Neurotransmission in neonatal rat cardiac ganglion in situ
RIS ID
106260
Abstract
The intrinsic cardiac ganglia of the neonatal heart in situ were studied using electrophysiological and histochemical techniques. The vagal branches innervating the atrial myocardium and cardiac ganglia were identified and individual ganglion cells visualized using Hoffman modulation contrast optics. Histochemical studies revealed the presence of acetylcholinesterase activity associated with neuronal cell bodies and fibers, catecholamine-containing, small intensely fluorescent cells, and cell bodies and nerve fibers immunoreactive for vasoactive intestinal polypeptide. Intracellular recordings from the 'principal' cells of the rat cardiac ganglion in situ revealed a fast excitatory postsynaptic potential (EPSP) evoked after electrical stimulation of the vagus nerve, which was inhibited by the nicotinic receptor antagonist, mecamylamine. No spontaneously firing neurons were found, although infrequent (< 2 min-1) spontaneous miniature EPSPs were observed in most neurons. The quantal content of neurally evoked responses was between 10 and 30 quanta, and the presence of multiple EPSPs in some cells suggested polyneuronal innervation. The neurally evoked EPSP amplitude was dependent on the rate of nerve stimulation, decreasing with increasing frequency of stimulation. Neurons exhibited a sustained depolarization during high frequency stimulation (> 1 Hz), and in ~ 15% of the cells a slow depolarization lasting 1-3 min was observed after a train of stimuli. The presence of catecholamine- and neuropeptide-containing neuronal cell body fibers in neonatal rat cardiac ganglia in situ, along with neurally evoked postsynaptic responses resistant to cholinergic ganglionic blockers, suggests a role for noncholinergic transmission in the regulation of the mammalian heart beat.
Publication Details
Seabrook, G. R., Fieber, L. A. & Adams, D. J. (1990). Neurotransmission in neonatal rat cardiac ganglion in situ. American Journal of Physiology: Heart and Circulatory Physiology, 259 (4), H997-H1005.