say that we got a "broken heart", or we have a "heavy heart", or still when we say that we love something with our very hearts. "Knowing by heart", such as when we memorize something, has the same origin. All this probably comes from the fact that the sympathetic branch of the autonomous nervous system is activated during strong emotions, causing a perceptible increase in heart rate and force of contractions. The temporal association of effect to its cause in its peripheral expression has led to the erroneous interpretation, which the natural philosophers tried to "explain" in scientific terms.
- Anyhow, the famous Roman physician Galen (130-200) rejected Aristotles’ ideas, arguing that there were no sense in believing that the brain could cool the passions of heart. Galen dissected a lot (the animal of choice was the ox) and paid more attention to the meninges and cerebral ventricles than to the brain itself. In those days, working with unfixed material, it is only natural that the ventricles would call more attention than the brain, that would resemble an amorphous paste. Galen For Galen, the nutrients absorbed in the guts went to the liver, where the natural spirit was formed. This spirit was taken to the heart and, in the left ventricle, was changed into a vital spirit. The vital spirit, going through the carotid arteries, would reach the rete mirabile , a net of vessels localized in the base of the skull. There, it was blended with the inspired air, forming the animal spirit, that was stored in the cerebral ventricles, from where it could reach the rest of the brain. The animal spirit, a product of the mixture of a liquid and the air, was considered as the essence of life and the source of intellectual skills. When necessary, it could travel along the hollow nerves, eliciting movements or mediating sensations. According to Galen, the substance refined in the rete mirabile would produce a certain amount of refuse, part of which was gaseous, the other part being liquid. The gaseous part escaped through the bone sutures and air sinuses of the skull, and its passage was not perceived by the senses. The liquid part leaked from the anterior ventricles to the openings of the cribiform plate of the ethmoid bones or, yet, from the third ventricle through the pituitary fossa. From there, it could reach the nasal cavity to be discharged as plhegm, or mucus. Greek physician in the Roman Empire who performed experiments to prove arteries contain blood (but thought the heart was a single --not double--pump) Many of Galen's conclusions were wrong because he used mostly animals after an early career using humans at a gladiatorial school outside Rome Human dissection was forbidden in ancient Rome From On Anatomical Procedure (Book I, Chapter II): "Pursue by hard study, then, not only the descriptions of the bones in the book, but also acquaint yourself with the appearance of each of the bones, by the use your own eyes handling each bone by itself so that you become a first-hand observer. . . . I once examined the skeleton of a robber, lying on a mountain-side a short distance from the road. This man had been killed. . . and his body was eaten by birds of prey. . . As regards yourself, then, even if you do not have the luck to see anything like this, still you can dissect an ape, and learn each of the bones from it." Galen was considered "the authority" until the Renaissance During the Middle Ages, questioning Galen was questioning authority and because authority came from God, it was heresy and punishable by death --so NOBODY questioned Galen's conclusions Diagram of Galen's concepts In the painting to the left, Galen is shown "cupping" a patient. In this procedure, heated cups are applied to the patient's back. As the warm air in the cups cools, the air contracts and forms sucking force that draws blood toward the surface of the skin. Sometimes, cuts in the skin allow the cupping procedure to draw out the blood (a treatment known as blood-letting). Cupping was probably borrowed from the Eastern tradition and is still used today by some traditional healers.
- Brain Ventricles and the Concept of Mind Nemesius (circa 320), bishop of Emesa, a city in Syria, embraced Galen’s ideas and based in the cerebral ventricles the intellectual faculties. In his book “ On the Nature of Man ”, a treatise of physiology modeled on Greek medicine, it is said that the soul could not be localized, but the functions of the mind could. The cerebral ventricles were supposed to be responsible for mental operations, from sensation to memorization. The first pair of ventricles were the seat of the “common senses”. They would make the analysis of the information originated in the sense organs. The resultant images were carried to the middle ventricle, the seat of reason, thinking and wisdom. Then came into action the last ventricle, the seat of memory. Up to the Middle Age, the figures depicting the brain would show the ventricles with great detail. The idea that spirits wandered in the ventricles, favored by the Church, prevailed up to the Renaissance. In a book published in the thirteenth century, named “ On the Properties of Things ”, a compilation made by Bartholomew the Englishman, it is stated that “the anterior cavity is soft and moist in order to facilitate association of sensual perceptions and imagination. The middle cell must also be warm, since thinking is a process of separation of pure from impure, comparable to digestion, and heat is known to be the main factor in digestion. The posterior cell, however, is a place for cold storage in which a cool and dry atmosphere must allow for the stocking of goods. That is why the cerebellum is harder, i.e. less medullary and airy, than the rest of the brain”.
- Andreas Vesalius (1514-1564 CE) of Brussels (later Padua, Italy) Flemish anatomist willing to "use his own eyes" in human dissections correcting over 200 mistakes of Galen During the middle ages, everyone had simply trusted Galen, but Vesalius and others during the Renaissance began to question and correct Galen Vesalius was one of the first to dissect cadavers himself (rather than rely on others or on animal dissections); even Leonardo da Vinci and other "artist-anatomists" didn't do their own dissection (of course, they lived nearly twice as long because they weren't exposed to infections in the dead bodies) Vesalius was obsessed with dissections, even stacking up cadavers in his bedroom as a medical student in Paris. Later in his life, he told his students to keep a list of their really sick patients so he'd know where to go to get a freshly dead body (yikes) Published Concerning the Structure of the Human Body - De Corporis Humani Fabrica in 1543 (first "modern" human anatomy text) will detailed illustrations by Jan Stephan van Calcar (student of Titian) The Illustrations from the Works of Andreas Vesalius of Brussels ACT This book was published the same year as Copernicus's text, marking this year as the beginning of the "Scientific Revolution" "It is perfectly clear to me that my attempt will have all too little authority because I have not yet passed the twenty-eighth year of my life; it is equally clear that, because of the numerous indications of the false dogmas of Galen, it will be exceedingly unsafe from the attacks of conservatives, who, as with us in the Italian schools, have constantly avoided anatomy, and who, being old men, will be consumed with envy because of the correct discoveries of the young, and will be ashamed at having been blind thus far, along with other followers of Galen."
