2 neural basis Flashcards
Why is the SCN considered to be the circadian clock?
- Lesions in animals cause a disruption in normal circadian rhythms. (Ibuku and Kawamura, 1995).
- Recording from the SCN shows 24 hour rhythms or record from a single cell. (Mohawk and Takeheshi, 2011).
How does the SCN maintain wakefulness?
In the morning light travels via photosensitive reinal ganglion cells to the SCN. This inhibits melatonin secretion in the pineal gland. This feedback to the SCN. Therefore, the SCN sends excitation projections to wake promoting areas: thalamus, basal forebrain (cholinergic activity). Ascending arousal system: Schwartz and Roth (2008).
This is modulated by Hypocretin (synthesised in the lateral and posteral hypothalamus).
How do we know when to sleep?
In the evening, when it gets dark the pineal secretes melatonin. This feedback to the SCN via melatonin receptors and has inhibitory effects-.
How does sleep pressure (homeostasis) effect sleep?
Throughout the day, ATP is used up and causes a bi-product- adenosine. This builds up in the basal forebrain and blocks excitation cholinergic activity.
- It also inhibits hypocretin.
Hypocretin is a neuromodulator which regulates the switch between sleep and wake.
Once inhibited it can no longer regulate wake promoting systems.
This activates the VLPO- ventrolateral preoptic area of the hypothalamus. This inhibits the neurotransmitters involved in arousal through the use of GABA and Galanin.
When is sleep initiated (Moore, 2007)
Sleep is initiated when the circadian drive for alertness is overtaken by sleep pressure.
How is sleep measured?
EEG, EOG, EMG - polysomnography.
stage 1 sleep.
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 a waves.
late stage 1 shows slowing in the EEG with low voltage desynchronized theta waves of moderate frequency (3-7Hz)
Stage 2 sleep.
Light NREM sleep
EEG has “sleep spindles” (High frequency bursts-12-14Hz) and K complexes which are related to d waves
stage 3 sleep
Transitional between light and deep NREM sleep (low % d waves)
stage 4 sleep (SWS)
Deep NREM sleep; highest threshold for arousal – difficult to wake up
EEG has highly synchronized, high amplitude, low frequency (0.5-2Hz) d waves
neural basis for NREM sleep: Deafferntation Theory of Sleep:
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
neural basis for NREM sleep: Sleep as an active process:
argues that hypothalamic inputs cause sleep
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
Tubero mammilary nucleus (TMN) – 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
REM sleep
EEG: low-voltage (<20 :V), high frequency (>12 Hz) waves, and sawtooth waves
EOG: episodic, conjugate rapid eye movements
EMG: Atonia occasional myoclonic twitches
PGO waves: Ponto-geniculo-occipital waves (have not been recorded in humans)EEG: low-voltage (<20 :V), high frequency (>12 Hz) waves, and sawtooth waves
EOG: episodic, conjugate rapid eye movements
EMG: Atonia occasional myoclonic twitches
PGO waves: Ponto-geniculo-occipital waves (have not been recorded in humans)
