Tzu Chi Medical Journal
Volume 20, Issue 1 , Pages 11-18, March 2008

Source and Action of Pituitary Adenylate Cyclase-Activating Polypeptide in Guinea Pig Intrinsic Cardiac Ganglia

Department of Anatomy and Neurobiology, College of Medicine, University of Vermont, Vermont, USA

Received 1 September 2007; received in revised form 5 December 2007; accepted 6 December 2007.

Article Outline

Abstract 

The mammalian parasympathetic cardiac ganglia form a complex intrinsic cardiac nervous system presumed to contain multiple neuron types and are innervated by extrinsic fibers from multiple sources, each containing specific neurotransmitters and neuropeptides. In the guinea pig, the preganglionic parasympathetic cholinergic fibers contain the neuropeptide, pituitary adenylate cyclase-activating polypeptide (PACAP), and essentially all cardiac neurons express the PACAP selective PAC1 receptor. Application of exogenous PACAP depolarizes and enhances the excitability of guinea pig cardiac neurons. The mechanism by which PACAP enhances excitability is not established. However, Ca2+ influx through PACAP-activated nonselective cation channels is required for the PACAP-induced increase in excitability of guinea pig cardiac neurons. In addition, a PACAP-induced shift in the voltage dependence of activation of the cyclic nucleotidegated, hyperpolarization-activated current, Ih, most likely participates in the peptide-induced increase in neuronal excitability. The release of endogenous PACAP by repetitive stimulation of preganglionic fibers in vitro contributes to the generation of a slow excitatory postsynaptic potential and also can enhance cardiac neuron excitability. We hypothesize that PACAP released during ongoing vagal activity may regulate cardiac neuron excitability in vivo. [Tzu Chi Med J 2008;20(1):11–18]

Keywords:  Cardiac neurons , Neuronal excitability , Neuropeptide , Slow synaptic transmission

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PII: S1016-3190(08)60002-6

doi:10.1016/S1016-3190(08)60002-6

Tzu Chi Medical Journal
Volume 20, Issue 1 , Pages 11-18, March 2008