GABAB Receptor-Activation Inhibits GABAergic Synaptic Transmission in Parvocellular Neurones of Rat Hypothalamic Paraventricular Nucleus

Autor: Eliane Tribollet, Xinhuai Liu, Mario Raggenbass
Rok vydání: 2006
Předmět:
Phosphinic Acids/pharmacology
Male
Baclofen
medicine.medical_specialty
Endocrinology
Diabetes and Metabolism
Hypothalamus
Paraventricular Hypothalamic Nucleus/cytology/ drug effects/metabolism
In Vitro Techniques
Biology
GABAB receptor
Neurotransmission
Inhibitory postsynaptic potential
Baclofen/pharmacology
Synaptic Transmission
Receptors
GABA-B/ agonists/antagonists & inhibitors/metabolism
GABA Antagonists
Propanolamines
Rats
Sprague-Dawley
Cellular and Molecular Neuroscience
Endocrinology
Hypothalamus/cytology/ drug effects/metabolism
Parvocellular cell
Internal medicine
medicine
Animals
GABA Agonists
Propanolamines/pharmacology
GABA Agonists/pharmacology
Neurons
Endocrine and Autonomic Systems
GABAA receptor
Immunohistochemistry
Phosphinic Acids
ddc:616.8
Rats
GABA Antagonists/pharmacology
Receptors
GABA-B
nervous system
GABA-B Receptor Agonists
GABAergic
Neurons/ drug effects/metabolism
GABA-B Receptor Antagonists
Neuroscience
Paraventricular Hypothalamic Nucleus
Ionotropic effect
Zdroj: Journal of Neuroendocrinology, Vol. 18, No 3 (2006) pp. 177-186
ISSN: 1365-2826
0953-8194
DOI: 10.1111/j.1365-2826.2005.01402.x
Popis: 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.
Databáze: OpenAIRE
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