Jj. Wang et al., Agatoxin-IVA-sensitive calcium channels mediate the presynaptic and postsynaptic nicotinic activation of cardiac vagal neurons, J NEUROPHYS, 85(1), 2001, pp. 164-168
Whole cell currents and miniature glutamatergic synaptic events (minis) wer
e recorded in vitro from cardiac vagal neurons in the nucleus ambiguus usin
g the patch-clamp technique. We examined whether voltage-dependent calcium
channels were involved in the nicotinic excitation of cardiac vagal neurons
. Nicotine evoked an inward current, increase in mini amplitude, and increa
se in mini frequency in cardiac vagal neurons. These responses were inhibit
ed by the nonselective voltage-dependent calcium channel blocker Cd (100 mu
M). The P-type voltage-dependent calcium channel blocker agatoxin IVA (100
nM) abolished the nicotine-evoked responses. Nimodipine (2 muM), an antagon
ist of L-type calcium channels, inhibited the increase in mini amplitude an
d frequency but did not block the ligand gated inward current. The N- and Q
-type voltage-dependent calcium channel antagonists conotoxin GVIA (1 muM)
and conotoxin MVIIC (5 muM) had no effect. We conclude that the presynaptic
and postsynaptic facilitation of glutamatergic neurotransmission to cardia
c vagal neurons by nicotine involves activation of agatoxin-IVA-sensitive a
nd possibly L-type voltage-dependent calcium channels. The postsynaptic inw
ard current elicited by nicotine is dependent on activation of agatoxin-IVA
-sensitive voltage-dependent calcium channels.