Thyrotropin-releasing hormone (TRH) content of rat striatum: modification by drugs and lesions

Two hours after injection, D-amphetamine sulfate (10 mg/kg, i.p.) lowered thyrotropin-releasing hormone (TRH) levels in rat striatum by 50%, but produced no significant changes in the TRH contents of hypothalamus, septum, brain stem or preoptic area. The effect peaked 2 h after amphetamine injection and declined slowly thereafter. The amphetamine-induced decrease in striatal TRH could be blocked by pretreatment with haloperidol or alpha-methyltyrosine, or by production of a 6-hydroxy-dopamine lesion in the ipsilateral substantia nigra. Amphetamine did not act by inhibiting protein synthesis in as much as cycloheximide did not similarly decrease striatal TRH. Kainic acid injected into the striatum lowered TRH by 30% after 5 days. In contrast, partial deafferentiation of the striatum (by cerebral hemitransection at mid-hypothalamic level) increased striatal TRH 2-3-fold, while lesions of the dorsal raphe did not significantly change striatal TRH. Thus TRH levels in rat striatum are closely regulated by dopaminergic and other neurotransmitter systems.