Cholinergic facilitation of thalamic relay transmission in the cat

The effects of intravenously injected atropine and physostigmine were tested on field potentials evoked in ventral anterior and ventral lateral, ventral posterolateral, and lateral geniculate nuclei of the thalamus by electrical stimulation of principal afferent pathways. Postsynaptic components of potentials evoked by stimulation of the brachium conjunctivum, medial lemniscus, and optic tract were usually selectively enhanced by physostigmine and depressed by atropine. Responses evoked in the ventral lateral nucleus by stimulation of the precruciate cortex were similarly altered, but in a smaller proportion of tests. In a small number of tests, the nicotinic blocker, mecamylamine, was also found to depress the postsynaptic responses to stimulation of the three major afferent pathways. Transmission in these pathways and the effects of drug administrations were partly dependent on the anesthetic state of the animal. Halothane and pentobarbital administration depressed the postsynaptic responses. It is possible that depression of thalamic relay transmission by anesthetic agents, by anticholinergic drugs, and during slow-wave sleep may all reflect interaction with a common cholinergic neuronal system.