NT, promotes wakefulness, NE levels in LC, amygdala, nucleus, accumbens, and prefrontal cortex greater during wakefulness than during sleep. most importantly LC.
REM sleep characteristics
Rapid eye movement sleep, aka paradoxical sleep. Characterized by rapid eye movements, muscle atonia, cortical activation. Occurs ~ 90 mins. after sleep onset, and in ~90 min. intervals after first REM stage. Irregular respiration and heart rates, and body temp. Dreaming usually occurs during REM.
REM sleep generation/inhibition
REM sleep generating neurons localized to pons. 5-HT and NE inhibit REM
Inhibits REM, promotes arousal. 5-HT levels in the dorsal raphé nucleus (DR), cortex, and thalamus are greatest during wakefulness, intermediate in NREM sleep, and lowest during REM sleep. However, can have biphasic effect on wakefulness by contributing to the production of one or more sleep-enhancing substance, or inhibiting wakefulness producing neurons.
ACh release high during high cortical activity (REM and Wake). Promotes REM. AChergic neurons located Basal Forebrain and LDT/PPT. ACh Release in the PRF is Greatest during REM Sleep. LDT/PPT cholinergic neurons are REM-On and Wake On/REM-On. Basal forebrain ACh lowest during NREM.
Increases wakefulness. DAergic neurons of importance project located in ventral tegmental area (VTA) and substantia nigra, project to dorsal raphe nucleus (DR), locus coeruleus, LDT/PPT, basal forebrain and thalamus. Mean firing rate stable across sleep states, but variability is significantly different. In prefrontal cortex and nucleus accumbens, DA levels higher in W and REM than NREM.
Wakefulness promoting drug that increases DA levels in caudate nucleus. But if DA transporters are knoecked out, has no effect.
REM Sleep Behavior Disorder
characterized by no muscle atonia during REM sleep; permits acting out of dreams • dreams are often violent or injurious • typically affects men > 50 y.o. • acute onset is induced by tricyclic antidepressants, SSRIs, SNRIs • effectively treated with clonazepam usually associated with reduced striatal DA.
inhibitory. In Brainstem : increases REM by inhibiting wakefulness neurons like LC and 5-HT DR. In Pontine Recticular Formation (PRF) neurons generate REM. GABA inhibits these neurons, decreasing REM. Anterior hypothalamus GABA greatest during REM: Sleep-on, GABAergic neurons in the VLPO and MnPN project to the major arousal-promoting, nuclei and inhibit them:• DR (5-HT) • LC (NE) • tubero-mammillary nucleus of the posterior hypothalamus (histamine) Posterior hypothalamus GABA induces sleep onset, greatest during NREM
Basal Forebrain and Hypothalamus sleep/wake generation
preoptic/anterior hypothalamus is sleep center. posterior hypothalamus is wakefulness center. Neurons that fire most during NREM in basal forebrain.
posterior hypothalamus (TM) HAergic neurons are Wake-on. project to ant. hypothalamus and LDT of brainstem to increase wakefulness.
Induces NREM, inhibits wakefulness. caffeine is adenosine receptor antagonist. Adenosine in ant. hyp decreases wakefulness, increases NREM. Only in basal forebrain, Adenosine levels increase during wakefulness, decreases during recovery sleep (sleep deprivation induced). Inhibits cholinergic basal forebrain neurons, disinhibits GABAergic sleep on neurons of VLPO
activates wake-promoting neurons in LC, DR, LatDorsTeg/PPT, PosHyp, SI. greater during actv. waking than quiet, and greater in slow wave (NREM) than REM (PS). H/O increases GABA in PRF, increasing wakefulness.
Kleitman and Richardson
Early biological clock studies, moved into a cave (dark all day). Figured out that biolocial clock is endogenously generated because we still have daily rhythms despite outside cues. (free running)
Master circadian pacemaker, endogenously generates circadian rhythms. Our biological clock is entrained to 24 hr environmental rhythm by acting in a phase dependent manner (rhythm peaks/troughs match up with zeitgeber peaks/troughs).
A time cue such as light, temp, food, social activity, attention etc.
your internal clock only reacts to a zeitgeber when it signals that environmental time is different from expected. Chronotype involves a coordinated phasing of multiple rhythms in the body
gene of SCN, expressed in circadian patterns. Responds to light, its relative abundance increases as light does.
Changes in plasticity over life
Synaptic network organization demands highest in developing/ learning brain. we get more REM and NREM as infants, both decrease w/ age.
a long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously.
Hippocampus and Memory
temporary memory assembly place & storehouse. Hippocmapus needed to form long-term memories (hours, days, weeks, years) Long term memories stored in parallel, distributed fashion in neocortex After which hippocampus can be cleared to avoid saturation (depotentiation).Hippocampal place cell patterns reactivate in sleep
ACh, NE, 5-HT and learning
ACh creates theta activity in the hippocampus Theta rhythm necessary for hippocampal learning (present only in REM and awakening) Absence of NE allows both sides of plasticity (LTP and LTD). Noradrenaline blocks depotentiation. But abnormal addition of NE via LC/noise/direct electrical stimulation enhances initial learning but prevents memory reoganization & reset in light of novel information.
antidepressants (desipramine) and learning
antidepressants like desipramine supress REM. impairs novel learning and familiar reconsolidation after reminders
sleep traits and learning
high Ach, low NE and 5HT, and high PG0 waves support learning and reorganization of memories
Two process model of sleep wake regulation
Process S = sleep propensity • Increases during waking • Decreases during sleep Process C = circadian rhythm • Sets thresholds for falling asleep and waking up limitations Model is phenomenological, S and C has no physiological basis, Does not include different sleep
Reciprocal interaction model for REM sleep cycling
predator/prey. 1) Illustrates that monoaminergic inhibition and cholinergic excitation between neural populations can generate cycling behavior 2) Dynamic model that captures cycling over time 3) Limit cycle properties can explain differences in 1st REM episode properties observed under different conditions.
Sleep-wake flip-flop model
neurons in VLPO more active in sleep, synapses are inhibitory to other wake active neurons.
REM sleep flip-flop models
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