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Absence of p75(NTR) causes increased basal forebrain cholinergic neuron size, choline acetyltransferase activity, and target innervation JOURNAL OF NEUROSCIENCE Yeo, T. T., CHUACOUZENS, J., Butcher, L. L., Bredesen, D. E., Cooper, J. D., Valletta, J. S., Mobley, W. C., LONGO, F. M. 1997; 17 (20): 7594-7605


Emerging evidence suggests that the p75 neurotrophin receptor (p75NTR) mediates cell death; however, it is not known whether p75NTR negatively regulates other neuronal phenotypes. We found that mice null for p75NTR displayed highly significant increases in the size of basal forebrain cholinergic neurons, including those that are TrkA-positive. Cholinergic hippocampal target innervation also was increased significantly. Activity of the cholinergic neurotransmitter synthetic enzyme choline acetyltransferase (ChAT) was increased in both the medial septum and hippocampus. Upregulation of these cholinergic features was not associated with increased basal forebrain or hippocampal target NGF levels. In contrast, striatal cholinergic neurons, which do not express p75NTR, showed no difference in neuronal number, size, or ChAT activity between wild-type and p75NTR null mutant mice. These findings indicate that p75NTR negatively regulates cholinergic neuronal phenotype of the basal forebrain cholinergic neurons, including cell size, target innervation, and neurotransmitter synthesis.

View details for Web of Science ID A1997XZ44900003

View details for PubMedID 9315882