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First published online on November 8, 2002.
 Copyright © 2002 by The Physiological Society
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2002.025890v1
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Received June 3, 2002
Accepted after revision October 10, 2002

Interaction between AMPA-glutamate and SST2-somatostatin receptors in rat mediobasal hypothalamus requires activation of NMDA and/or metabotropic glutamate receptors and depends on intracellular calcium

Stéphane Peineau1, Brigitte Potier1, Florence Petit1, Pascal Dournaud1, Jacques Epelbaum1, and R. Gardette1*

1 INSERM U549, IFR Broca Sainte Anne, 2ter rue d'Alésia, 75014 Paris, France

* To whom correspondence should be addressed. E-mail: gardette{at}broca.inserm.fr.

Modulation of glutamatergic transmission by neuropeptides is an essential aspect of neuronal network activity. Activation of the hypothalamic somatostatin sst2 receptor subtype by octreotide decreases AMPA glutamate responses, indicating a central link between a neurohormonal and neuromodulatory peptide and the main hypothalamic fast excitatory neurotransmitter. In mediobasal hypothalamic slices, sst2 activation inhibits the AMPA component of glutamatergic synaptic responses but is ineffective when AMPA currents are pharmacologically isolated. In mediobasal hypothalamic cultures, the decrease of AMPA currents induced by octreotide requires a concomitant activation of sst2 receptors with either NMDA and/or metabotropic glutamate receptors. This modulation depends on changes in intracellular calcium concentration induced by calcium flux through NMDA receptors or calcium release from intracellular stores following metabotropic glutamate receptor activation. These results highlight an unusual regulatory mechanism in which the simultaneous activation of at least three different types of receptor is necessary to allow somatostatin-induced modulation of fast synaptic glutamatergic transmission in the hypothalamus.




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