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J Neurophysiol (February 16, 2005). doi:10.1152/jn.00770.2004
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Submitted on July 29, 2004
Accepted on February 11, 2005

5-HT1B Receptor-Mediated Presynaptic Inhibition of GABA Release in the Suprachiasmatic Nucleus

Jayne R. Bramley1*, Patricia J. Sollars1, Gary E. Pickard1, and F. Edward Dudek1

1 Department of Biomedical Sciences - Anatomy & Neurobiology Section, Colorado State University, Fort Collins, CO, USA

* To whom correspondence should be addressed. E-mail: jbramley{at}lamar.colostate.edu.

The suprachiasmatic nucleus (SCN) receives a dense serotonergic innervation that modulates photic input to the SCN via serotonin 1B (5-HT1B) presynaptic receptors on retinal glutamatergic terminals. However, the majority of 5-HT1B binding sites in the SCN are located on non-retinal terminals and most axonal terminals in the SCN are GABAergic. We therefore tested the hypothesis that 5-HT1B receptors might also be located on SCN GABAergic terminals by examining the effects of the highly selective 5-HT1B receptor agonist CP-93,129 on SCN miniature inhibitory postsynaptic currents (mIPSCs). Whole-cell patch-clamp recordings of mIPSCs were obtained from rat and mouse SCN neurons in hypothalamic slices. Using CsCl-containing microelectrodes with QX314, we isolated mPSCs that were sensitive to the GABAA receptor antagonist, bicuculline. Bath application of CP-93,129 (1 µM) decreased the frequency of mIPSCs by an average of 22% (n=7) in rat SCN neurons and by an average of 30% (n=8) in mouse SCN neurons with no clear effect on mIPSC amplitude. In mice lacking functional 5-HT1B receptors, CP-93,129 (1 µM) had no clear effect on the frequency or the amplitude of mIPSCs recorded in any of the cells tested (n=4). The decrease in the frequency of mIPSCs of SCN neurons produced by the selective 5-HT1B receptor agonist CP-93,129 is consistent with the interpretation that 5-HT1B receptors are located on GABA terminals in the SCN and that 5-HT inhibits GABA release via a 5-HT1B presynaptic receptor-mediated mechanism.




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