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Axonal transport of angiotensin-converting enzyme in the rat striatonigral pathway
M Aiso1, W Z Potter, J M Saavedra
1Unit on Preclinical Neuropharmacology, National Institute of Mental Health, Bethesda, MD 20892.
Abstract:
We analyzed the transport of angiotensin-converting enzyme (kininase II, EC 3.4.15.1) in the striatonigral pathway by quantitative autoradiography using the specific converting enzyme inhibitor, 125I-351A. 125I-351A binding was studied at different time intervals after knife cut lesions of the striatonigral pathway. Twenty-four h after the lesion, accumulations of 125I-351A binding sites were observed both rostral and caudal to the lesioned site. No change in 125I-351A binding was observed at this time in the caudate putamen and substantia nigra. Ten days after the lesion, a significant decrease (58%) in 125I-351A binding was found in the pars reticulata of the ipsilateral substantia nigra. These results suggest that the angiotensin-converting enzyme is transported axonally in the rat striatonigral pathway.