The role of p75NTR in cholinergic basal forebrain structure and function

The role of the p75 neurotrophin receptor (p75(NTR)) in adult cholinergic basal forebrain (cBF) neurons is unclear due to conflicting results from previous studies and to limitations of existing p75(NTR)-knock-out mouse models. In the present study we used a novel conditional knock-out line (ChAT-cr...

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Published inThe Journal of neuroscience Vol. 34; no. 39; pp. 13033 - 13038
Main Authors Boskovic, Zoran, Alfonsi, Fabienne, Rumballe, Bree A, Fonseka, Sachini, Windels, Francois, Coulson, Elizabeth J
Format Journal Article
LanguageEnglish
Published United States Society for Neuroscience 24.09.2014
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Abstract The role of the p75 neurotrophin receptor (p75(NTR)) in adult cholinergic basal forebrain (cBF) neurons is unclear due to conflicting results from previous studies and to limitations of existing p75(NTR)-knock-out mouse models. In the present study we used a novel conditional knock-out line (ChAT-cre p75(in/in)) to assess the role of p75(NTR) in the cBF by eliminating p75(NTR) in choline acetyl-transferase-expressing cells. We show that the absence of p75(NTR) results in a lasting increase in cBF cell number, cell size, and cholinergic innervation to the cortex. Analysis of adult ChAT-cre p75(in/in) mice revealed that mutant animals show a similar loss of cBF neurons with age to that observed in wild-type animals, indicating that p75(NTR) does not play a significant role in mediating this age-related decline in cBF neuronal number. However, the increased cholinergic axonal innervation of the cortex, but not the hippocampus, corresponded to alterations in idiothetic but not allothetic navigation. These findings support a role for p75(NTR)-mediated regulation of cholinergic-dependent cognitive function, and suggest that the variability in previous reports of cBF neuron number may stem from limited spatial and temporal control of p75(NTR) expression in existing knock-out models.
AbstractList The role of the p75 neurotrophin receptor (p75(NTR)) in adult cholinergic basal forebrain (cBF) neurons is unclear due to conflicting results from previous studies and to limitations of existing p75(NTR)-knock-out mouse models. In the present study we used a novel conditional knock-out line (ChAT-cre p75(in/in)) to assess the role of p75(NTR) in the cBF by eliminating p75(NTR) in choline acetyl-transferase-expressing cells. We show that the absence of p75(NTR) results in a lasting increase in cBF cell number, cell size, and cholinergic innervation to the cortex. Analysis of adult ChAT-cre p75(in/in) mice revealed that mutant animals show a similar loss of cBF neurons with age to that observed in wild-type animals, indicating that p75(NTR) does not play a significant role in mediating this age-related decline in cBF neuronal number. However, the increased cholinergic axonal innervation of the cortex, but not the hippocampus, corresponded to alterations in idiothetic but not allothetic navigation. These findings support a role for p75(NTR)-mediated regulation of cholinergic-dependent cognitive function, and suggest that the variability in previous reports of cBF neuron number may stem from limited spatial and temporal control of p75(NTR) expression in existing knock-out models.
The role of the p75 neurotrophin receptor (p75 NTR ) in adult cholinergic basal forebrain (cBF) neurons is unclear due to conflicting results from previous studies and to limitations of existing p75 NTR -knock-out mouse models. In the present study we used a novel conditional knock-out line (ChAT-cre p75 in/in ) to assess the role of p75 NTR in the cBF by eliminating p75 NTR in choline acetyl-transferase-expressing cells. We show that the absence of p75 NTR results in a lasting increase in cBF cell number, cell size, and cholinergic innervation to the cortex. Analysis of adult ChAT-cre p75 in/in mice revealed that mutant animals show a similar loss of cBF neurons with age to that observed in wild-type animals, indicating that p75 NTR does not play a significant role in mediating this age-related decline in cBF neuronal number. However, the increased cholinergic axonal innervation of the cortex, but not the hippocampus, corresponded to alterations in idiothetic but not allothetic navigation. These findings support a role for p75 NTR -mediated regulation of cholinergic-dependent cognitive function, and suggest that the variability in previous reports of cBF neuron number may stem from limited spatial and temporal control of p75 NTR expression in existing knock-out models.
Author Coulson, Elizabeth J
Alfonsi, Fabienne
Windels, Francois
Rumballe, Bree A
Boskovic, Zoran
Fonseka, Sachini
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Issue 39
Keywords navigation
Morris water maze
cholinergic basal forebrain
hippocampus
knock-out
p75 neurotrophin receptor
Language English
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Z.B. and F.A. contributed equally to this work.
Author contributions: Z.B., F.A., F.W., and E.J.C. designed research; Z.B., F.A., B.A.R., and S.F. performed research; Z.B., F.A., and E.J.C. analyzed data; Z.B., F.W., and E.J.C. wrote the paper.
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Snippet The role of the p75 neurotrophin receptor (p75(NTR)) in adult cholinergic basal forebrain (cBF) neurons is unclear due to conflicting results from previous...
The role of the p75 neurotrophin receptor (p75 NTR ) in adult cholinergic basal forebrain (cBF) neurons is unclear due to conflicting results from previous...
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SubjectTerms Animals
Brief Communications
Cholinergic Neurons - metabolism
Cholinergic Neurons - physiology
Cognition
Female
Male
Maze Learning
Mice
Mice, Inbred C57BL
Prosencephalon - cytology
Prosencephalon - growth & development
Prosencephalon - metabolism
Prosencephalon - physiology
Receptors, Nerve Growth Factor - genetics
Receptors, Nerve Growth Factor - metabolism
Synaptic Transmission
Title The role of p75NTR in cholinergic basal forebrain structure and function
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Volume 34
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