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Corticotropin-releasing factor injected intracerebroventricularly in a dose of 1 µg produced a prolonged locomotor activation (3 h) in rats previously habituated to the test cage environment. This activation was reversed by α-flupenthixol (intraperitoneally), a dopamine receptor antagonist, only at cataleptic doses and not at all by naloxone (subcutaneously) in doses of 0.02–5.0 mg/kg. The effective dose 50% (ED₅₀) for the α-flupenthixol reversal of locomotor activity induced by corticotropin-releasing factor was 0.13 mg/kg; similar to the 0.14 mg/kg ED₅₀ needed to reverse the locomotor activation produced by caffeine (10 mg/kg s.c). The ED₅₀ necessary to reverse amphetamine (0.75 mg/kg s.c.) locomotion with this drug was 0.07 mg/kg. The results suggest that the corticotropin-releasing factor acts independently of direct activation of the dopamine or opioid peptide systems.

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