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J Neurophysiol (January 22, 2003). doi:10.1152/jn.00934.2002
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Submitted on October 17, 2002
Accepted on January 14, 2003

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

Jijiang Wang1, Xin Wang1, Mustapha Irnaten1, Priya Venkatesan1, Cory Evans1, Sunit Baxi1, and David Mendelowitz*

1 Pharmacology, George Washington University, Washington, DC, USA

* To whom correspondence should be addressed. E-mail: dmendel{at}gwu.edu.

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 cardio-respiratory 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 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 post-synaptic 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 (DH{beta}E) at a concentration (3 µM) specific for {alpha}4{beta}2 nicotinic receptors. In the presence of tetrodotoxin nicotine increased the frequency of GABAergic and glycinergic miniature synaptic events (mIPSCs), which were also abolished by DH{beta}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}4{beta}2 nicotinic receptors at presynaptic terminals facilitates GABAergic and glycinergic neurotransmission to cardiac vagal neurons. Nicotinic facilitation of inhibitory neurotransmission to cardiac vagal neurons may be involved in generating respiratory sinus arrhythmia.




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