In:
Science, American Association for the Advancement of Science (AAAS), Vol. 375, No. 6584 ( 2022-03-04), p. 972-973
Abstract:
How human brains regulate sleep remains an enduring puzzle ( 1 ). How sleep subserves human dreaming—rapid eye movement (REM) sleep—is especially puzzling. There is considerable mechanistic understanding of the synaptic, cellular, and circuit bases of REM sleep ( 2 , 3 ). However, despite pharmacological evidence that dopamine (DA) can potently modulate REM sleep, this neurotransmitter is conspicuously absent from most prevailing REM sleep circuit models. DA is historically associated with pleasure and addiction. On page 994 of this issue Hasegawa et al. ( 4 ) report that the release of DA in the basolateral amygdala (BLA), a brain structure associated with emotional processing, can trigger REM sleep in mice and also that selective manipulation of DA release within the BLA can trigger cataplexy, which occurs in the sleep disorder narcolepsy and manifests as a crippling pathologic intrusion of REM sleep into wakefulness that results in loss of postural motor control.
Type of Medium:
Online Resource
ISSN:
0036-8075
,
1095-9203
DOI:
10.1126/science.abo1987
Language:
English
Publisher:
American Association for the Advancement of Science (AAAS)
Publication Date:
2022
detail.hit.zdb_id:
128410-1
detail.hit.zdb_id:
2066996-3
detail.hit.zdb_id:
2060783-0
SSG:
11
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