%0 Journal Article %A Thomas Naumann %A Elisabeth Casademunt %A Ewald Hollerbach %A Jutta Hofmann %A Georg Dechant %A Michael Frotscher %A Yves-Alain Barde %T Complete Deletion of the Neurotrophin Receptor p75NTRLeads to Long-Lasting Increases in the Number of Basal Forebrain Cholinergic Neurons %D 2002 %R 10.1523/JNEUROSCI.22-07-02409.2002 %J The Journal of Neuroscience %P 2409-2418 %V 22 %N 7 %X 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 p75NTR. We have analyzed cholinergic septohippocampal neurons of the medial septal nucleus inp75exonIII (partial p75NTR knock-out) andp75exonIV (complete p75NTR knock-out) mice, in their original genetic background and in congenic strains. At postnatal day 15, thep75exonIII mutation leads to a moderate increase (+13%) in these neurons among littermates only after back-crossing in a C57BL/6 background. In contrast, the nullp75exonIV mutation, which prevents expression of both the full-length and the shorter p75NTR isoforms, results in a 28% neuronal increase, independent of genetic background. The incomplete nature of the p75NTR 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 p75NTR in regulating cholinergic neuron numbers in the mouse forebrain. %U https://www.jneurosci.org/content/jneuro/22/7/2409.full.pdf