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Voltage‐gated Ca 2+ channel subtypes mediating GABAergic transmission in the rat supraoptic nucleus
Author(s) -
Bhaukaurally Khaleel,
Panatier Aude,
Poulain Dominique A.,
Oliet Stéphane H. R.
Publication year - 2005
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.1460-9568.2005.04097.x
Subject(s) - metabotropic glutamate receptor , neurotransmission , chemistry , voltage dependent calcium channel , supraoptic nucleus , metabotropic receptor , gabaergic , inhibitory postsynaptic potential , glutamate receptor , neuroscience , receptor , biology , nucleus , calcium , biochemistry , organic chemistry
The supraoptic nucleus receives an abundant γ‐aminobutyric acid (GABA)ergic input which is inhibited by activation of various presynaptic metabotropic receptors. We here analysed the subtypes of voltage‐gated Ca 2+ channels intervening in the control of transmitter release at these synapses. To address this issue, we tested various specific inhibitors of Ca 2+ channels on evoked inhibitory postsynaptic currents (IPSCs). Blocking N‐ and P‐type voltage‐gated Ca 2+ channels with 1 µ m ω‐conotoxin‐GVIA and 20 n m ω‐agatoxin‐IVA, respectively, dramatically reduced IPSC amplitude. Q‐ and l ‐type Ca 2+ channels also contributed to GABAergic transmission, although to a lesser extent, as revealed by applications of 200 n m ω‐agatoxin‐IVA and of the dihydropyridines nifedipine (10 µ m ) and nimodipine (10 µ m ). Evoked IPSCs were insensitive to SNX‐482 (300 n m ), a blocker of some R‐type Ca 2+ channels. Analysis of selective blockade by the various antagonists suggested that multiple types of Ca 2+ channels synergistically interact to trigger exocytosis at some individual GABA release sites. We next investigated whether inhibition of GABA release in response to the activation of metabotropic glutamate, GABA and adenosine receptors involved the modulation of these presynaptic Ca 2+ channels. This was not the case, as the inhibitory actions of selective agonists of these receptors were unaffected by the presence of the different Ca 2+ channel antagonists. This finding suggests that these metabotropic receptors modulate GABAergic transmission through a different mechanism, downstream of Ca 2+ entry in the terminals, or upstream through the activation of K + channels.