Dopamine agonist action in mesolimbic, cortical and extrapyramidal areas to modify spontaneous climbing behaviour of the mouse

Dopamine and apomorphine were injected directly into limbic, extrapyramidal and cortical areas of mouse brain to determine relative sensitivities to the inhibitory effects of these agents on mouse spontaneous climbing behaviour. Injections of 0.06-2 micrograms apomorphine or dopamine into the nucleus accumbens, central area of the amygdala, septum or ventral tegmental nucleus caused dose-dependent motor inhibition with maximal reductions in the order of 60-70% of control value. In the extrapyramidal nuclei, caudate-putamen and globus pallidus, apomorphine and dopamine were required at 0.5-2.5 micrograms to produce inhibition, but the degree of inhibition never achieved 50% of control. Apomorphine and dopamine (0.001-10 micrograms) failed to cause any inhibition of mouse spontaneous climbing behaviour when injected into the anteromedial, supragenual or suprarhinal cortex. The higher doses of dopamine or apomorphine could effect stimulation of climbing behaviour from the limbic, extrapyramidal and cortical areas. Bilateral injections of haloperidol or (-)sulpiride (0.001-1 microgram) into the selected limbic and extrapyramidal areas caused dose-related depression of mouse spontaneous climbing, the limbic areas, particularly the nucleus accumbens, being the most sensitive. Doses of these neuroleptics selected as having minimal effect in their own right were shown to antagonise the marked motor inhibition effected by dopamine and apomorphine from the limbic areas, and the modest inhibition effected from the extrapyramidal areas. In contrast, intracerebral pretreatments with prazosin or yohimbine failed to antagonise the motor inhibitory effects of dopamine or apomorphine from any brain area.