Specificity of function of acetylcholinergic receptors in the caudate and vestibular nuclei.

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Electrophysiological studies, using slice preparation of the rat brain, were undertaken to examine the regulatory mechanism of acetylcholine receptors in the caudate and vestibular nuclei. Either carbachol or milscarine dosedependently inhibited extracellular action potentials orthodromically elicited by local stimulation in the caudate nucleus. A combination of acetylcholine with physostigmine also inhibited the orthodromic responses, but nicotine had no effects on the neuronal activity. Carbachol or muscarine decreased the amplitude of excitatory postsynaptic potential and increased firing induced by intracellular depolarizing pulsesinto the cells, whereas nicotine did not affect these potentials. The inhibitory and excitatory effects of carbachol were blocked by atropine. These results suggest that muscarinic receptors located on the presynaptic and postsynaptic sites of the neuron mediate cholinergic inhibition and excitation in the caudate nucleus, respectively.Bromocriptine, a dopamine D-2 agonist, produced a depolarization of the membrane potential of the caudate neurons, and an increase in the spontaneous firing rate as well as the number of action potentials evoked by depolarizing pulses applied into the cells. The bromocriptine-induced excitation was antagonized by domperidone (D-2 antagonist) and haloperidol, but not affected by SCH 23390 (D-1 antagonist). The medial vestibular nucleus neurons fired spikes spontaneously. Carbachol dose-dependently increased the spontaneous firing, and the addition of atropine attenuated the carbachol-induced excitation of the neurons. Acetylcholine in the presence of physostigmine also increased the firing rate, while nicotine had no effects. These results suggest that firing rate of the spontaneously active neurons in the medial vestibular nucleus are regulated by acetylcholine via muscarinic receptors.