Effect of preganglionic stimulation on neuropeptide-like immunoreactivity in the stellate ganglion of the cat.

In pentobarbital-anesthetized cats, treated with hexamethonium and atropine, 40 Hz stimulation of the preganglionic input to the decentralized right stellate ganglion caused cardioacceleration. When the 40-Hz stimulation is maintained for 2 h, this cardioacceleration was progressively attenuated and eventually irreversibly lost. At this time, neurotensin-like and leucine-enkephalin-like immunoreactivity associated with intraganglionic fibers and presumptive axon terminals was also lost. Preganglionic 40 Hz stimulation for 2 h did not change substance P-like, somatostatin-like, vasoactive intestinal peptide-like and corticotropin-releasing factor-like immunoreactivity in the stellate ganglion. A 40-Hz 2-h stimulation of the intact stellate ganglion output caused no change of the neuropeptide immunoreactivity pattern. These findings suggest that neurotensin and leucine-enkephalin are released by sympathetic preganglionic axon terminals and that the releasable pool of these peptides is depleted by prolonged preganglionic stimulation. The association of peptide depletion with loss of the cardioacceleration, evoked by stimulation of the input to the stellate ganglion in the presence of cholinergic antagonists, suggests the possibility that peptides are involved in the non-cholinergic mechanism of ganglionic transmission mediating the cardioacceleration.