The developmental decrease in REM sleep: the role of transmitters and electrical coupling.
OBJECTIVE
This mini-review considers certain factors related to the developmental decrease in rapid eye movement (REM) sleep, which occurs in favor of additional waking time, and its relationship to developmental factors that may influence its potential role in brain development.


METHODS
Specifically, we discuss some of the theories proposed for the occurrence of REM sleep and agree with the classic notion that REM sleep is, at the least, a mechanism that may play a role in the maturation of thalamocortical pathways. The developmental decrease in REM sleep occurs gradually from birth until close to puberty in the human, and in other mammals it is brief and coincides with eye and ear opening and the beginning of massive exogenous activation. Therefore, the purported role for REM sleep may change to involve a number of other functions with age.


RESULTS
We describe recent findings showing that morphologic and physiologic properties as well as cholinergic, gamma amino-butyric acid, kainic acid, n-methyl-d-aspartic acid, noradrenergic, and serotonergic synaptic inputs to mesopontine cholinergic neurons, as well as the degree of electrical coupling between mostly noncholinergic mesopontine neurons and levels of the neuronal gap-junction protein connexin 36, change dramatically during this critical period in development. A novel mechanism for sleep-wake control based on well-known transmitter interactions, as well as electrical coupling, is described.


CONCLUSIONS
We hypothesize that a dysregulation of this process could result in life-long disturbances in arousal and REM sleep drive, leading to hypervigilance or hypovigilance such as that observed in a number of disorders that have a mostly postpubertal age of onset.
Center for Translational Neuroscience, Department of Neurobiology & Developmental Science, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. GarciaRillEdgar@uams.edu
Edgar
E
Garcia-Rill
Amanda
A
Charlesworth
David
D
Heister
Meijun
M
Ye
Abdallah
A
Hayar
D000293:Adolescent; D000328:Adult; D000818:Animals; D001921:Brain / Q000502:physiology*; D002540:Cerebral Cortex / Q000502:physiology; D002648:Child; D002675:Child, Preschool; D017630:Connexins / Q000502:physiology; D005260:Female; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D020646:Intralaminar Thalamic Nuclei / Q000502:physiology; D008297:Male; D009415:Nerve Net / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology; D009474:Neurons / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology*; D011149:Pons / Q000502:physiology; D012154:Reticular Formation / Q000502:physiology; D012895:Sleep, REM / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*; D014851:Wakefulness / Q000502:physiology*; D000097004:Gap Junction delta-2 Protein
D017630:Connexins; D018377:Neurotransmitter Agents; D000097004:Gap Junction delta-2 Protein