The striatonigral fibres and the feedback control of dopamine metabolism.
It proved possible to make lesions which interrupted the striatonigral GABA-containing pathway in the rat brain without causing concomitant damage to the nigrostriatal dopamine containing system. Estimations of striatal concentrations of dopamine (DA), dihydroxyphenyl-acetic acid (DOPAC) and homovanillic acid (HVA) inducated that these lesions had no influence either on normal striatal DA turnover or on the enhancement of DA turnover induced by neuroleptics. Behavioural experiments suggested a motor output function for the striatonigral pathway.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D014150:Antipsychotic Agents / Q000494:pharmacology; D001058:Apomorphine / Q000494:pharmacology; D001345:Autoradiography; D003342:Corpus Striatum / Q000378:metabolism* / Q000502:physiology; D004298:Dopamine / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D006220:Haloperidol / Q000494:pharmacology; D006719:Homovanillic Acid / Q000378:metabolism; D009434:Neural Pathways / Q000502:physiology*; D009638:Norepinephrine / Q000378:metabolism; D011954:Receptors, Dopamine / Q000187:drug effects; D013378:Substantia Nigra / Q000378:metabolism* / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D014150:Antipsychotic Agents; D011954:Receptors, Dopamine; D015102:3,4-Dihydroxyphenylacetic Acid; D005680:gamma-Aminobutyric Acid; D006220:Haloperidol; D001058:Apomorphine; D004298:Dopamine; D009638:Norepinephrine; D006719:Homovanillic Acid