Behavioral recovery following kainic acid lesions and fetal implants of the striatum occurs independent of dopaminergic mechanisms.
Transplantation of fetal striatal tissue into rats with kainic acid lesions of the striatum reversed the spontaneous locomotor abnormalities caused by the lesions, but had no effect on the lesion-induced hyperactivity that followed amphetamine or apomorphine injection. Conversely, transplants into intact (non-lesioned) striatum led to abnormalities in spontaneous locomotion, but did not effect locomotion under amphetamine or apomorphine conditions. Dopamine autoradiography found a relative absence of dopamine receptors within the transplants. These results suggest that the mechanism which accounts for transplant-induced recovery of spontaneous locomotion is independent of striatal dopamine mechanisms.
D000818:Animals; D001927:Brain Diseases / Q000139:chemically induced / Q000628:therapy; D003342:Corpus Striatum / Q000378:metabolism / Q000637:transplantation*; D004298:Dopamine / Q000502:physiology*; D005260:Female; D005333:Fetus; D007608:Kainic Acid; D009069:Movement Disorders / Q000628:therapy*; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000378:metabolism; D009435:Synaptic Transmission
D011954:Receptors, Dopamine; D007608:Kainic Acid; D004298:Dopamine