- Descartes, Brain and Mind During the seventeenth century, spirits still commanded behavior. At that time Rene Descartes (1596-1650) had chosen the pineal body, not properly as the seat of the soul, but as the place of its activity. The pineal was picked because it is a single organ, unlike the other brain structures, that come in pairs. Descartes’ neurophysiology was independent of neuroanatomy, which he deliberately ignored. It was based in the animal spirits , pores and ways by means of which they flew to exert their actions. According to him, the “most active and quickest particles of the blood” were taken by the arteries from the heart to the brain, where they were transformed in a very subtle air or wind, a very pure and active flame: the “animal spirits” [ 5 ]. The arteries were supposed to come together around the gland localized at the center of the brain: the pineal. Descartes presumed that filaments in the nerves (supposed to be tubes) could move little valvules, opening pores that would allow the flowing or the animal spirits. A stimulus in the skin, for example, would move those filaments, inducing a contraction as a reflex response. Starting in the brain, the animal spirits wold travel along the nerves up to the muscles, inflating them to cause movements. That would be the mechanism for voluntary acts. A reflex response according to Descartes’ physiology. The fire elicits movement of animal spirits in hollow nerves. The movement opens pores in the ventricle (F), letting flow spirits that will inflate the muscles of the leg, that moves away from the heat. External stimuli should open pores in the brain and the spirits would be carried to the pineal gland, which had in its surface a complete sensorial and motor map. The will was under pineal’s control, which could manage the flow of the animal spirits into different nerves. A drawing from the book by Rene Descartes, De Homine, published in 1662. Visual information is taken to the brain by hollow optic nerves. From there, it reaches the Pineal body (H), which regulates the flowing of animal spirits into the nerves. The spirits will go to the muscles of the arm, to produce motion.
- Sleep and wajing, according to Descartes (1662), would depend on the flow of animal spirits in the brain, which were regulated by the pineal gland (H). In the upper drawing, there is a small flow of spirits and the brain is is an "flacid state" during sleep. The lower drawing represents the state of awakeness, when the greater inflow of spirits distents brain matter. Diversity of sensations would be explained by the manner that the pores were open. A strong stimulus, for example, would cause pain. A uniform stimulation of many fibers in the skin would be felt as a smooth surface. The irregular stimulation would cause a feeling of a rough surface. According to Descartes, the animal spirits could dilate the brain, just as the wind acts on the sails of a boat. This action would wake up the brain and allow reception of sensorial information. The absence or small intensity of the animal spirits would induce sleep and dreams. The animal spirits were also the base for his theory of a cerebral localization of movements and sensations. Each person’s distinct temperament and natural skills should be due to differences in number, size, shape and movement of the animal spirits.
- The first roots of cognitive neuroscience lie in phrenology, which was a pseudoscientific theory that claimed that behavior could be determined by the shape of the scalp . In the early 19th century, Franz Joseph Gall and J. G. Spurzheim believed that the human brain was localized into approximately 35 different sections. In his book, The Anatomy and Physiology of the Nervous System in General, and of the Brain in Particular , Gall claimed that a larger bump in one of these areas meant that that area of the brain was used more frequently by that person. This theory gained significant public attention, leading to the publication of phrenology journals and the creation of phrenometers, which measured the bumps on a human subject's head.
- Bioelectricity and the Neuronal Dogma The belief in animal spirits travelling along the nerves, born among the Greeks, remained current up to the eighteen century, when the electric nature of nerve conduction was verified. For that, it was important the work of Luigi Galvani (1737-1798) and, in the following century, the work of Emil du Bois-Reymond (1818-1896). Du Bois-Reymond made his studies on nervous transmission in the 1840 decade and in the 1870 decade he proposed that the effector organs were excited by the nerves via currents or by means of chemical substances liberated by the nerve endings. The nineteenth century brought the acknowledgment that brain’s tissue was important for nervous functions. Theodor Schwann (1810-1882), who described the myelin sheath, was the first to propose that the body is made of individual cells. His cellular theory was accepted for the whole body, with the exception of the nervous system, that was supposed to be made of cells whose branches formed a continuous net. Only after the discovery of the staining method of silver impregnation of nervous elements (Golgi method) an accurate analysis was possible, introducing the works of Santiago Ramon y Cajal (1852-1934) who affirmed, in 1889, that the nervous cells were isolated units. Wilhelm von Waldeyer (1836-1921), in 1891, coined the term “neuron” to designate the anatomical and functional unit of the nervous tissue. Finally, spaces in the junctions between nervous cells or between nervous and muscular cells were described by Charles Scott Sherrington (1857-1952). Sherrington gave these structures the name of “synapses”.
- Before the neuron doctrine was accepted, it was widely believed that the nervous system was a reticulum, or a connected meshwork, rather than a system made up of discrete cells . [3] This theory, the reticular theory , held that neurons' somata mainly provided nourishment for the system. [4] The nineteenth century brought the acknowledgment that brain’s tissue was important for nervous functions. Theodor Schwann (1810-1882), who described the myelin sheath, was the first to propose that the body is made of individual cells. His cellular theory was accepted for the whole body, with the exception of the nervous system, that was supposed to be made of cells whose branches formed a continuous net. Only after the discovery of the staining method of silver impregnation of nervous elements (Golgi method) an accurate analysis was possible, introducing the works of Santiago Ramon y Cajal (1852-1934) who affirmed, in 1889, that the nervous cells were isolated units. Wilhelm von Waldeyer (1836-1921), in 1891, coined the term “neuron” to designate the anatomical and functional unit of the nervous tissue. Finally, spaces in the junctions between nervous cells or between nervous and muscular cells were described by Charles Scott Sherrington (1857-1952). Sherrington gave these structures the name of “synapses”. Drawing by Ramón y Cajal from "Structure of the Mammalian Retina " Madrid, 1900. The initial failure to accept the doctrine was due in part to inadequate ability to visualize cells using microscopes , which were not developed enough to provide clear pictures of nerves. With the cell staining techniques of the day, a slice of neural tissue appeared under a microscope as a complex web and individual cells were difficult to make out. Since neurons have a large number of neural processes an individual cell can be quite long and complex, and it can be difficult to find an individual cell when it is closely associated with many other cells. Thus, a major breakthrough for the neuron doctrine occurred in the late 1800s when Ramón y Cajal used a technique developed by Camillo Golgi to visualize neurons. The staining technique, which uses a silver solution, only stains one in about a hundred cells, effectively isolating the cell visually and showing that cells are separate and do not form a continuous web. Further, the cells that are stained are not stained partially, but rather all their processes are stained as well. Ramón y Cajal altered the staining technique and used it on samples from younger, less myelinated brains, because the technique did not work on myelinated cells. [1] He was able to see neurons clearly and produce drawings like the one at right. For their technique and discovery respectively, Golgi and Ramón y Cajal shared the 1906 Nobel Prize in Physiology or Medicine . Golgi could not tell for certain that neurons were not connected, and in his acceptance speech he defended the reticular theory. Ramón y Cajal , in his speech, contradicted that of Golgi and defended the now accepted neuron doctrine. A paper written in 1891 by Wilhelm von Waldeyer , a supporter of Ramón y Cajal , debunked the reticular theory and outlined the Neuron Doctrine. Updating the neuron doctrine Wiki While the neuron doctrine is a central tenet of modern neuroscience , recent studies suggest that there are notable exceptions and important additions to our knowledge about how neurons function. First, electrical synapses are more common in the central nervous system than previously thought. Thus, rather than functioning as individual units, in some parts of the brain large ensembles of neurons may be active simultaneously to process neural information. [5] Electrical synapses are formed by gap junctions that allow molecules to directly pass between neurons, creating a cytoplasm-to-cytoplasm connection. Second, dendrites, like axons, also have voltage-gated ion channels and can generate electrical potentials that carry information to and from the soma. This challenges the view that dendrites are simply passive recipients of information and axons the sole transmitters. It also suggests that the neuron is not simply active as a single element, but that complex computations can occur within a single neuron. [6] Third, the role of glia in processing neural information has begun to be appreciated. Neurons and glia make up the two chief cell types of the central nervous system. There are far more glial cells than neurons: glia outnumber neurons by as many as 10:1. Recent experimental results have suggested that glia play a vital role in information processing. [7] Finally, recent research has challenged the historical view that neurogenesis , or the generation of new neurons, does not occur in adult mammalian brains. It is now known that the adult brain continuously creates new neurons in the hippocampus and in an area contributing to the olfactory bulb . This research has shown that neurogenesis is environment-dependent (eg. exercise, diet, interactive surroundings), age-related, upregulated by a number of growth factors, and halted by survival-type stress factors. [8] [9] Of particularly compelling interest, Charles Gross and Elizabeth Gould provided evidence suggesting that neurogenesis occurred in neocortex after birth, in areas of the brain known to be important for cognitive function. [10] Strong challenges to this work have come from more well-controlled studies by Pasko Rakic and others which support Rakic's original hypothesis that neurogenesis after birth is restricted to the olfactory bulb and hippocampus. [11] [12] [13] Rakic argues that the Princeton group's work has not been substantiated by multiple other groups. [14]
