Abstract
Rapid eye movement sleep (REMS) is generated in the brainstem by a distributed network of neurochemically distinct neurons. In the pons, the main subtypes are cholinergic and glutamatergic REMS-on cells and aminergic REMS-off cells. Pontine REMS-on cells send axons to the ventrolateral medulla (VLM), but little is known about REMS-related activity of VLM cells. In urethane-anesthetized rats, dorsomedial pontine injections of carbachol trigger REMS-like episodes that include cortical and hippocampal activation and suppression of motoneuronal activity; the episodes last 4–8 min and can be elicited repeatedly. We used this model to determine whether VLM catecholaminergic cells are silenced during REMS, as is typical of most aminergic neurons studied to date, and to investigate other REMS-related cells in this region. In 18 anesthetized, paralyzed and artificially ventilated rats, we obtained extracellular recordings from VLM cells when REMS-like episodes were elicited by pontine carbachol injections (10 mM, 10 nl). One major group were the cells that were activated during the episodes (n = 10). Their baseline firing rate of 3.7±2.1 (SD) Hz increased to 9.7±2.1 Hz. Most were found in the adrenergic C1 region and at sites located less than 50 µm from dopamine β-hydroxylase-positive (DBH+) neurons. Another major group were the silenced or suppressed cells (n = 35). Most were localized in the lateral reticular nucleus (LRN) and distantly from any DBH+ cells. Their baseline firing rates were 6.8±4.4 Hz and 15.8±7.1 Hz, respectively, with the activity of the latter reduced to 7.4±3.8 Hz. We conclude that, in contrast to the pontine noradrenergic cells that are silenced during REMS, medullary adrenergic C1 neurons, many of which drive the sympathetic output, are activated. Our data also show that afferent input transmitted to the cerebellum through the LRN is attenuated during REMS. This may distort the spatial representation of body position during REMS.
Highlights
Rapid eye movement sleep (REMS) is a state characterized by wake-like activation of the cortex and hippocampus accompanied by a loss of activity in postural muscles and a host of phasic phenomena, such as rapid eye movements, twitches of the distal limb and orofacial muscles, and variable breathing and arterial blood pressure [1]
Single cell recordings obtained from the pons indicated the presence of two major cell types likely to play a key role in the generation of REMS: the REMS-on cells that are tonically activated in association with the occurrence of REMS episodes and REMS-off cells that are suppressed or silenced in a reciprocal manner relative to the activity of the REMS-on neurons
We suggest that the REMS-related suppression of activity in lateral reticular nucleus (LRN) neurons may be of particular relevance in the condition known as the REMS behavior disorder (RBD) in which patients can execute complex motor task while they are in REMS based on all other electrophysiologic criteria
Summary
Rapid eye movement sleep (REMS) is a state characterized by wake-like activation of the cortex and hippocampus accompanied by a loss of activity in postural muscles (atonia) and a host of phasic phenomena, such as rapid eye movements, twitches of the distal limb and orofacial muscles, and variable breathing and arterial blood pressure [1]. REMS is the state when dreams occur and it plays an important role in brain development and processing of memories acquired during the waking states [2,3,4] It is a state whose expression characteristically changes with aging and neurodegenerative disorders [5,6,7,8]. The pontine REMS-on cells include cholinergic and glutamatergic neurons, whereas the best identified pontine REMS-off cells are those containing serotonin (dorsal raphe nucleus) and norepinephrine (locus coeruleus (LC)), designated as the A6 noradrenergic group) [11,12,13,14,15,16,17,18,19] Based on these findings, a reciprocal cholinergic-aminergic network model has been proposed to explain the generation of REMS [20], and it was subsequently modified to include pontine excitatory glutamatergic and inhibitory (GABA-ergic) neurons [21]. Further tests and refinements of the existing models are needed to advance our understanding of the mechanisms responsible for the generation of REMS and, to understand its physiologic role
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