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The Journal of Neurophysiology Vol. 81 No. 2 February 1999, pp. 447-454
Copyright ©1999 by the American Physiological Society
Department of Pharmacology, School of Medicine and Health Sciences, The George Washington University, Washington, DC 20037
N-type voltage-dependent calcium channels mediate the nicotinic
enhancement of GABA release in chick brain. The role of
voltage-dependent calcium channels (VDCCs) in the nicotinic
acetylcholine receptor (nAChR)-mediated enhancement of spontaneous
GABAergic inhibitory postsynaptic currents (IPSCs) was investigated in
chick brain slices. Whole cell recordings of neurons in the lateral
spiriform (SpL) and ventral lateral geniculate (LGNv) nuclei showed
that cadmium chloride (CdCl2) blocked the carbachol-induced
increase of spontaneous GABAergic IPSCs, indicating that VDCCs might be involved. To conclusively show a role for VDCCs, the presynaptic effect
of carbachol on SpL and LGNv neurons was examined in the presence of
selective blockers of VDCC subtypes.
-Conotoxin GVIA, a selective
antagonist of N-type channels, significantly reduced the nAChR-mediated
enhancement of
-aminobutyric acid (GABA) release in the SpL by 78%
compared with control responses. Nifedipine, an L-type channel blocker,
and
-Agatoxin-TK, a P/Q-type channel blocker, did not inhibit the
enhancement of GABAergic IPSCs. In the LGNv,
-Conotoxin GVIA also
significantly reduced the nAChR-mediated enhancement of GABA release by
71% from control values. Although
-Agatoxin-TK did not block the
nicotinic enhancement, L-type channel blockers showed complex effects
on the nAChR-mediated enhancement. These results indicate that the
nAChR-mediated enhancement of spontaneous GABAergic IPSCs requires
activation of N-type channels in both the SpL and LGNv.
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