Molecular Mechanisms of Pain. Part 1
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AACIMP 2011 Summer School. Neuroscience Stream. Lecture by Nana Voitenko.
![Bogomoletz Institute of Physiology, Kiev, Ukraine [email_address] Dr. NANA VOITENKO AACIMP KIEV - 2011 Molecular Mechanisms of Pain part I](https://image.slidesharecdn.com/kpi2011voitenko1-110909124958-phpapp01/85/molecular-mechanisms-of-pain-part-1-1-320.jpg)
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Molecular Mechanisms of Pain. Part 1
- 1. Bogomoletz Institute of Physiology, Kiev, Ukraine [email_address] Dr. NANA VOITENKO AACIMP KIEV - 2011 Molecular Mechanisms of Pain part I
- 4. Long term chronic pain, mainly inflammatory or neuropathic, afflicts about 25% of the general world population. More than 60% of people aged 65 plus complain of daily pains. This degree of disability has a huge economic toll in terms of loss of employment and disability payments but quality of life is equally compromised. Pain is thus a major medical issue but is not simply a sensation but an event that also triggers aversive and threatening psychological feelings. Intolerable pain is one of the main reason for euthanasia .
- 8. Organization of Cutaneous, Primary Afferent Input to the Dorsal Horn of the Spinal Cord Millan M.J. , 1999
- 9. NATURE CLINICAL PRACTICE NEUROLOGY, 2006 Mechanisms of peripheral and central sensitization in neuropathic pain P2X receptor ASICs
- 10. Receptors and Ionic Channels
- 12. Lingueglia, E. J. Biol. Chem. 2007;282:17325-17329 The ASIC family of ion channels
- 17. Ionic currents through different subunits of P2X receptors P2X3 P2X2/3 P2X2 P2X3+P2X2/3
- 18. [Ca 2+ ] i increase under activation of P2X receptors
- 19. GEOFFREY BURNSTOCK 2007 Physiology and Pathophysiology of Purinergic Neurotransmission Mechanisms of ATP-induced sensitization
- 21. Modulation of pain by AppCH 2 ppG – antagonist of P2X3 receptor Viatchenko-Karpinski et al, 2011 in press
- 25. T-channel subunits Iftinca et. al., 2006
- 26. Copyright ©2007 Society for Neuroscience Jagodic, M. M. et al. J. Neurosci. 2007;27:3305-3316 I ncrease in T-type current density in DRG neurons from diabetic rats.
Editor's Notes
- Neuropathic pain syndromes—pain after a lesion or disease of the peripheral or central nervous system—are clinically characterized by spontaneous and evoked types of pain, which are underpinned by various distinct pathophysiological mechanisms in the peripheral and central nervous systems. In some patients, the nerve lesion triggers molecular changes in nociceptive neurons, which become abnormally sensitive and develop pathological spontaneous activity. Inflammatory reactions of the damaged nerve trunk can induce ectopic nociceptor activity, causing spontaneous pain. The hyperactivity in nociceptors induces secondary changes in processing neurons in the spinal cord and brain, so that input from mechanoreceptive A-fibers is perceived as pain. Neuroplastic changes in the central pain modulatory systems can lead to further hyperexcitability.
- The time-dependent activation, the time to peak, measured over a range of test potentials from -65 mV to -30 mV. No significant difference was found The “window period” of T-type current is under neuropathic conditions has widened in comparison to control. The window period is the area were the activation and inactivation curves overlap. A window current can occur. Window current means the small range of voltage where T-type channels can open but not inactivate completely. There was a larger overlap area between activation and inactivation curves in the neuropathic cells. This indicated that more T-type calcium channels are available at physiological membrane potentials. Enhanced function of the T-type calcium channels under neuropathic condition.