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This Article Full Text Full Text (PDF) All Versions of this Article: 98/3/1323    most recent 00575.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, U. Articles by Chung, L.-y. Search for Related Content PubMed PubMed Citation Articles by Kim, U. Articles by Chung, L.-y.

Dual GABAergic Synaptic Response of Fast Excitation and Slow Inhibition in the Medial Habenula of Rat Epithalamus

¹Department of Neurosurgery and Interdisciplinary Neuroscience Program, College of Medicine, Pennsylvania State University, Hershey, Pennsylvania; and ²Department of Psychiatry, Duke University Medical Center, Durham, North Carolina

Submitted 22 May 2007; accepted in final form 29 June 2007

We report here a novel action of GABAergic synapses in regulating tonic firing in the 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 at postnatal days 18–25 generates a combinatorial activation of fast excitation and slow inhibition. The fast excitation, mediated by -aminobutyric acid type A receptors (GABA_ARs), is alone capable of triggering robust action potentials to increase cell firing. This excitatory influence of GABAergic input results from the Cl^– homeostasis that maintains intracellular Cl^– at high levels. The GABA_A excitation is often followed by a slow inhibition mediated by GABA_BRs that suppresses tonic firing. Interestingly, in a subpopulation of the cells, the GABA_B inhibition exhibits a remarkably low threshold for synaptic activation in that low-strength GABAergic input often activates selectively the GABA_B slow inhibition, whereas the GABA_A excitation requires further increases in stimulus strength. Our study demonstrates that the dual activation of GABAergic excitation and inhibition through GABA_ARs and GABA_BRs generates distinct temporal patterns of cell firing that alter the cellular output in an activity-dependent manner.

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