- Overview Perhaps the major reason that neuroscience remains such an exciting field is the wealth of unanswered questions about the fundamental structure and functions of the human brain. To understand this remarkable organ (and the rest of the nervous system), the myriad cell types that constitute the nervous system must be identified, their interconnections traced, and the physiological role of the resulting circuits defined. Adding to these several challenges is the fact that a specialized anatomical vocabulary has arisen to describe the structure of the nervous system, as well as a specialized set of physiological terms to describe its functions. In light of these conceptual and semantic difficulties, comprehending the brain and the rest of the nervous system is greatly facilitated by a general picture of the organization of the nervous system, and by a review of the basic terms and anatomical conventions used in discussing its structure and function. Summary Nerve cells generate electrical signals to convey information over substantial distances and to transmit it to other cells by means of synaptic connections. The action potential—the signal that conveys information along nerve cell axons—ultimately depends on the resting electrical potential across the neuronal membrane. A resting potential occurs because nerve cell membranes are permeable to one or more ion species subject to an electrochemical gradient. More specifically, a negative membrane potential at rest results from a net efflux of K+ across neuronal membranes that are predominantly permeable to K+. In contrast, an action potential occurs when a transient rise in Na+ permeability allows a net flow of Na+ in the opposite direction across the membrane that is now predominantly permeable to Na+. The brief rise in membrane Na+ permeability is followed by a secondary, transient rise in membrane K+ permeability that repolarizes the neuronal membrane and produces a brief undershoot of the action potential. As a result of these processes, the membrane is depolarized in an all-or-none fashion during an action potential. When these active permeability changes subside, the membrane potential returns to its resting level because of the high resting membrane permeability to K+.
- Factors That Affect Net Rate of Diffusion By now it is evident that many substances can diffuse through the cell membrane.What is usually important is the net rate of diffusion of a substance in the desired direction. This net rate is determined by several factors. Effect of Concentration Difference on Net Diffusion Through a Membrane. Figure 4–8 A shows a cell membrane with a substance in high concentration on the outside and low concentration on the inside.The rate at which the substance diffuses inward is proportional to the concentration of molecules on the outside, because this concentration determines how many molecules strike the outside of the membrane each second. Conversely, the rate at which molecules diffuse outward is proportional to their concentration inside the membrane. Therefore, the rate of net diffusion into the cell is proportional to the concentration on the outside minus the concentration on the inside, or: Net diffusion μ (Co - Ci) in which Co is concentration outside and Ci is concentration inside. Effect of Membrane Electrical Potential on Diffusion of Ions— The “Nernst Potential.” If an electrical potential is applied across the membrane, as shown in Figure 4–8 B, the electrical charges of the ions cause them to move through the membrane even though no concentration difference exists to cause movement. Thus, in the left panel of Figure 4–8 B, the concentration of negative ions is the same on both sides of the membrane, but a positive charge has been applied to the right side of the membrane and a negative charge to the left, creating an electrical gradient across the membrane. The positive charge attracts the negative ions, whereas the negative charge repels them. Therefore, net diffusion occurs from left to right.After much time, large quantities of negative ions have moved to the Factors That Affect Net Rate of Diffusion By now it is evident that many substances can diffuse through the cell membrane.What is usually important is the net rate of diffusion of a substance in the desired direction. This net rate is determined by several factors. Effect of Concentration Difference on Net Diffusion Through a Membrane. Figure 4–8 A shows a cell membrane with a substance in high concentration on the outside and low concentration on the inside.The rate at which the substance diffuses inward is proportional to the concentration of molecules on the outside, because this concentration determines how many molecules strike the outside of the membrane each second. Conversely, the rate at which molecules diffuse outward is proportional to their concentration inside the membrane. Therefore, the rate of net diffusion into the cell is proportional to the concentration on the outside minus the concentration on the inside, or: Net diffusion μ (Co - Ci) in which Co is concentration outside and Ci is concentration inside. Effect of Membrane Electrical Potential on Diffusion of Ions— The “Nernst Potential.” If an electrical potential is applied across the membrane, as shown in Figure 4–8 B, the electrical charges of the ions cause them to move through the membrane even though no concentration difference exists to cause movement. Thus, in the left panel of Figure 4–8 B, the concentration of negative ions is the same on both sides of the membrane, but a positive charge has been applied to the right side of the membrane and a negative charge to the left, creating an electrical gradient across the membrane. The positive charge attracts the negative ions, whereas the negative charge repels them. Therefore, net diffusion occurs from left to right.After much time, large quantities of negative ions have moved to the right, creating the condition shown in the right panel of Figure 4–8 B, in which a concentration difference of the ions has developed in the direction opposite to the electrical potential difference. The concentration difference now tends to move the ions to the left, while the electrical difference tends to move them to the right. When the concentration difference rises high enough, the two effects balance each other. At normal body temperature (37°C), the electrical difference that will balance a given concentration difference of univalent ions—such as sodium (Na+) ions—can be determined from the following formula, called the Nernst equation: in which EMF is the electromotive force (voltage) between side 1 and side 2 of the membrane, C1 is the concentration on side 1, and C2 is the concentration on side 2. This equation is extremely important in understanding the transmission of nerve impulses and is discussed in much greater detail in Chapter 5. Effect of a Pressure Difference Across the Membrane. At times, considerable pressure difference develops EMF in millivolts 61 log C C right, creating the condition shown in the right panel of Figure 4–8 B, in which a concentration difference of the ions has developed in the direction opposite to the electrical potential difference. The concentration difference now tends to move the ions to the left, while the electrical difference tends to move them to the right. When the concentration difference rises high enough, the two effects balance each other. At normal body temperature (37°C), the electrical difference that will balance a given concentration difference of univalent ions—such as sodium (Na+) ions—can be determined from the following formula, called the Nernst equation: in which EMF is the electromotive force (voltage) between side 1 and side 2 of the membrane, C1 is the concentration on side 1, and C2 is the concentration on side 2. This equation is extremely important in understanding the transmission of nerve impulses and is discussed in much greater detail in Chapter 5. Effect of a Pressure Difference Across the Membrane. At times, considerable pressure difference develops EMF in millivolts 61 log C C between the two sides of a diffusible membrane. This occurs, for instance, at the blood capillary membrane in all tissues of the body. The pressure is about 20 mm Hg greater inside the capillary than outside. Pressure actually means the sum of all the forces of the different molecules striking a unit surface area at a given instant.Therefore, when the pressure is higher on one side of a membrane than on the other, this means that the sum of all the forces of the molecules striking the channels on that side of the membrane is greater than on the other side. In most instances, this is caused by greater numbers of molecules striking the membrane per second on one side than on the other side.The result is that increased amounts of energy are available to cause net movement of molecules from the high-pressure side toward the low-pressure side. This effect is demonstrated in Figure 4–8 C, which shows a piston developing high pressure on one side of a “pore,” thereby causing more molecules to strike the pore on this side and, therefore, more molecules to “ diffuse” to the other side.
