Rem Sleep: Receptors Activated And Their Functions

Several receptors are activated during REM sleep, and their functions are still being discovered. MCH neurons, for example, are most active during REM sleep, but a subpopulation is only activated during wakefulness. The role of neurotransmitters, such as GABAA receptor agonism and antagonism in the amygdala, has been found to alter REM sleep expression. Additionally, serotonin application during non-REM sleep can induce rapid transitions into REM sleep, and cholinergic excitation increases the frequency of REM episodes. A recent hypothesis suggests that REM sleep regulates noradrenergic receptor sensitivity by upregulating or preventing the downregulation of brain norepinephrine (NE) receptors.

GABAA receptor agonism increases REM sleep amounts

GABAA receptor agonists are able to reduce sleep latency, increase sleep continuity, and promote non-rapid-eye-movement (NREM) sleep as well as the occurrence of spindles. In both rats and normal sleeping individuals, GABAA receptor agonists can also increase REM sleep amounts.

The activation of the BZ binding site by GABAA receptor agonism increases REM sleep amounts by increasing the EC50 for GABA greater than five-fold. This indicates an allosteric alteration of GABAA receptors and antagonism of GABA activity.

The activation of the BZ binding site by GABAA receptor agonism increases REM sleep amounts by increasing the EC50 for GABA greater than five-fold. This indicates an allosteric alteration of GABAA receptors and antagonism of GABA activity.

Serotonin produces rapid transitions into REM sleep

Serotonin is a neurotransmitter that is involved in the regulation of REM sleep. Serotonin is produced by neurons in the raphe nuclei (a midline system extending from the midbrain to the medulla). These serotonin cells are inactive during sleep, and their inactivity during REM sleep allows high voltage electrical activity to propagate from the pons to the thalamus and cortex, releasing associated eye movements and twitches.

Serotonin promotes the wake state and inhibits REM sleep. Serotonin cells in the dorsal raphe fail to switch off during REM sleep in cats with experimentally induced REM sleep without atonia. An increased serotonergic tone may induce REM sleep without atonia.

Serotonin, histamine, and norepinephrine cells normally turn off during REM sleep. The cessation of activity of these cells during REM sleep may be related to the loss of muscle tone during sleep.

Cholinergic excitation increases the frequency of REM episodes

Direct cholinergic activation and GABAergic inhibition induce the transition into REM sleep by activating SubC glutamatergic neurons. This interaction between the core of the REM-generating circuit and other forebrain, hypothalamic, and brainstem structures generates REM sleep and its characteristics, such as muscle paralysis.

The regulation of noradrenergic receptor sensitivity is also thought to be a function of REM sleep. This hypothesis is based on the observation that NE neurons of the locus coeruleus (LC) are tonically active in waking and non-REM sleep, but the entire population of LC NE neurons is inactive during REM sleep. The continuous presence of NE or adrenoceptor agonists downregulates NE receptors, while a reduction in NE availability upregulates these receptors.

Pharmacological agents can also have an impact on REM sleep duration. The release of NE or its functional enhancement through pharmacological agents that prevent its reuptake or degradation, or the direct activation of NE receptors by agonists, is thought to suppress or 'substitute' for REM sleep. This is achieved by increasing the activity of negative feedback circuits monitoring the efficiency of NE receptor action.

MCH neurons are most active during REM sleep

MCH neurons are activated by the accumulation of calcium ions. They are synchronised during REM sleep and are also activated during exploratory behaviour. They are thought to be involved in memory consolidation.

NE receptor downregulation is linked to REM sleep deprivation

Sleep is a complex process involving various neurotransmitters and brain structures. One of the critical aspects of sleep is REM (rapid-eye movement) sleep, which is associated with dreaming and memory consolidation. During REM sleep, the brain exhibits intense activity, and understanding the underlying mechanisms is essential for comprehending sleep regulation.

One hypothesis suggests that REM sleep plays a role in regulating noradrenergic receptor sensitivity. This hypothesis is based on the observation that norepinephrine (NE) neurons in the locus coeruleus (LC) exhibit different activity patterns during wakefulness, non-REM sleep, and REM sleep. Specifically, these neurons are tonically active during wakefulness and non-REM sleep but become entirely inactive during REM sleep.

The regulation of NE receptor sensitivity is crucial for maintaining a balance in the body. Prolonged exposure to NE or the continuous presence of adrenoceptor agonists leads to downregulation of NE receptors, while a reduction in NE availability upregulates these receptors. This regulatory mechanism is significant because the effects of REM sleep deprivation are similar to those observed with NE receptor downregulation.

Recent biochemical studies have provided strong support for the link between REM sleep and NE receptor regulation. These studies suggest that REM sleep may serve to upregulate or prevent the downregulation of brain NE receptors. This regulatory function of REM sleep could be essential for maintaining optimal NE receptor sensitivity and ensuring that the body can respond appropriately to changes in NE levels.

Furthermore, pharmacological manipulations of NE levels or receptor activity have been shown to impact REM sleep duration. Increasing NE levels or enhancing its function through pharmacological agents can suppress REM sleep by activating negative feedback circuits that monitor NE receptor efficiency. These findings highlight the intricate relationship between NE receptors and REM sleep, providing valuable insights into the complex nature of sleep regulation.

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