Pharmacological characterization of dopaminergic influence on expression of neuropeptide Y immunoreactivity by rat striatal neurons.
Selective unilateral lesion of the nigrostriatal dopamine pathway by the cytotoxin 6-hydroxydopamine was previously shown to enhance the number and staining intensity of neurons expressing neuropeptide Y immunoreactivity in the ipsilateral striatum. This effect was completely reversed by treatment of the 6-hydroxydopamine-injected animals with the directly acting dopamine agonist apomorphine. This finding reinforces our previous hypothesis that changes in striatal neuropeptide Y staining subsequent to 6-hydroxydopamine lesions of this kind reflect changes in intraneuronal neuropeptide Y levels which are directly attributable to the suppression of a tonic dopaminergic control. In contrast to the effect of 6-hydroxydopamine lesion, non-destructive impairment of striatal dopamine transmission by treatments with either the dual dopamine D1/D2 receptor antagonist haloperidol or the dopamine synthesis inhibitor alpha-methylparatyrosine induced a decrease in both the number of neuropeptide Y striatal cells (-29.8% and -34.8%, respectively) and in their labeling intensity. The selective D2-antagonist sulpiride also showed a tendency to reduce the number of neuropeptide Y immunoreactive cells, whereas the selective D1 antagonist SCH 23390 induced a small but constant increase in this number. Taken as a whole, these results suggest that the dopaminergic D1 and D2 receptor subtypes play opposite roles in the dopaminergic control of the striatal neuropeptide Y neuronal system, which may account for the different changes in striatal neuropeptide Y immunostaining observed after 6-hydroxydopamine injury and after non-destructive impairment of nigrostriatal dopaminergic transmission.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001552:Benzazepines / Q000494:pharmacology; D002452:Cell Count; D003342:Corpus Striatum / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism / Q000502:physiology*; D005260:Female; D006220:Haloperidol / Q000494:pharmacology; D006892:Hydroxydopamines; D007150:Immunohistochemistry; D008781:Methyltyrosines / Q000494:pharmacology; D009478:Neuropeptide Y / Q000378:metabolism*; D016627:Oxidopamine; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology; D013378:Substantia Nigra / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D019805:alpha-Methyltyrosine
D001552:Benzazepines; D006892:Hydroxydopamines; D008781:Methyltyrosines; D009478:Neuropeptide Y; D011954:Receptors, Dopamine; D019805:alpha-Methyltyrosine; D016627:Oxidopamine; D006220:Haloperidol; D001058:Apomorphine; D004298:Dopamine