- Resting Potential There is normally a charge difference across the plasma membrane of a neuron. The outside of the membrane has a positive charge. The inside has a negative charge. Resting potential results from differences between sodium and potassium positively charged ions and negatively charged ions in the cytoplasm. Sodium ions are more concentrated outside the membrane, while potassium ions are more concentrated inside the membrane. This imbalance is maintained by the active transport of ions across the membrane known as the sodium potassium pump. This difference or potential is measured in millivolts. The resting potential is usually about -70mv. Two properties of the neuron membrane permit a resting potential: The lipid bilayer bars the free passage of potassium ions and sodium ions. Ions can flow from one side to the other through channels in transport proteins. There are more potassium ions inside and more sodium ions outside the resting neuron membrane. Potassium ions have a tendency to leak out by facilitated diffusion through channel proteins. Most of the sodium channels are "gated" and remain closed most of the time, keeping the concentration outside high. However, small amounts of sodium do leak in and must be pumped out (and potassium pumped in) by the sodium-potassium pump. Electrical potentials are generated across the membranes of neurons—and, indeed, all cells—because (1) there are differences in the concentrations of specific ions across nerve cell membranes, and (2) the membranes are selectively permeable to some of these ions. These two facts depend in turn on two different kinds of proteins in the cell membrane ( Figure 2.2 ). The ion concentration gradients are established by proteins known as active transporters , which, as their name suggests, actively move ions into or out of cells against their concentration gradients. The selective permeability of membranes is due largely to ion channels , proteins that allow only certain kinds of ions to cross the membrane in the direction of their concentration gradients. Thus, channels and transporters basically work against each other, and in so doing they generate the resting membrane potential, action potentials, and the synaptic potentials and receptor potentials that trigger action potentials. The structure and function of these channels and transporters are described in Chapter 4 . To appreciate the role of ion gradients and selective permeability in generating a membrane potential, consider a simple system in which a membrane separates two compartments containing solutions of ions. In such a system, it is possible to determine the composition of the two solutions and, thereby, control the ion gradients across the membrane. For example, take the case of a membrane that is permeable only to potassium ions (K+). If the concentration of K+ on each side of this membrane is equal, then no electrical potential will be measured across it ( Figure 2.3A ). However, if the concentration of K+ is not the same on the two sides, then an electrical potential will be generated. For instance, if the concentration of K+ on one side of the membrane (compartment 1) is 10 times higher than the K+ concentration on the other side (compartment 2), then the electrical potential of compartment 1 will be negative relative to compartment 2 ( Figure 2.3B ). This difference in electrical potential is generated because the potassium ions flow down their concentration gradient and take their electrical charge (one positive charge per ion) with them as they go. Because neuronal membranes contain pumps that accumulate K+ in the cell cytoplasm, and because potassium-permeable channels in the plasma membrane allow a transmembrane flow of K+, an analogous situation exists in living nerve cells. A continual resting efflux of K+ is therefore responsible for the resting membrane potential. In the hypothetical case just described, an equilibrium will quickly be reached. As K+ moves from compartment 1 to compartment 2 (the initial conditions on the left of Figure 2.3B ), a potential is generated that tends to impede further flow of K+. This impediment results from the fact that the potential gradient across the membrane tends to repel the positive potassium ions that would otherwise move across the membrane. Thus, as compartment 2 becomes positive relative to compartment 1, the increasing positivity makes compartment 2 less attractive to the positively charged K+. The net movement (or flux) of K+ will stop at the point (at equilibrium on the right of Figure 2.3B ) where the potential change across the membrane (the relative positivity of compartment 2) exactly offsets the concentration gradient (the 10× excess of K+ in compartment 1). At this electrochemical equilibrium , there is an exact balance between two opposing forces: (1) the concentration gradient that causes K+ to move from compartment 1 to compartment 2, taking along positive charge, and (2) an opposing electrical gradient that increasingly tends to stop K+ from moving across the membrane ( Figure 2.3B ). The number of ions that needs to flow to generate this electrical potential is very small (per cm2 of membrane, approximately 10-12 moles of K+, or 1012 K+ ions). This last fact is significant in two ways. First, it means that the concentrations of permeant ions on each side of the membrane remain essentially constant, even after the flow of ions has generated the potential. Second, the tiny fluxes of ions required to establish the membrane potential do not disrupt chemical electroneutrality because each ion has an oppositely charged counter ion (chloride ions in the example shown in Figure 2.3 ) to maintain the neutrality of the solutions on each side of the membrane. The concentration of K+ remains equal to the concentration of Cl- in the solutions in compartments 1 and 2, meaning that the separation of charge that creates the potential difference is restricted to the immediate vicinity of the membrane.
