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Local γ‐aminobutyric acid and glutamate circuit control of hypophyseotrophic corticotropin‐releasing factor neuron activity in the paraventricular nucleus of the hypothalamus
Author(s) -
Bartanusz V.,
Muller D.,
Gaillard R. C.,
Streit P.,
Vutskits L.,
Kiss J. Z.
Publication year - 2004
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2004.03167.x
Subject(s) - kainate receptor , cnqx , bicuculline , glutamatergic , ampa receptor , gabaergic , neuroscience , chemistry , neurotransmission , inhibitory postsynaptic potential , gabaa receptor , premovement neuronal activity , hypothalamus , gamma aminobutyric acid , glutamate receptor , medicine , endocrinology , biology , receptor , biochemistry
Paraventricular corticotropin‐releasing factor (CRF) neurons play a pivotal role in regulating neuroendocrine responses to stress. The mechanisms by which synaptic inputs control the activity of these neurons are not well understood. The present study was undertaken to determine the role of the intrinsic γ‐aminobutyric acid (GABA)‐ and glutamatergic neural circuits of the hypothalamic paraventricular nucleus (PVN) in the control of CRF neural activity. We show that in organotypic cultures of the PVN, blockade of the intrinsic GABAergic neurotransmission by the GABA A receptor antagonist bicuculline resulted in a significant increase in CRF secretion. The bicuculline‐induced CRF secretory activity was abolished by the coadministration of the selective α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazoleprionic acid (AMPA)/kainate receptor antagonist 6‐cyano‐7‐nitroquinoxaline‐2,3‐dione (CNQX). Electrical stimulation of the CRF cell division elicited glutamatergic extracellular field potentials that were dramatically enhanced by bicuculline and were suppressed by CNQX. These results show that the functional activity of CRF neurons in organotypic cultures of the PVN is under a tonic inhibitory influence of an intrinsic GABAergic circuit. Suppression of GABAergic transmission appears to have a permissive role for inducing an increased secretory activity of CRF neurons that is driven by an excitatory glutamatergic network via AMPA/kainate receptors.