AJP - Regu Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 271: R1707-R1712, 1996;
0363-6119/96 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nitz, D.
Right arrow Articles by Siegel, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nitz, D.
Right arrow Articles by Siegel, J. M.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 271, Issue 6 1707-R1712, Copyright © 1996 by American Physiological Society

ARTICLES

GABA release in posterior hypothalamus across sleep-wake cycle

D. Nitz and J. M. Siegel
Department of Neuroscience, University of California at Los Angeles 90024, USA.

The activity of neurons in the posterior hypothalamus (PH) is thought to contribute to the production of wakefulness and electroencephalograph 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 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 high-performance liquid chromatography methods for the quantification of glutamate, glycine, and gamma-aminobutyric acid (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 GABAA-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.


This article has been cited by other articles:


Home page
 J. Neurophysiol.Home page
Y.-P. Fan, E. M. Horn, and T. G. Waldrop
Biophysical Characterization of Rat Caudal Hypothalamic Neurons: Calcium Channel Contribution to Excitability
J Neurophysiol, December 1, 2000; 84(6): 2896 - 2903.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
A. May, A. Bahra, C. Buchel, R. S. J. Frackowiak, and P. J. Goadsby
PET and MRA findings in cluster headache and MRA in experimental pain
Neurology, November 14, 2000; 55(9): 1328 - 1335.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
T. Scammell, D. Gerashchenko, Y. Urade, H. Onoe, C. Saper, and O. Hayaishi
Activation of ventrolateral preoptic neurons by the somnogen prostaglandin D2
PNAS, June 23, 1998; 95(13): 7754 - 7759.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
J. E. Sherin, J. K. Elmquist, F. Torrealba, and C. B. Saper
Innervation of Histaminergic Tuberomammillary Neurons by GABAergic and Galaninergic Neurons in the Ventrolateral Preoptic Nucleus of the Rat
J. Neurosci., June 15, 1998; 18(12): 4705 - 4721.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online