Separate neural substrates of the locomotor-activating properties of amphetamine, heroin, caffeine and corticotropin releasing factor (CRF) in the rat.
Destruction of dopamine terminals within the nucleus accumbens (N.Acc.) with 6-hydroxydopamine blocked the locomotor activating properties of d-amphetamine, but not caffeine or corticotropin-releasing factor (CRF). Infusion of muscimol into the region of nucleus accumbens efferent terminals in the substantia innominata and lateral preoptic region (SI/LPO) blocked amphetamine-, but not caffeine- or CRF-stimulated locomotion. These muscimol infusions also blocked heroin-stimulated locomotion. These results suggest that amphetamine, acting through a process dependent on N.Acc. dopamine transmission, stimulates locomotion by decreasing GABAergic activity within this N.Acc.-SI/LPO projection; heroin, known to act through a process dependent on N.Acc. opiate receptor activation, also stimulates locomotion by decreasing GABAergic activity within the SI/LPO; caffeine and CRF produce their activation through different neural substrates.
D000661:Amphetamine / Q000494:pharmacology*; D000818:Animals; D002110:Caffeine / Q000494:pharmacology*; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology*; D003932:Heroin / Q000494:pharmacology*; D007267:Injections; D008297:Male; D009043:Motor Activity / Q000187:drug effects*; D009474:Neurons / Q000502:physiology*; D011301:Preoptic Area; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D002110:Caffeine; D003932:Heroin; D003346:Corticotropin-Releasing Hormone; D000661:Amphetamine