JN Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


J Neurophysiol (July 5, 2007). doi:10.1152/jn.00575.2007
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
98/3/1323    most recent
00575.2007v1
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 Google Scholar
Google Scholar
Right arrow Articles by Kim, U.
Right arrow Articles by Chung, L.-y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kim, U.
Right arrow Articles by Chung, L.-y.
Submitted on May 22, 2007
Accepted on June 29, 2007

Dual GABAergic synaptic response of fast excitation and slow inhibition in the medial habenula of rat epithalamus.

Uhnoh Kim1* and Lee-yup Chung2

1 Neurosurgery, Penn State University College of Medicine, Hershey, Pennsylvania, United States
2 Psychiatry, Duke University Medical Center, Durham, North Carolina, United States

* To whom correspondence should be addressed. E-mail: ukim{at}hmc.psu.edu.

We report here a novel action of GABAergic synapses in regulating tonic firing in the mature mammalian brain. By using gramicidin-perforated patch recording in rat brain slices, we show that cells of the medial habenula of the epithalamus generate tonic firing in basal conditions. The GABAergic input onto these cells generates a combinatorial activation of fast excitation and slow inhibition. The fast excitation is mediated by GABAA receptors and alone capable of triggering robust action potentials to increase cell firing. This excitatory influence of the GABAergic input results from the Cl- homeostasis that maintains intracellular Cl- at high levels. The GABAA excitation is often followed by a slow inhibition mediated by GABAB receptors that suppresses tonic firing. Interestingly, in a subpopulation of the cells, the GABAB inhibition exhibits a remarkably low threshold for synaptic activation in that low-strength GABAergic input often activates selectively the GABAB slow inhibition, whereas the GABAA excitation requires further increases in stimulus strength. Our study demonstrates that the dual activation of GABAergic excitation and inhibition through GABAA and GABAB receptors generates distinct temporal patterns of cell firing that alter the cellular output in an activity-dependent manner.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2007 by the The American Physiological Society.