Medial-to-lateral gradient of neostriatal NGF receptors: relationship to cholinergic neurons and NGF-like immunoreactivity

• Published in: The Journal of neuroscience 1991-03, Vol.11 (3), p.828-836
• Main Authors: Altar, CA, Dugich-Djordjevic, M, Armanini, M, Bakhit, C
• Format: Article
• Language: English
• Subjects: Anatomy; Animals; Binding, Competitive; Biological and medical sciences; Caudate Nucleus - metabolism; Central nervous system; Choline O-Acetyltransferase - analysis; Corpus Striatum - anatomy & histology; Corpus Striatum - cytology; Corpus Striatum - metabolism; Dopamine - physiology; Dopamine Antagonists; Fundamental and applied biological sciences. Psychology; Hydroxydopamines - pharmacology; Kinetics; Male; Mazindol - metabolism; Nerve Growth Factors - analysis; Nerve Growth Factors - metabolism; Neurons - cytology; Neurons - metabolism; Oxidopamine; Putamen - metabolism; Rats; Rats, Inbred Strains; Receptors, Cell Surface - metabolism; Receptors, GABA-A - metabolism; Receptors, Nerve Growth Factor; Recombinant Proteins - metabolism; Vertebrates: nervous system and sense organs
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/JNEUROSCI.11-03-00828.1991

High-affinity binding sites for recombinant human NGF (rhNGF) were studied in the caudate-putamen of the adult rat and rabbit. Displaceable 125I-rhNGF binding sites were densely distributed throughout the caudate-putamen and were 2-3-fold more prevalant in the ventrolateral and lateral than in the medial caudate-putamen. The amount of nondisplaceable binding did not vary throughout the caudate-putamen. The medial-to-lateral receptor gradient was correlated (r = +0.99) with a 2-3-fold medial-to-lateral increase in ChAT activity. In contrast, NGF-like immunoreactivity (NGF-LI) was prevalent but uniformly distributed in the caudate-putamen. Lesions of intrinsic cholinergic neurons by quinolinic acid produced extensive gliosis in the medial, central, and lateral caudate-putamen, yet 125I-rhNGF binding was decreased in each of these regions. The activity of ChAT and 125I-rhNGF binding throughout the caudate-putamen were each decreased by 40% following quinolinic acid. Binding was not changed after 70-77% dopamine nerve terminal depletions induced by 6-hydroxydopamine, demonstrating a nonglial, nondopaminergic locus for striatal NGF binding sites. The cholinergiclike topography of NGF binding sites throughout the intact caudate-putamen, the parallel decreases of cholinergic neurons and NGF binding sites following intrinsic neuronal loss, and the uniform neostriatal gradient of NGF-LI are consistent with the trophic role of endogenous NGF for cholinergic interneurons of the caudate-putamen.