Gaba release in the posterior hypothalamus across the sleep/wake
cycle.
Nitz, Douglas, and Jerome Siegel.
UCLA Depts. of Neuroscience and Psychiatry and Sepulveda, Sepulveda
Veterans Administration Medical Center, Neurobiology Research, 151A3,
16111 Plummer Street, Sepulveda, CA 91343
APStracts 3:0241R, 1996.
The activity of neurons in the posterior hypothalamus (PH) is thought
to contribute to the production of wakefulness and EEG
desynchronization. Inactivation of neuronal activity in this area is
known to induce sleep. Most PH neurons decrease unit discharge during
slow-wave sleep (SWS) relative to wake and rapid-eye-movement (REM)
sleep. In the present study, we sought to examine potential sources
of inhibition or disfacilitation underlying the reduction of PH unit
activity during SWS in the cat. We employed the microdialysis
technique in conjunction with HPLC methods for the quantification of
glutamate, glycine, and GABA release. We found a selective increase
in GABA release during SWS in the PH. Glutamate and glycine levels
were unchanged across the sleep/wake cycle. Microinjection of the
GABA-A receptor agonist muscimol, into the same areas from which
microdialysis samples were collected, increased SWS time. Our studies
support the hypothesis that GABA release in the posterior
hypothalamus mediates inhibition of posterior hypothalamic neurons,
thereby facilitating SWS.
Received 25 January 1996; accepted in final form 5 June 1996.
APS Manuscript Number R36-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96