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GABA B Receptor‐Activation Inhibits GABAergic Synaptic Transmission in Parvocellular Neurones of Rat Hypothalamic Paraventricular Nucleus
Author(s) -
Liu X.,
Tribollet E.,
Raggenbass M.
Publication year - 2006
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2005.01402.x
Subject(s) - gabaergic , gabab receptor , parvocellular cell , neuroscience , postsynaptic potential , inhibitory postsynaptic potential , chemistry , medicine , gabaa receptor , endocrinology , muscimol , receptor , biology , hypothalamus
The paraventricular nucleus of the hypothalamus contains three classes of neurones: (i) magnocellular and (ii) parvocellular neurosecretory neurones and (iii) nonendocrine projection neurones. The present study aimed to determine whether functional GABA B receptors are present on axon terminals that synapse with parvocellular neurosecretory and nonendocrine paraventricular neurones and to determine how activation of GABA B receptors control GABAergic input to these neurones. Whole‐cell recordings were performed in coronal hypothalamic slices of the rat containing the paraventricular nucleus. GABA A receptor–mediated inhibitory postsynaptic currents (i.p.s.c.) were isolated pharmacologically in the presence of antagonists of glutamatergic ionotropic receptors. We found that baclofen, an agonist of GABA B receptors, decreased the frequency of spontaneous and miniature i.p.s.c. It also decreased the amplitude of evoked i.p.s.c. These effects were suppressed by CGP55845A, a competitive antagonist of GABA B receptors. CGP55845A also increased the frequency of miniature i.p.s.c. and the amplitude of evoked i.p.s.c., suggesting that, in physiological conditions, presynaptic GABA B receptors exert a tonic inhibition on GABA release. Baclofen had no effect on GABA‐evoked postsynaptic currents, suggesting that the baclofen‐dependent suppression of GABAergic i.p.s.c. was exclusively due to a presynaptic action of the agonist. Our data indicate that GABA B receptors are present on axon terminals of GABAergic presynaptic neurones contacting parvocellular neurosecretory and nonendocrine paraventricular neurones, and suggest that GABA B receptors exert a tonic inhibition of GABA release from GABAergic terminals. Activation of these receptors causes disinhibition of parvocellular neurosecretory and nonendocrine paraventricular neurones.