Compensatory bilateral changes in dopamine turnover after striatal kainate lesion.
Diseases of the extrapyramidal systems like Parkinson's disease and Huntington's chorea have been closely associated with the basal ganglia. In particular, the prominent symmetrical nigrostriatal dopaminergic systems play an important role in pathogenesis and symptomatology of motor disorders. Biochemical and electrophysiological data indicate a functional relationship between the nigrostriatal pathways on the two brain hemispheres. Unilateral pharmacological manipulations result in short-term changes in contralateral dopamine (DA) release, and surgical lesions on one side lead to long-term alterations in the firing rate of contralateral dopaminergic neurones. We report here the effects of unilateral kainic acid-induced lesions of striatal cell bodies on ipsi- and contralateral striatal DA turnover. We present evidence that morphologically intact dopaminergic neurones on both sides possess compensatory mechanisms which can counteract striatal synaptic asymmetries. Such mechanisms could be responsible at least in part for the maintenance of symmetrical motor behaviour in unilaterally lesioned animals.
D000818:Animals; D002421:Caudate Nucleus / Q000378:metabolism; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism*; D007839:Functional Laterality; D006801:Humans; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D009043:Motor Activity / Q000187:drug effects; D011759:Pyrrolidines / Q000494:pharmacology*; D051381:Rats; D013239:Stereotyped Behavior / Q000187:drug effects
D011759:Pyrrolidines; D007608:Kainic Acid; D004298:Dopamine