- Figure 2.1. Recording passive and active electrical signals in a nerve cell. (A) Two microelectrodes are inserted into a neuron; one of these measures membrane potential while the other injects current into the neuron. (B) Inserting the voltage-measuring microelectrode into the neuron reveals a negative potential, the resting membrane potential. Injecting current through the current-passing microelectrode alters the neuronal membrane potential. Hyperpolarizing current pulses produce only passive changes in the membrane potential. While small depolarizing currents also elict only passive responses, depolarizations that cause the membrane potential to meet or exceed threshold additionally evoke action potentials. Action potentials are active responses in the sense that they are generated by changes in the permeability of the neuronal membrane. The best way to observe an action potential is to use an intracellular microelectrode to record directly the electrical potential across the neuronal plasma membrane ( Figure 2.1 ). A typical microelectrode is a piece of glass tubing pulled to a very fine point (with an opening of less than 1 μm diameter) and filled with a good electrical conductor, such as a concentrated salt solution. This conductive core can then be connected to a voltmeter, such as an oscilloscope, to record the transmembrane voltage of the nerve cell. When a microelectrode is inserted through the membrane of the neuron, it records a negative potential, indicating that the cell has a means of generating a constant voltage across its membrane when it is at rest. This voltage, called the resting membrane potential , depends on the type of neuron being examined, but it is always a fraction of a volt (typically -40 to -90 mV). Action potentials represent transient changes in the resting membrane potential of neurons. One way to elicit an action potential is to pass electrical current across the membrane of the neuron. In normal circumstances, this current would be generated by the action of neurotransmitters released by other neurons, or by the transduction of an external stimulus at specialized regions of sensory neurons (sensory receptors in the skin, for example; see Unit II). In the laboratory, however, electrical current suitable for initiating an action potential can be readily produced by inserting a second microelectrode into the same neuron and then connecting the electrode to a battery. If the current delivered in this way is such as to make the membrane potential more negative ( hyperpolarization ), nothing very dramatic happens. The membrane potential simply changes in proportion to the magnitude of the injected current. Such hyperpolarizing responses do not require any unique property of neurons and are therefore called passive electrical responses. A much more interesting phenomenon is seen if current of the opposite polarity is delivered, so that the membrane potential of the nerve cell becomes more positive than the resting potential ( depolarization ). In this case, at a certain level of membrane potential called the threshold potential , an action potential occurs (see Figure 2.1B ). The action potential, which is an active response generated by the neuron, appears on an oscilloscope as a brief (about 1 ms) change from negative to positive in the transmembrane potential. Importantly, the amplitude of the action potential is independent of the magnitude of the current used to evoke it; that is, larger currents do not elicit larger action potentials. The action potentials of a given neuron are therefore said to be all-or-none, because they occur fully or not at all. If the amplitude or duration of the stimulus current is increased sufficiently, multiple action potentials occur, as can be seen in the responses to the three different current intensities shown at the right of Figure 2.1B . It follows, therefore, that the intensity of a stimulus is encoded in the frequency of action potentials rather than in their amplitude. This chapter addresses the underlying question of how nerve cells can generate electrical potentials by distributing ions across the neuronal membrane. Chapter 3 explores more specifically the means by which action potentials are produced and how these signals solve the problem of long-distance electrical conduction within nerve cells. Chapter 4 examines the properties of membrane molecules responsible for producing action potentials. Finally, Chapters 5 – 8 consider how electrical signals are transmitted from one nerve cell to another at synaptic contacts.
- Figure 2.5. Resting and action potentials entail permeabilities to different ions. (A) Hypothetical situation in which a membrane variably permeable to Na+ (red) and K+ (yellow) separates two compartments that contain both ions. For simplicity, Cl- ions are not shown in the diagram. (B) Schematic representation of the membrane ionic permeabilities associated with resting and action potentials. At rest, neuronal membranes are more permeable to K+ (yellow) than to Na+ (red); accordingly, the resting membrane potential is negative and approaches E K. During an action potential, the membrane becomes very permeable to Na+ (red); thus the membrane potential becomes positive and approaches E Na. The rise in Na+ permeability is transient, however, so that the membrane again becomes primarily permeable to K+ (yellow), causing the potential to return to its negative resting value. When a neuron receives signals, an abrupt, temporary reversal in the polarity is generated (an action potential). The inside becomes more positive. Any membrane that can produce action potentials is said to show membrane excitability. Voltage change causes voltage-gated channels in the membrane to open. As a result of ion flow through these channels, the inside of a neuron briefly becomes more positive than outside. This animation (Audio - Important) describes sodium - potassium pumps. "Graded" means that the signals at the input zone vary in magnitude depending on the intensity and duration of the stimulus. "Local" means the signal does not usually spread beyond the input zone. However, if the stimulation is strong enough, an adjacent trigger zone may respond. When a stimulus reaches a certain minimum, a threshold-gated channels open and sodium rushes in. In an accelerating way, more and more gates open (this is an example of positive feedback). At threshold, the opening of more gates no longer depends on the stimulus but is self-propagating. These two animations (Audio - Important) describe an action potential: action potential 1. action potential 2. Action potentials are all-or-nothing events. All action potentials are the same size. If stimulation is below threshold level, no action potential occurs. If it is above threshold level, the cell is always depolarized to the same level.
- Figure 3.12. Action potential conduction requires both active and passive current flow. Depolarization at one point along an axon opens Na+ channels locally (Point 1) and produces an action potential at this point (A) of the axon (time point t =1). The resulting inward current flows passively along the axon (2), depolarizing the adjacent region (Point B) of the axon. At a later time ( t =2), the depolarization of the adjacent membrane has opened Na+ channels at point B, resulting in the initiation of the action potential at this site and additional inward current that again spreads passively to an adjacent point (Point C) farther along the axon (3). At a still later time ( t =3), the action potential has propagated even farther. This cycle continues along the full length of the axon (5). Note that as the action potential spreads, the membrane potential repolarizes due to K+ channel opening and Na+ channel inactivation, leaving a “wake” of refractoriness behind the action potential that prevents its backward propagation (4). Panel to the left of the figure legend shows the changing membrane potential as a function of time at the points indicated.
- The Refractory Period The depolarization that produces Na+ channel opening also causes delayed activation of K+ channels and Na+ channel inactivation, leading to repolarization of the membrane potential as the action potential sweeps along the length of an axon (see Figure 3.12 ). In its wake, the action potential leaves the Na+ channels inactivated and K+ channels activated for a brief time. These transitory changes make it harder for the axon to produce subsequent action potentials during this interval, which is called the refractory period . Thus, the refractory period limits the number of action potentials that a given nerve cell can produce per unit time. As might be expected, different types of neurons have different maximum rates of action potential firing due to different types and densities of ion channels. The refractoriness of the membrane in the wake of the action potential explains why action potentials do not propagate back toward the point of their initiation as they travel along an axon.
