This presentation discusses in detail the transients that occur mainly in late stage 1 and stage 2 of sleep, and may be confused to be pathological. The prototype here are theK complexes and the Sleep Spindles.
6. Sleep Spindles
• Compared to alpha rhythm !!
• One of the earliest described events
• Hallmark of Synchronization
• Requires an oscillator
7. Midpontine pre- trigeminal
Cerebellum
Encephale isole‘
Klimesch VO: BioIII
Normal sleep-wake cycle including REM
Cerveau isole‘
SWS
Thalamus
Sleep-wake cycle without REM
pproximate location of the three cuts for the human brain are
below.
7
12. T type calcium channel genes in
thalamus
α1G
α1H
α1I
Courtesy of E Talley, D Bayliss & E
Perez-Reyes
13. Post inhibitory rebound in thalamic
relay neurons
-60
Vm
-70
-80
Ca2+depende
nt
rebound
burst
IPSP
threshold
1
hT
0
T channels reprimed
100 ms
14. Thalamo-cortical reentrant loops.
Steriade, M. (1999). Coherent oscillations and
short-term plasticity in corticothalamic networks. TINS, Vol. 22 (8), 337-344.
Basic Circuitry:
Cortex
RE
Cortex
Dorsal Thal. = Relay Nuclei
RE
L-circ
Th-cx
Dendro-dendr.
Th-cx
RE
L-circ
Aff
‚Secondary neurons‘
15. 1,2
Afferent brainstem input to Th-cx (1),
Activation of RE and Cortex (2)
Cortex
L-circ
RE
Th-cx
Dendro-dendr.
Th-cx
RE
L-circ
Aff
16. 3 Excitatory processes in Cortex;
Inhibition of primary L-circ;
Inhibition of other RE cells
Cortex
L-circ
RE
Th-cx
Dendro-dendr.
Th-cx
RE
L-circ
Aff
17. 4
Excitatory feedback response from cortex.
Disinhibition of primary L-circ neurons.
Inhibition of secondary Th-cx neurons.
The resulting effect is that during time 4, Th-cx are again under inhibitory control from L-circ neurons and, at the same time are activated
from cortico-thalamic cells. Thus, only strong (converging and/or amplified) cortical feedback will trigger another excitatory activation
wave into the cortex in time 5.
Cortex
The strong
inhibition of the
secondary Th-cx
cell may lead to low
threshold spikes
(LTS) and, thus, to
a 10 Hz oscillation.
L-circ
RE
Th-cx
Th-cx
RE
L-circ
Aff
18. 5 The primary Th-cx cell may start a new excitatory burst into the cortex. At this stage
(because released from the L-circ inhibition), a new afferent input will have a strong effect.
The secondary Th-cx cells remain under inhibition
RESULT: Center-surround ‚on-off‘ effect with a resulting strong focal activation of
cortical target neurons.
Cortex
RE
L-circ
Th-cx
Th-cx
RE
L-circ
Aff
19. Summary of findings:
Afferent brainstem activation is missing and cortical activation is strong:
- Th-cx cells are hyperpolarized and oscillate with spindle frequency Note that a depol.
current pulse during maximal hyperpol. leads to high frequency bursts. The result is
increased oscillatory cortical activation leading to Delta activity.
- The effect of increased cortical activation is even larger if stimulation patterns are
oscillatory
SLEEP: Spindles and Delta
RE
Cortex
Th-cx hyperpolarized,
Sleep spindles
L-circ
Th-cx
Missing brainstem afferents
20. Spindle oscillations in thalamus
A M P A /N M D A R
T h a la m u s
G A B A AR
nR t
T C
+
timing
R ebound
B u rs t
E P S P &
B u rs t
IP S P
20 m V
C o rte x
-
200 m s
21. RE Cell Rapidly bursting type
A Mathematical model
Foundations II - Neuroimaging
29. K Complexes
• stage 2 sleep, arousing stimuli.
• Loomis et al. (1938);
• reason for calling them K complexes
remains obscure
• spur of the moment
• Knocking
• K complex shows a maximum over the
vertex,
• also K complexes with an indubitable
maximum over the frontal midline.
30. • H. Davis et al. - central and frontal K
complexes
• Brazier (1949) presumed two distinct
generators; these were area 6,
corresponding with the vertex, and area 9,
corresponding with frontal midline.
• initial sharp component, followed by a slow
component that fuses with a superimposed
fast component.
• The sharp component is biphasic and not
seldom multiphasic.
• The slow component is represented by a
large slow wave that may exceed 1,000
msec in duration
31.
32. Positive occipital sharp transients of sleep
POSTS start to occur in healthy people at age 4 years, become fairly common
by age 15 years, remain common through age 35 years, and start to disappear
by age 50 years.
POSTS are seen very commonly on EEG and have been said to be more
common during daytime naps than during nocturnal sleep.
Most characteristics of POSTS are contained in their name. They have a
positive maximum at the occiput, are contoured sharply, and occur in early
sleep (stages I and II). Their morphology classically is described as "reverse
check mark," and their amplitude is 50-100 µV. They typically occur in runs of
4-5 Hz and are bisynchronous, although they may be asymmetric. They persist
in stage II sleep but usually disappear in subsequent stag
33. Vertex sharp transients
Also called vertex waves or V waves, these transients are almost
universal. Although they often are grouped together with K complexes,
strictly speaking, vertex sharp transients are distinct from K
complexes. Like K complexes, vertex waves are maximum at the
vertex (central midline placement of electrodes [Cz]), so that,
depending on the montage, they may be seen on both sides, usually
symmetrically. Their amplitude is 50-150 µV. They can be contoured
sharply and occur in repetitive runs, especially in children. They persist
in stage II sleep but usually disappear in subsequent stages. Unlike K
complexes, vertex waves are narrower and more focal and by
themselves do not define stage II.
Notas do Editor
Incomplete synchrony, sparseness, also seen in vitro, higher synchrony seen during seizures
Roaming cortical activation, perhaps semi-random to reactivate cortical circuits during slow wave sleep
IMPORTANCE OF RT, inhibitory nucleus
A1g in dt, ai,h in nrt , leads to differences in bursts
A1g yellow, a1h red, a1i blue
Inhibition, excitation, rebound burst firing resulting from t type ca channels, next