Neurally released pituitary adenylate cyclase-activating polypeptide enhances guinea pig intrinsic cardiac neurone excitability

摘要: Intracellular recordings were made in vitro from guinea-pig cardiac ganglia to determine whether endogenous neuropeptides such as pituitary adenylate cyclase-activating polypeptide (PACAP) or substance P released during tetanic neural stimulation modulate neurone excitability and/or contribute slow excitatory postsynaptic potentials (sEPSPs). When nicotinic and muscarinic receptors blocked by hexamethonium atropine, 20 Hz for 10 s initiated a sEPSP all innervated neurones. In 40% of the cells, was enhanced after termination sEPSP. This suggested that non-cholinergic receptor-mediated mechanisms contributed modulated neuronal excitability. Exogenous PACAP depolarization neurones whereas only increased PACAP. treated with PAC1 antagonist PACAP6-38 (500 nm), evoked reduced ∼50% an occurred 10% cells. These observations preganglionic nerve terminals sEPSPs. After addition 1 nm bath, 7 9 exhibited tonic firing pattern untreated preparations, neurons had phasic pattern. nm) diminished increase caused so 4 13 other cells retained findings indicate can be intrinsic We hypothesize vivo may neurotransmission within ganglia.