- Criteria That Define a Neurotransmitter Three primary criteria have been used over the years to confirm that a molecule acts as a neurotransmitter at a given chemical synapse. 1. The substance must be present within the presynaptic neuron. Clearly, a chemical cannot be secreted from a presynaptic neuron unless it is present there. Because elaborate biochemical pathways are required to produce neurotransmitters, showing that the enzymes and precursors required to synthesize the substance are present in presynaptic neurons provides additional evidence that the substance is used as a transmitter. Note, however, that since the transmitters glutamate, glycine, and aspartate are also needed for protein synthesis and other metabolic reactions in all neurons, their presence is not sufficient evidence to establish them as neurotransmitters. 2. The substance must be released in response to presynaptic depolarization, and the release must be Ca2+-dependent . Another essential criterion for identifying a neurotransmitter is to demonstrate that it is released from the presynaptic neuron in response to presynaptic electrical activity, and that this release requires Ca2+ influx into the presynaptic terminal. Meeting this criterion is technically challenging, not only because it may be difficult to selectively stimulate the presynaptic neurons, but also because enzymes and transporters efficiently remove the secreted neurotransmitters. 3. Specific receptors for the substance must be present on the postsynaptic cell. A neurotransmitter cannot act on its target unless specific receptors for the transmitter are present in the postsynaptic membrane. One way to demonstrate receptors is to show that application of exogenous transmitter mimics the postsynaptic effect of presynaptic stimulation. A more rigorous demonstration is to show that agonists and antagonists that alter the normal postsynaptic response have the same effect when the substance in question is applied exogenously. High-resolution histological methods can also be used to show that specific receptors are present in the postsynaptic membrane (by detection of radioactively labeled receptor antibodies, for example). Fulfilling these criteria establishes unambiguously that a substance is used as a transmitter at a given synapse. Practical difficulties, however, have prevented these standards from being applied at many types of synapses. It is for this reason that so many substances must be referred to as "putative" neurotransmitters. Demonstrating the identity of a neurotransmitter at a synapse requires showing (1) its presence, (2) its release, and (3) the postsynaptic presence of specific receptors.
- Brain Plasticity--An Overview What is brain plasticity ? Does it mean that our brains are made of plastic? Of course not. Plasticity, or neuroplasticity, is the lifelong ability of the brain to reorganize neural pathways based on new experiences. As we learn, we acquire new knowledge and skills through instruction or experience. In order to learn or memorize a fact or skill, there must be persistent functional changes in the brain that represent the new knowledge. The ability of the brain to change with learning is what is known as neuroplasticity . To illustrate the concept of plasticity, imagine the film of a camera. Pretend that the film represents your brain. Now imagine using the camera to take a picture of a tree. When a picture is taken, the film is exposed to new information -- that of the image of a tree. In order for the image to be retained, the film must react to the light and “change” to record the image of the tree. Similarly, in order for new knowledge to be retained in memory, changes in the brain representing the new knowledge must occur. To illustrate plasticity in another way, imagine making an impression of a coin in a lump of clay. In order for the impression of the coin to appear in the clay, changes must occur in the clay -- the shape of the clay changes as the coin is pressed into the clay. Similarly, the neural circuitry in the brain must reorganize in response to experience or sensory stimulation FACT 1 : Neuroplasticity includes several different processes that take place throughout a lifetime. Neuroplasticity does not consist of a single type of morphological change, but rather includes several different processes that occur throughout an individual’s lifetime. Many types of brain cells are involved in neuroplasticity, including neurons, glia, and vascular cells. FACT 2 : Neuroplasticity has a clear age-dependent determinant. Although plasticity occurs over an individual’s lifetime, different types of plasticity dominate during certain periods of one’s life and are less prevalent during other periods. FACT 3 : Neuroplasticity occurs in the brain under two primary conditions: 1. During normal brain development when the immature brain first begins to process sensory information through adulthood (developmental plasticity and plasticity of learning and memory). 2. As an adaptive mechanism to compensate for lost function and/or to maximize remaining functions in the event of brain injury. FACT 4 : The environment plays a key role in influencing plasticity. In addition to genetic factors, the brain is shaped by the characteristics of a person's environment and by the actions of that same person. Developmental Plasticity: Synaptic Pruning Gopnick et al. (1999) describe neurons as growing telephone wires that communicate with one another. Following birth, the brain of a newborn is flooded with information from the baby’s sense organs. This sensory information must somehow make it back to the brain where it can be processed. To do so, nerve cells must make connections with one another, transmitting the impulses to the brain. Continuing with the telephone wire analogy, like the basic telephone trunk lines strung between cities, the newborn’s genes instruct the "pathway" to the correct area of the brain from a particular nerve cell. For example, nerve cells in the retina of the eye send impulses to the primary visual area in the occipital lobe of the brain and not to the area of language production (Wernicke’s area) in the left posterior temporal lobe. The basic trunk lines have been established, but the specific connections from one house to another require additional signals. Over the first few years of life, the brain grows rapidly. As each neuron matures, it sends out multiple branches (axons, which send information out, and dendrites, which take in information), increasing the number of synaptic contacts and laying the specific connections from house to house, or in the case of the brain, from neuron to neuron. At birth, each neuron in the cerebral cortex has approximately 2,500 synapses . By the time an infant is two or three years old, the number of synapses is approximately 15,000 synapses per neuron (Gopnick, et al., 1999). This amount is about twice that of the average adult brain. As we age, old connections are deleted through a process called synaptic pruning . Synaptic pruning eliminates weaker synaptic contacts while stronger connections are kept and strengthened. Experience determines which connections will be strengthened and which will be pruned; connections that have been activated most frequently are preserved. Neurons must have a purpose to survive. Without a purpose, neurons die through a process called apoptosis in which neurons that do not receive or transmit information become damaged and die. Ineffective or weak connections are "pruned" in much the same way a gardener would prune a tree or bush, giving the plant the desired shape. It is plasticity that enables the process of developing and pruning connections, allowing the brain to adapt itself to its environment. Plasticity of Learning and Memory It was once believed that as we aged, the brain’s networks became fixed. In the past two decades, however, an enormous amount of research has revealed that the brain never stops changing and adjusting. Learning, as defined by Tortora and Grabowski (1996), is “the ability to acquire new knowledge or skills through instruction or experience. Memory is the process by which that knowledge is retained over time.” The capacity of the brain to change with learning is plasticity. So how does the brain change with learning? According to Durbach (2000), there appear to be at least two types of modifications that occur in the brain with learning: A change in the internal structure of the neurons, the most notable being in the area of synapses. An increase in the number of synapses between neurons. Initially, newly learned data are "stored" in short-term memory, which is a temporary ability to recall a few pieces of information. Some evidence supports the concept that short-term memory depends upon electrical and chemical events in the brain as opposed to structural changes such as the formation of new synapses. One theory of short-term memory states that memories may be caused by “reverberating” neuronal circuits -- that is, an incoming nerve impulse stimulates the first neuron which stimulates the second, and so on, with branches from the second neuron synapsing with the first. After a period of time, information may be moved into a more permanent