The Journal of Neurophysiology Vol. 85 No. 1 January 2001, pp. 164-168
Copyright ©2001 by the American Physiological Society
Agatoxin-IVA-Sensitive Calcium Channels Mediate the Presynaptic
and Postsynaptic Nicotinic Activation of Cardiac Vagal Neurons
Jijiang
Wang,
Mustapha
Irnaten, and
David
Mendelowitz
Department of Pharmacology, George Washington University,
Washington, DC 20037
Wang, Jijiang,
Mustapha Irnaten, and
David Mendelowitz.
Agatoxin-IVA-Sensitive Calcium Channels Mediate the Presynaptic
and Postsynaptic Nicotinic Activation of Cardiac Vagal Neurons. J. Neurophysiol. 85: 164-168, 2001. Whole cell currents and miniature glutamatergic synaptic events (minis)
were recorded in vitro from cardiac vagal neurons in the nucleus
ambiguus using 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 increase in mini frequency in cardiac
vagal neurons. These responses were inhibited by the nonselective
voltage-dependent calcium channel blocker Cd (100 µM). The P-type
voltage-dependent calcium channel blocker agatoxin IVA (100 nM)
abolished the nicotine-evoked responses. Nimodipine (2 µM), an
antagonist of L-type calcium channels, inhibited the increase in mini
amplitude and frequency but did not block the ligand gated inward
current. The N- and Q-type voltage-dependent calcium channel
antagonists conotoxin GVIA (1 µM) and conotoxin MVIIC (5 µM) had no
effect. We conclude that the presynaptic and postsynaptic facilitation
of glutamatergic neurotransmission to cardiac vagal neurons by nicotine
involves activation of agatoxin-IVA-sensitive and possibly L-type
voltage-dependent calcium channels. The postsynaptic inward current
elicited by nicotine is dependent on activation of
agatoxin-IVA-sensitive voltage-dependent calcium channels.
