Dihydroergotoxine potentiation of thioridazine-induced hypomotility.

Dihydroergotoxine (DHET), a dopamine (DA) receptor agonist, induced hypomotility in rats at doses of 0.125-0.5 mg/kg s.c., (-)sulpiride a D-2 receptor antagonist, a dose which did not affect spontaneous activity (10 mg/kg s.c.) counteracted the hypomotility induced by DHET. Thioridazine (THR), a widely used neuroleptic, reduced motility (2.5-10 mg/kg i.p.) when given alone; this effect was potentiated by DHET when the two drugs administered in doses of 1 mg/kg THR/0.05 mg/kg DHET and 2.5 mg/kg THR/0.125 mg/kg DHET; higher doses of THR (5 and 10 mg/kg i.p.) which by themselves induced marked inhibition of motility, were not potentiated by doses of DHET of 0.25 and 0.5 mg/kg s.c. THR and DHET influenced in an opposite manner the levels of DA-metabolites dihydroxyphenylacetic acid and homovanillic acid in the caudate; while THR (1-10 mg/kg i.p.) increased, DHET (0.25-0.5 mg/kg s.c.), decreased DA-metabolite levels. The association of THD and DHET resulted in a reciprocal antagonism of their effects on DA-metabolite levels.