The physiological role of striatal cholinergic interneurons was investigate
d with immunotoxin-mediated cell targeting (IMCT). Unilateral cholinergic c
ell ablation caused an acute abnormal turning behavior. These mice showed g
radual recovery but displayed abnormal turning by both excess stimulation a
nd inhibition of dopamine actions. In the acute phase, basal ganglia functi
on was shifted to a hyperactive state by stimulation and suppression of str
iatonigral and striatopallidal neurons, respectively. D1 and D2 dopamine re
ceptors were then down-regulated, relieving dopamine-predomimant synaptic p
erturbation but leaving a defect in controlling dopamine responses. The ace
tylcholine-dopamine interaction is concertedly and adaptively regulated for
basal ganglia synaptic integration.