The localization of receptor binding sites in the substantia nigra and striatum of the rat.
Neurotransmitter receptor binding of 5 ligands was examined in the striatum, substantia nigra (SN) and frontal cortex of rats which had received either unilateral 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal pathway (NSP) or unilateral kainic acid lesions of the striatum. 6-OHDA lesions of the NSP significantly reduced [3H]dihydroalprenolol ([3H]DHA) and [3H]naloxone ([3H]Nal) binding by 31% and 28% respectively, in the denervated striatum compared to the contralateral side. Scatchard analysis revealed that the alteration in [3H]DHA binding was not due to a change in the affinity of the beta-adrenergic receptor for [3H]DHA. In marked contrast to these changes in the striatum, destruction of the NSP resulted in a significant increase in [3H]DHA and [3H]Nal binding by 44% and 26%, respectively, in the frontal cortex of the lesioned compared to the control side. 6-OHDA lesions in the NSP did not alter striatal receptor binding for [3H]quinuclidinyl benzilate ([3H]QNB), [3H]muscimol ([3H]Mus) or [3H]flunitrazepam ([3H]Flu). Similarily, intrastriatal kainic acid injections did not alter striatal receptor binding for [3H]Nal, [3H]Flu or [3H]Mus. Of the various receptor densities measured in the SN after the above lesions the only alteration observed was a 43% increase in [3H]Flu binding following 6-OHDA lesions of the NSP. Scatchard analysis indicated no change in the affinity of the benzodiazepine receptor for [3H]Flu. 6-OHDA lesions of the NSP did not alter [13H]QNB or [3H]Nal binding in the SN. Striatal kainic acid lesions did not alter nigral [3H]QNB or [3H]Flu binding. The results are discussed in terms of neurotransmitter localization and plasticity within the striatum, SN and frontal cortex.
D000818:Animals; D001931:Brain Mapping; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism*; D004082:Dihydroalprenolol / Q000378:metabolism; D005476:Fluphenazine / Q000378:metabolism; D006892:Hydroxydopamines / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D009118:Muscimol / Q000378:metabolism; D009270:Naloxone / Q000378:metabolism; D009434:Neural Pathways / Q000187:drug effects; D009474:Neurons / Q000187:drug effects; D011813:Quinuclidinyl Benzilate / Q000378:metabolism; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000378:metabolism; D011950:Receptors, Cholinergic / Q000378:metabolism; D011954:Receptors, Dopamine / Q000187:drug effects; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D011957:Receptors, Opioid / Q000378:metabolism; D013378:Substantia Nigra / Q000187:drug effects / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D006892:Hydroxydopamines; D011943:Receptors, Adrenergic, beta; D011950:Receptors, Cholinergic; D011954:Receptors, Dopamine; D017981:Receptors, Neurotransmitter; D011957:Receptors, Opioid; D009118:Muscimol; D009270:Naloxone; D005680:gamma-Aminobutyric Acid; D004082:Dihydroalprenolol; D011813:Quinuclidinyl Benzilate; D005476:Fluphenazine; D007608:Kainic Acid