Brain electrical activity differs markedly between wakefulness and sleep. Concomitant shifts in the ion composition of brain extracellular fluids. The ventrolateral preoptic nucleus contains GABAergic and galaninergic neurons that are active during sleep and are necessary for normal sleep. The posterior lateral hypothalamus contains orexin/hypocretin neurons that are crucial for maintaining normal wakefulness. Contrary to current scientific theories, our brains do not use several areas to control sleep and wakefulness, suggests a new study.
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Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement NREM sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights.
Single brain 'switch' controls both sleep and wakefulness
Rapid-eye-movement REM sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle control of sleep and wakefulness, REMs, dreaming, and cortical activation.
Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function.
These changes affect the level of depolarization of thalamic spindle pacemaker neurons as well as thalamocortical projection neurons. At this time, NREM sleep becomes increasingly characterized by high voltage, slow wave delta activity in the cortex.
The cellular basis of this activity depends on thalamocortical neurons, maintained in a hyperpolarized state by the absence of depolarizing input and generating synchronous bursts of discharges McCormick and Bal, ; Steriade et al. Control of sleep and wakefulness waves reflect these bursts of activity, transferred through the thalamocortical network, and synchronized as oscillations with cortical pyramidal cells, which are themselves discharging control of sleep and wakefulness a similar mode.
Importantly, this burst discharge mode in thalamic cells prevents the transfer of sensory information through the thalamus to the cortex, so maintaining the block on sensory input that is characteristic of sleep.
- CONTROL OF SLEEP AND WAKEFULNESS
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- Thalamic neurons drive sleep-wake cycle
control of sleep and wakefulness As noted above, another major influence on cortical activation originates in the BF, an important site for sleep homeostatic control and whose inactivation leads to increased slow wave activity.
Conversely, increased bursting activity of BF cholinergic neurons is associated with cortical activation and the appearance of gamma and theta frequencies on the EEG Lee et al.
EEG activation and the block of delta waves Neurotransmitters that depolarize thalamocortical and cortical cells will therefore prevent the appearance of delta waves. At this time, depolarized thalamocortical relay cells show the single-spike discharge mode, which allows the transfer of sensory input through the thalamus to the cortex.
Control of sleep and wakefulness.
During REM sleep, in contrast, the cholinergic and glutamatergic influence provide the depolarizing input without a contribution from the monoaminergic cells which are quiescent.
Principles and Practice of Sleep Medicine, 4th edition. Elsevier Saunders, Philadelphia, PA, pp. Unitary characteristics of presumptive cholinergic tegmental neurons during the sleep-waking cycle in freely moving cats.
Neurobiology of sleep and wakefulness - Scholarpedia
Persistence of circadian rhythmicity in a mammalian hypothalamic "island" containing the suprachiasmatic nucleus. From waking to sleeping: Trends Pharmacol Sci, What does a cat dream about? Cholinergic basal forebrain neurons burst with theta during waking and paradoxical sleep.
J Control of sleep and wakefulness, 25, A putative flip-flop switch for control of REM sleep.
Cholinergic and noradrenergic modulation of thalamocortical processing.