Muscarinic inhibition as a dominant role in cholinergic regulation of transmission in the caudate nucleus.

The effects of cholinergic agonists and antagonists were investigated using slice preparations of the rat caudate nucleus (CN) to elucidate the role of the cholinergic system in the CN. Either carbachol (10(-7) to 10(-5) M) or muscarine (10(-7) to 10(-5) M) dose-dependently inhibited extracellular action potentials orthodromically elicited by local stimulation in the CN. A combination of acetylcholine (10(-6) to 10(-4) M) with physostigmine (10(-6) M) also inhibited the orthodromic response of CN neuron, but nicotine (10(-6) to 10(-3) M) had no effects on the neuronal activity. Atropine (10(-8) to 10(-6) M) antagonized the carbachol-induced inhibition of CN neuron with pA2 of 7.58. Carbachol (10(-5) M) or muscarine (10(-5) M) decreased the amplitude of excitatory postsynaptic potential (EPSP) without altering the resting membrane potential or input impedance of the CN neuron, whereas nicotine (10(-5) M) did not affect either the resting membrane potential or amplitude of EPSP. When carbachol (10(-5) M) was added to the bath, the number of action potentials elicited by applying a depolarizing current into the cell was increased, whereas action potentials transsynaptically elicited by local stimulation were inhibited conversely. The excitatory effects of carbachol on the postsynaptic site of the neuron were also blocked by atropine (3 x 10(-7) M). Carbachol (10(-5) M) did not affect the time courses of the rise and decay phases of EPSP induced by the local stimulation, but did reduce the amplitude of the EPSP.(ABSTRACT TRUNCATED AT 250 WORDS)