neurobiology of sleep Flashcards

(26 cards)

1
Q

EEG (Electroencephalogram)

A

measures the EPSP and IPSPs of cerebral cortical neurons

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2
Q

EOG (Electro-oculogram

A

measures eye movements

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3
Q

EMG (Electromyogram)

A

measures skeletal muscle activity as well as heart rate and breathing pattern.

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4
Q

Phases of sleep are distinguished by

A

Synchronized or Desynchronized EEG

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5
Q

Desynchronized

A

means the EPSPs and IPSPs are not summing on the EEG

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6
Q

temporally Synchronized

A

when the EPSPs and IPSPs are temporally Synchronized, they sum up to a wave with greater amplitude on EEG

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7
Q

EEG findings memory key

A

BATS Drink Blood (b waves when awake, a in stage 1, q waves during late stage 1, sleep spindles during stage 2, d waves during stage 4, b waves return during REM)

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8
Q

Non-Rapid Eye Movement Sleep

A

(characterized by Synchronized EEG) “Idling brain in a movable body”

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9
Q

Non rapid eye movement sleep: ‘vagal tone’

A

regular HR, RR, BP, muscle tone, ß brain O2 consumption, homeothermic, ß erections

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10
Q

Stage 1

A

Transitional between wakefulness and stage 2
- during wakefulness and early stage 1, the EEG is desynchronized

  • during drowsiness, there is synchronizing of EEG that is especially apparent over occipital cortex forming alpha waves.
  • late stage 1 shows slowing in the EEG with low voltage desynchronized theta waves of moderate frequency (3-7Hz)
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11
Q

Stage 2

A

Light NREM sleep

EEG has “sleep spindles” (High frequency bursts-12-14Hz) and K complexes which are related to d waves

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12
Q

Stage 3

A

Transitional between light and deep NREM sleep (low % d waves)

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13
Q

Stage 4

A

Deep NREM sleep; highest threshold for arousal – difficult to wake up
EEG has highly synchronized, high amplitude, low frequency (0.5-2Hz) d waves

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14
Q

Deafferntation Theory of Sleep:

A

loss of sensory input from brainstem Þ sleep

  • ascending Reticular Activating System (MRF, PRF, Med RF) is very important for wakefulness, as are LC, LDT/PPT and Raphe nuclei
  • lesions through the rostral brainstem cause synchronized EEG at first, due to the disconnection of above structures with cortex
  • eventually desynchronized waves will return after lesion is made
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15
Q

Sleep as an active process

A

argues that hypothalamic inputs cause sleep

VLPO
TMN

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16
Q

Sleep as an active process: VLPO

A

VLPO: Ventrolateral preoptic nucleus is small, contains adenosine receptors (caffeine blocks these) and is in anterior hypothalamus

  • lesions of VLPO results in insomnia = permanently desynchronized EEG
  • suprachiasmatic nucleus (sets circadian rhythms) interacts with VLPO
  • Theory = VLPO has active control over the process of sleep
17
Q

Sleep as an active process:

Tubero mammilary nucleus (TMN)

A

In posterior hypothalamus; projects to and activates broad areas of cortex; stimulation causes EEG to de-synchronize

  • histamine is neurotransmitter, so antihistamine may cause drowsiness by interrupting this system
  • studies show that NREM sleep is an actively controlled process by VLPO which contains inhibitory GABA in its projections to the posterior hypothalamus, shutting off TMN as well as LC, Dorsal Raphe and LDT/PPT
18
Q

Mechanism for Synchronized EEG of Sleep:

A

loop of cortical thalamic neurons

  • 3-cell loop contains neurons in the reticular thalamic nucleus, thalamic cortical neurons and cortico-thalamic neurons
  • during wakefulness there is activation of cortical neurons by LC, Dorsal Raphe, LDT/PPT and TMN of hypothalamus
  • during wakefulness the thalamic cells spend most of their time depolarized
  • during sleep there is loss of excitatory input from reticular nuclei which allows thalamic neurons to hyperpolarize
  • the intrinsic pattern of cortico-neurons is slow oscillation of there membrane potential
  • summation results from the hyperpolarized thalamic-cortico loops expressing their intrinsic properties which gives rise to rhythmic, repetitive, synchronized, inputs to the cortex which allow recording of Synchronized EEG
  • so the cortex is deafferntated, but it is done actively. (nucleus solitarius can also do this but unknown how)
19
Q

REM

A

Rapid Eye Movement Sleep (characterized by Desynchronized EEG) “Highly active brain in a paralyzed
body”

20
Q

also called Paradoxical sleep because EEG pattern is the same as awake; EEG characterized by saw tooth waves.

21
Q

REM: tone

A

spiking “sympathetic tone”: irregular HR, RR, BP, atonia, Ý brain O2 consumption, polkilothermic, Ý erections, etc.

22
Q

2 stages of REM

A

Phasic: associated with eye movements and myoclonic twitches.
Tonic: period between these phasic events.

23
Q

Polysomnography:

A

which records EEG, EOG and EMG at the same time help distinguish REM from NREM and Wakefulness.

24
Q

EMG in wakefulness versus REM

A

during wakefulness there is tonic and phasic EMG activity vs REM in which EMG shows muscle Atonia (paralysis)

25
REM activity in excitatory ACH cells of LDT/PPT project to:
1) Thalamus and remove inhibitory currents from VLPO which results in Desynchronization on the EEG (2) area of Magoun and Rhines located in MedR which inhibits a motor neurons when stimulated Þ Atonia
26
Monoaminergic cell groups
such as LC(norepinephrine), Raphe (serotonin) and TMN (histamine), which are also active during wakeful Desynchronization are inactive during REM sleep.