Cholinergic excitation and inhibition in the visual thalamus of the cat--influences of cortical inactivation and barbiturate anesthesia.

Neuronal responses to microiontophoretically applied pulses of acetylcholine (ACh) were recorded in the perigeniculate nucleus (PGN) and dorsal lateral geniculate nucleus (dLGN) of the cat. In the PGN, ACh inhibited 95% of the cells under N2O/O2-halothane anesthesia. Systemic application of sodium pentobarbitone did not abolish ACh inhibition. In the dLGN with N2O-halothane, ACh increased firing rates of neurons before (88%) and after (78%) interruption of their direct retinal inputs by photocoagulation of the receptive field area on the retina. Functional inactivation of the corticogeniculate loop by cooling of the ipsilateral visual cortex did not selectively influence ACh sensitivity in the retinally deafferented dLGN. It is concluded that ACh exerts a direct, excitatory action on geniculate neurons. Infusion of sodium pentobarbitone resulted in reduction of ACh firing rates to about 30% of the control values in 35% of the normally innervated cells (65% of that sample not being excited by ACh), whereas excitatory ACh responses after retinal deafferentation were completely blocked by the barbiturate. It is concluded that pentobarbitone influences direct ACh excitation, but not cholinergic disinhibition in the dLGN or ACh inhibition in the PGN. Possible differential effects of pentobarbitone on nicotinic and muscarinic types of ACh responses are discussed.