ABSTRACTThis study was undertaken to determine if muscarinic mechanisms are involved in synaptic transmission in the parasympathetic ciliary ganglion as has been clearly shown for sympathetic ganglia. Cats were anesthetized, and following topical ephedrine, pupillary constrictions were elicited by electrical stimulation of the intracranial oculomotor nucleus. Nictitating membrane contractions were evoked by electrical stimulation of the preganglionic cervical nerve. Frequency-response curves were repeated after infusion with hexamethonium (0.6-1.0 mg/kg min−1) and after subsequent administration of atropine (500 μg/kg. i.v.). In other experiments, effects of nicotinic (DMPP) and muscarinic (McN-A-343) agonists on postganglionic ciliary nerve activity were measured. Treatment with hexamethonium reduced nictitating membrane responses at all frequencies of stimulation (by about 75 at 16-32 Hz). The residual nictitating membrane contractions were subsequently blocked by the addition of atropine. In contrast, hexamethonium totally abolished miosis produced by CNS preganglionic oculomotor nerve stimulation. The nicotinic agonist, DMPP, produced nictitating membrane contractions, miosis, and increased ciliary nerve firing. In contrast, McN-A-343 contracted the nictitating membrane but failed to increase postganglionic ciliary nerve activity. These results suggest that, unlike sympathetic ganglia, a significant degree of muscarinic transmission does not occur in the parasympathetic ciliary gangli
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