Abstract
Electrical and cholinergic (physostigmine) stimulation of the mesencephalic reticular formation (MRF) blocks ciliary nerve activity. Pentobarbitone increases the spontaneous ciliary nerve potential and lowers the threshold to electrical MRF stimulation. Atropine has no significant effect on spontaneous activity, but diminishes the response to electrical MRF stimulation and blocks the physostigmine-induced inhibition. In contrast, electrical stimulation and physostigmine activation of the MRF generally increases vagal efferent discharges and tends to induce rhythmicity or increase the rate of pre-existing rhythmicity. Pentobarbitone depresses spontaneous activity and blocks effects induced by electrical MRF stimulation. Atropine, per se , may increase, decrease, or modify vagal efferent activity, suggesting selective effects on different neuronal aggregates of the vagal system. Physostigmine-induced alterations of vagal outflow are antagonized by atropine. From these results it is concluded that the differential effect of MRF stimulation, physostigmine, atropine and pentobarbitone on the upper (ciliary) and lower (vagal) parasympathetic outflow represents the consequence of a different organization of those substrates which govern the two parasympathetic activities.
Published Version
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