Voltage-gated Ca2+ channel subtypes mediating GABAergic transmission in the rat supraoptic nucleus.

Khaleel Bhaukaurally, Aude Panatier, Dominique A. Poulain, Stéphane H. R. Oliet
European Journal of Neuroscience. 2005-05-01; 21(9): 2459-2466
DOI: 10.1111/j.1460-9568.2005.04097.x

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The supraoptic nucleus receives an abundant gamma-aminobutyric acid (GABA)ergic
input which is inhibited by activation of various presynaptic metabotropic
receptors. We here analysed the subtypes of voltage-gated Ca2+ channels
intervening in the control of transmitter release at these synapses. To address
this issue, we tested various specific inhibitors of Ca2+ channels on evoked
inhibitory postsynaptic currents (IPSCs). Blocking N- and P-type voltage-gated
Ca2+ channels with 1 micromomega-conotoxin-GVIA and 20 nmomega-agatoxin-IVA,
respectively, dramatically reduced IPSC amplitude. Q- and L-type Ca2+ channels
also contributed to GABAergic transmission, although to a lesser extent, as
revealed by applications of 200 nmomega-agatoxin-IVA and of the dihydropyridines
nifedipine (10 microm) and nimodipine (10 microm). Evoked IPSCs were insensitive
to SNX-482 (300 nm), a blocker of some R-type Ca2+ channels. Analysis of
selective blockade by the various antagonists suggested that multiple types of
Ca2+ 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 Ca2+ channels. This was
not the case, as the inhibitory actions of selective agonists of these receptors
were unaffected by the presence of the different Ca2+ channel antagonists. This
finding suggests that these metabotropic receptors modulate GABAergic
transmission through a different mechanism, downstream of Ca2+ entry in the
terminals, or upstream through the activation of K+ channels.


Auteurs Bordeaux Neurocampus