type of memory, long-term memory, which is the result of anatomical or biochemical changes that occur in the brain (Tortora and Grabowski, 1996). Injury-induced Plasticity: Plasticity and Brain Repair During brain repair following injury, plastic changes are geared towards maximizing function in spite of the damaged brain. In studies involving rats in which one area of the brain was damaged, brain cells surrounding the damaged area underwent changes in their function and shape that allowed them to take on the functions of the damaged cells. Although this phenomenon has not been widely studied in humans, data indicate that similar (though less effective) changes occur in human brains following injury. WHAT IS NEUROPLASTICITY, ANYWAY? The human brain is incredibly adaptive. Our mental capacity is astonishingly large, and our ability to process widely varied information and complex new experiences with relative ease can often be surprising. The brain’s ability to act and react in ever-changing ways is known, in the scientific community, as “neuroplasticity.” This special characteristic allows the brain’s estimated 100 billion nerve cells, also called neurons (aka “gray matter”), to constantly lay down new pathways for neural communication and to rearrange existing ones throughout life, thereby aiding the processes of learning, memory, and adaptation through experience. Without the ability to make such functional changes, our brains would not be able to memorize a new fact or master a new skill, form a new memory or adjust to a new environment; we, as individuals, would not be able to recover from brain injuries or overcome cognitive disabilities. Because of the brain’s neuroplasticity, old dogs, so to speak, regularly learn new tricks of every conceivable kind. WHAT PARTS OF THE BRAIN HAVE PLASTICITY? Plasticity Happens Wherever Neuro-processing Occurs Neuroplasticity is not a trait found in a single brain structure, nor does it consist of just one simple type of physical or chemical event. Rather, the brain’s ability to be molded – its plasticity – is the result of many different, complex processes that occur in our brains throughout our lifetime . A host of different structures and types of cells play some part in making neuroplasticity possible. There are even different types of plasticity that, depending on one’s age, are more or less involved in reshaping the brain as it handles new information. Plasticity works throughout the brain not just in the normal processes of learning and adaptation (most obvious in the early developmental years, though continuing throughout life), but also in response to injuries or diseases that cause loss of mental functioning. NEUROPLASTICITY AND THE NATURE/NURTURE DEBATE: WHICH IS IT? On The One Hand There’s Nature, On The Other, Nurture. While genetics certainly play a role in establishing the brain’s plasticity, the environment also exerts heavy influence in maintaining it. Take, for example, the newborn’s brain, which every day is flooded with new information. When the infant body receives input through its many different sensory organs, neurons are responsible for sending that input back to the part of the brain best equipped to handle it – and this requires each neuron to “know” something about the proper neural pathways through which to send its bits and pieces of information. To make this mental roadmap work, each neuron develops an axon to send information to other brain cells via electrical impulses, and also develops many dendrites that connect it to other neurons so that it can receive information from them. Each point of connection between two neurons is termed a “ synapse.” Our genes have, at birth, laid down the basic directions for neurons to follow along this roadmap, and have built its major “highways” between the basic functional areas of the brain. Environmental influence then plays the key role in forging a much denser, more complex network of interconnections. These smaller avenues and side roads, always under construction, can make the transfer of information between neurons more efficient and rich with situation-specific detail. This is clearly evidenced by the rapid increase in synaptic density that can be seen in a normally developing human. Genetics form a neural framework that, at birth, starts each neuron off with roughly 2,500 connections. By age two or three, however, sensory stimulation and environmental experience have taken full advantage of the brain’s plasticity; each neuron now boasts around 15,000 synapses. This number will have declined somewhat by the time we enter adulthood, as many of the more ineffective or rarely used connections – formed during the early years, when neuroplasticity is at its peak -- are done away with. HOW DOES NEUROPLASTICITY WORK? A Matter Of Neuron Networks And Connections. Complete neuron cell diagram. Neuroplasticity can work in two directions; it is responsible for deleting old connections as frequently as it enables the creation of new ones. Through this process, called “synaptic pruning,” connections that are inefficient or infrequently used are allowed to fade away, while neurons that are highly routed with information will be preserved, strengthened, made even more synaptically dense. Closely tied in with the pruning process, then, is our ability to learn and to remember. While each neuron acts independently, learning new skills may require large collections of neurons to be active simultaneously to process neural information; the more neurons activated, the better we learn. DOES NEUROPLASTICITY HELP ME LEARN AND REMEMBER? Remolding Connections Through Synaptic Transmission. Learning affects the brain in two different ways, neither of which would be possible without the special plasticity of our brains. In response to a new experience or novel information, neuroplasticity allows either an alteration to the structure of already-existing connections between neurons, or forms brand-new connections between neurons; the latter leads to an increase in overall synaptic density, while the former merely makes existing pathways more efficient or suitable. In either way, the brain is remolded to take in this new data and, if useful, retain it. While the precise mechanism that allows this process to occur is still unclear, some scientists theorize that long-term memories are formed successfully when something called “reverbration” occurs. When we are first exposed to something new, that information enters our short-term memory, which depends mostly upon chemical and electrical processes known as synaptic transmission to retain information, rather than deeper and more lasting structural changes such as those mentioned above. The electrochemical impulses of short-term memory stimulate one neuron, which then stimulates another; the key to making information last, however, occurs only when the second neuron repeats the impulse back again to the first. This is most likely to happen when we perceive the new information as especially important or when a certain experience is repeated fairly often. In these cases, the neural “echo” is sustained long enough to kick plasticity into high gear, leading to lasting structural changes that hard-wire the new information into the neural pathways of our brains. These changes result either in an alteration to an existing brain pathway, or in the formation of an all-new one. In this way, the new information or sensory experience is cemented into what seems, at its present moment, to be the most useful and efficient location within the massive neurocommunication network. Further repetition of the same information or experience may lead to more modifications in the connections that house it, or an increase in the number of connections that can access it – again, as a result of the amazing plasticity of our brains. THE DAMAGED OR DISABLED BRAIN: CAN NEUROPLASTICITY HELP? Rebuilding Connections That Rebuild Skills. Neuroplasticity is the saving grace of the damaged or disabled brain; without it, lost functions could never be regained, nor could disabled processes ever hope to be improved. Plasticity allows the brain to rebuild the connections that, because of trauma, disease, or genetic misfortune, have resulted in decreased abilities. It also allows us to compensate for irreparably damaged or dysfunctional neural pathways by strengthening or rerouting our remaining ones. While these processes are likely to occur in any number of ways, scientists have identified four major patterns of plasticity that seem to work best in different situations. Take, for example, the case in which healthy cells surrounding an injured area of the brain change their function, even their shape, so as to perform the tasks and transfer the signals previously dealt with by the now-damaged neurons at the site of injury. This process, called “functional map expansion,” results in changes to the amount of brain surface area dedicated to sending and receiving signals from some specific part of the body. Brain cells can also reorganize existing synaptic pathways; this form of plasticity, known as a “compensatory masquerade,” allows already-constructed pathways that neighbor a damaged area to respond to changes in the body’s