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J Neurophysiol 89: 2473-2481, 2003. First published January 22, 2003; doi:10.1152/jn.00934.2002
0022-3077/03 $5.00
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J Neurophysiol (May 1, 2003). 10.1152/jn.00934.2002
Submitted on Submitted 25 October 2002; accepted in final form 14 January 2003

Endogenous Acetylcholine and Nicotine Activation Enhances GABAergic and Glycinergic Inputs to Cardiac Vagal Neurons

Jijiang Wang, Xin Wang, Mustapha Irnaten, Priya Venkatesan, Cory Evans, Sunit Baxi, and David Mendelowitz

Department of Pharmacology, George Washington University, Washington, DC 20037

Wang, Jijiang, Xin Wang, Mustapha Irnaten, Priya Venkatesan, Cory Evans, Sunit Baxi, and David Mendelowitz. Endogenous Acetylcholine and Nicotine Activation Enhances GABAergic and Glycinergic Inputs to Cardiac Vagal Neurons. J. Neurophysiol. 89: 2473-2481, 2003. The heart slows during expiration and heart rate increases during inspiration. This cardiorespiratory interaction is thought to occur by increased inhibitory synaptic events to cardiac vagal neurons during inspiration. Since cholinergic receptors have been suggested to be involved in this cardiorespiratory interaction, we tested whether endogenous cholinergic activity modulates GABAergic and glycinergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus, whether nicotine can mimic this facilitation, and we examined the nicotinic receptors involved. Cardiac vagal neurons in the rat were labeled with a retrograde fluorescent tracer and studied in an in vitro slice using patch-clamp techniques. Application of neostigmine (10 µM), an acetylcholinerase inhibitor, significantly increased the frequency of both GABAergic and glycinergic inhibitory postsynaptic currents (IPSCs) in cardiac vagal neurons. Exogenous application of nicotine increased the frequency and amplitude of both GABAergic and glycinergic IPSCs. The nicotinic facilitation of both GABAergic and glycinergic IPSCs were insensitive to 100 nM alpha -bungarotoxin but were abolished by dihydro-beta -erythrodine (DHbeta E) at a concentration (3 µM) specific for alpha 4beta 2 nicotinic receptors. In the presence of TTX, nicotine increased the frequency of GABAergic and glycinergic miniature synaptic events, which were also abolished by DHbeta E (3 µM). This work demonstrates that there is endogenous cholinergic facilitation of GABAergic and glycinergic synaptic inputs to cardiac vagal neurons, and activation of alpha 4beta 2 nicotinic receptors at presynaptic terminals facilitates GABAergic and glycinergic neurotransmission to cardiac vagal neurons. Nicotinic facilitation of inhibitory neurotransmission to premotor cardiac parasympathetic neurons may be involved in generating respiratory sinus arrhythmia.




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