Metabolic abnormalities caused by 3-acetylpyridine in the cerebral motor regions of rats: Partial recovery by thyrotropin-releasing hormone

Although 3-acetylpyridine (3-AP) induces several motor disturbances and it degenerates the olivocerebellar pathway, abnormalities caused by 3-AP in ce rebral motor regions remain to be elucidated. Here we investigated the meta bolic changes caused by 3-AP (75 mg/kg, i.p.) on local cerebral glucose uti lization (LCGU) in various brain regions. The effects of anti-ataxic agents , thyrotropin-releasing hormone (TRH) (10 mg/kg, i.p.) and its mimetic agen t taltirelin hydrate (1 mg/kg, i.p.), on the 3-AP-induced change in LCGU we re also investigated. The LCGU in the nuclei of the basal ganglia, thalamus , limbic structures and brainstem of 3-AP-treated rats was significantly lo wer than that of naive animals. However 3-AP increased the LCGU of the cere bellar nuclei. TRH restored depressed LCGU in the substantia nigra and vent ral tegmental area. TRH tended to restore the lowered LCGU in several nucle i of 3-AP-treated rats. Moreover, taltirelin further increased the LCGU in the cerebellar nuclei. These results suggest that the motor disturbance of the 3-AP-treated rats may be due to not only degeneration of the olivocereb ellar pathway but also dysfunction of the several areas that play a role in motor coordination. Moreover, the anti-ataxic action by TRH could result f rom metabolic restoration of the multiple motor-coordination-related areas.