demands caused by lost function in some other area. Yet another neuroplastic process, “homologous region adoption,” allows one entire brain area to take over functions from another distant brain area (one not immediately neighboring the compensatory area, as in functional map expansion) that has been damaged. And, finally, neuroplasticity can occur in the form of “cross model reassignment,” which allows one type of sensory input to entirely replace another damaged one. Cross-model reassignment allows the brain of a blind individual, in learning to read Braille, to rewire the sense of touch so that it replaces the responsibilities of vision in the brain areas linked with reading. One or several of these neuroplastic responses enable us to recover, sometimes with astonishing completeness, from head injury, brain disease, or cognitive disability. fMRI Images courtesy of Dr. Susan Bookheimer, Ahmanson-Lovelace Brain Mapping Center, UCLA The Brain showing plasticity with regeneration of function below, after the right hemisphere is removed. Reorganization after Hemispherectomy - 12 year old girl. NEUROPLASTICITY CAN’T LAST FOREVER . . . CAN IT? From Fresh Experiences Throughout Your Lifetime. Contrary to widespread belief, the “garden” of the brain never ceases being pruned and newly planted. Though long believed by scientists to be the case, research over the past decade or so has proven that our neural connections do not ever reach, by some age, a fixed pattern that thereafter cannot change. Rather, the ongoing process of synaptic reformation and death is what gives the brain its plasticity – its ability to learn and remember, to adapt to its environment and all the challenges brought with it, to acquire new knowledge and learn from fresh experiences – throughout an individual’s lifetime. Groundbreaking new research suggests that, beyond modifying pathways and forming new ones between existing neurons, the human brain is even able to generate entirely new brain cells. While this neural regeneration was long believed to be impossible after age three or four, research now shows that new neurons can develop late into the life span, even into the golden years of age 70 and beyond. Thus, the old adage “use it or lose it” is brought soundly home. If one’s brain is constantly challenged by and engaged with a variety of stimulations and new experiences, while also exposed regularly to that which it already knows, it is better able to retain its adaptive flexibility, regenerative capacity, and remarkable efficiency throughout life. WHAT DIRECTIONS MIGHT NEUROPLASTICITY TAKE IN THE FUTURE? Seeking A World Without Mental Health Issues. Current research suggests that neuroplasticity may be key to the development of many new and more effective treatments for brain damage, whether resulting from traumatic injury, stroke, age-related cognitive decline, or any number of degenerative diseases (Alzheimer’s, Parkinson’s, and cerebral palsy, among many others). Plasticity also offers hope to people suffering from cognitive disabilities such as ADHD, dyslexia, and Down Syndrome; it may possibly lead to breakthroughs in the treatment of depression, anorexia, and other behavioral and emotional disorders as well. Some scientists have even ventured to suggest that, one day, neuroplasticity could be used in short-circuiting the brain’s racist, sexist, or otherwise culturally unacceptable thinking patterns; even the body’s ability to perform intricate sequences of activities necessary for sports and other highly complex physical processes might eventually be perfected through the power of neuroplasticity. Whether currently in use or only the product of futuristic hopes, the theory upon which harnessing the brain’s plasticity is based is a relatively simple one. With “directed neuroplasticity,” scientists and clinicians can deliver calculated sequences of input, and/or specific repetitive patterns of stimulation, to cause desirable and specific changes in the brain. As further research reveals the best ways to create and direct these stimuli, the amazing potential of the brain’s plasticity can begin to be taken advantage of in medicine, mental health, and a wealth of as-yet-uncharted territory in human behavior and consciousness. Thus, increasing our understanding of neuroplasticity holds great promise – through its complex workings – skills lost can be relearned; the decline of abilities can be staved off, even reversed; and entirely new functions can even, perhaps, be gained.
- A flexure in the long axis of the nervous system arose as humans evolved upright posture, leading to an approximately 120° angle between the long axis of the brainstem and that of the forebrain (A). The consequences of this flexure for anatomical terminology are indicated in (B). The terms anterior, posterior , superior , and inferior refer to the long axis of the body, which is straight. Therefore, these terms indicate the same direction for both the forebrain and the brainstem. In contrast, the terms dorsal , ventral , rostral , and caudal refer to the long axis of the central nervous system. The dorsal direction is toward the back for the brainstem and spinal cord, but toward the top of the head for the forebrain. The opposite direction is ventral. The rostral direction is toward the top of the head for the brainstem and spinal cord, but toward the face for the forebrain. The opposite direction is caudal. (C) The major planes of section used in cutting or imaging the brain. To understand the spatial organization of these systems, some additional vocabulary employed to describe them needs to be defined. The terms used to specify location in the central nervous system are the same as those used for the gross anatomical description of the rest of the body ( Figure 1.9 ). Thus, anterior and posterior indicate front and back; rostral and caudal, toward the head and tail; dorsal and ventral, top and bottom; and medial and lateral, the midline or to the side. Nevertheless, the comparison between these coordinates in the body versus the brain can be confusing. For the entire body these anatomical terms refer to the long axis, which is straight. The long axis of the central nervous system, however, has a bend in it. In human and other bipeds, a compensatory tilting of the rostral/caudal axis for the brain is necessary to properly compare body axes to brain axes. Once this adjustment has been made, the other axes for the brain can be easily assigned. The proper assignment of these anatomical axes then dictates the standard planes for histological sections or tomographic images used to study the internal anatomy of the brain (see Figure 1.9C) . Horizontal sections are taken parallel to the rostral/caudal axis of the brain. Sections taken in the plane dividing the two hemispheres are sagittal , and can be further categorized as median and paramedian according to whether the section is near the midline (median or midsagittal) or more lateral (paramedian). Sections in the plane of the face are called frontal or coronal. Different terms are usually used to refer to sections of the spinal cord. The plane of section orthogonal to the long axis of the cord is called transverse , whereas sections parallel to the long axis of the cord are called longitudinal . In a transverse section through the human spinal cord, the dorsal and ventral axes and the anterior and posterior axes indicate the same directions. Tedious though this terminology may be, it is essential for understanding the basic subdivisions of the nervous system.
- The central nervous system (defined as the brain and spinal cord) is usually considered to have seven basic parts: the spinal cord , the medulla , the pons , the cerebellum , the midbrain , the diencephalon , and the cerebral hemispheres ( Figure 1.10 ; see also Figure 1.8 ). The medulla, pons, and midbrain are collectively called the brainstem ( Box A ); the diencephalon and cerebral hemispheres are collectively called the forebrain . Within the brainstem are found cranial nerve nuclei that either receive input from cranial sensory ganglia via their respective cranial sensory nerves or give rise to axons that constitute cranial motor nerves ( Table 1.1 ). In addition, the brainstem is the conduit for several major tracts in the central nervous system. These tracts either relay sensory information from the spinal cord and brainstem to the midbrain and forebrain, or relay motor commands from the midbrain and forebrain back to motor neurons in the brainstem and spinal cord. Figure 1.10. The subdivisions and components of the central nervous system. (A) A lateral view indicating the seven major components of the central nervous system. (Note that the position of the brackets on the left side of the figure refers to the vertebrae, not the spinal segments.) (B) The central nervous system in ventral view, indicating the emergence of the segmental nerves and the cervical and lumbar enlargements. (C) Diagram of several spinal cord segments, showing the relationship of the spinal cord to the bony canal in which it lies.
- Left Brain Logical Sequential Rational Analytical Objective Looks at parts Right Brain Random Intuitive Holistic Synthesizing Subjective Looks at wholes