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The Journal of Neuroscience, April 1, 2002, 22(7):2409-2418

Complete Deletion of the Neurotrophin Receptor p75^NTR Leads to Long-Lasting Increases in the Number of Basal Forebrain Cholinergic Neurons

Thomas Naumann^{1, *}, Elisabeth Casademunt^{2, *}, Ewald Hollerbach¹, Jutta Hofmann¹, Georg Dechant², Michael Frotscher¹, and Yves-Alain Barde²

¹ Institute of Anatomy, University of Freiburg, D-79104 Freiburg, Germany, and ² Department of Neurobiology, Max Planck Institute of Neurobiology, D-82152 Martinsried, Germany

Cholinergic neurons innervating cortical structures are among the most affected neuronal populations in Alzheimer's disease. In rodents, they express high levels of the neurotrophin receptor p75^NTR. We have analyzed cholinergic septohippocampal neurons of the medial septal nucleus in p75^exonIII (partial p75^NTR knock-out) and p75^exonIV (complete p75^NTR knock-out) mice, in their original genetic background and in congenic strains. At postnatal day 15, the p75^exonIII mutation leads to a moderate increase (+13%) in these neurons among littermates only after back-crossing in a C57BL/6 background. In contrast, the null p75^exonIV mutation, which prevents expression of both the full-length and the shorter p75^NTR isoforms, results in a 28% neuronal increase, independent of genetic background. The incomplete nature of the p75^NTR mutation used previously, coupled with difficulties in delineating the mouse medial septum and the impact of the genetic background on cell numbers, all contribute to explain previous difficulties in establishing the role of p75^NTR in regulating cholinergic neuron numbers in the mouse forebrain.

Key words: p75^NTR; cholinergic neurons; medial septum; cell death; genetic background; optical fractionator; NGF

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^* T.N. and E.C. contributed equally to this study.

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Copyright © 2002 Society for Neuroscience  0270-6474/02/2272409-10$05.00/0

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