Functional neuronal replacement by grafted striatal neurones in the ibotenic acid-lesioned rat striatum.
In rats, striatal neuronal destruction by so-called excitotoxic amino acids, kainic acid or ibotenic acid (IA) produce neuropathological and neurochemical changes in the basal ganglia which resemble those seen in patients with Huntington's chorea. Such lesioned animals show a behavioural syndrome which is reminiscent of the cardinal symptoms of the disease, accompanied by a substantial increase in local cerebral metabolic activity in several striatal target structures within the extrapyramidal motor system. The study was designed to explore the potential of grafted fetal striatal neurones implanted into the IA-lesioned striatum to compensate for the structural, neurochemical, metabolic and behavioural defects of IA-lesioned rats. Extending previous studies, we report here that such striatal implants can significantly ameliorate the lesion-induced locomotor hyperactivity and at least partly normalize the metabolic hyperactivity in the extrapyramidal neuronal system.
D000818:Animals; D002421:Caudate Nucleus / Q000378:metabolism; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism / Q000637:transplantation*; D003847:Deoxyglucose / Q000378:metabolism; D005260:Female; D007051:Ibotenic Acid / Q000494:pharmacology; D009043:Motor Activity / Q000502:physiology*; D011699:Putamen / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D007051:Ibotenic Acid; D005680:gamma-Aminobutyric Acid; D003847:Deoxyglucose