ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Complete deletion of the neurotrophin receptor p75NTR leads to long-lasting increases in the number of basal forebrain cholinergic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 162 citations in OpenAlex.
- An antisense-long-noncoding-RNA modulates p75iScience · 2025Article
- NgfrNature communications · 2024Article
- Redundancy of p75NTR neurotrophin receptor function in development, growth and fertility in the rat.Transgenic research · 2024Article
- Review
- Cholinergic neurodegeneration and cholesterol metabolism dysregulation by constitutive p75Frontiers in molecular neuroscience · 2023Article
- Single neonatal dexamethasone administration has long-lasting outcome on depressive-like behaviour, Bdnf, Nt-3, p75ngfr and sorting receptors (SorCS1-3) stress reactive expression.Scientific reports · 2021Article
- Ablation of p75Translational psychiatry · 2021Article
- c-Jun N-terminal Kinase Mediates Ligand-independent p75Neuroscience · 2021Article
- Basal Forebrain Cholinergic Neurons: Linking Down Syndrome and Alzheimer's Disease.Frontiers in aging neuroscience · 2021Review
- Regulation of cholinergic basal forebrain development, connectivity, and function by neurotrophin receptors.Neuronal signaling · 2019Review
- Cellular Trafficking of Amyloid Precursor Protein in Amyloidogenesis Physiological and Pathological Significance.Molecular neurobiology · 2019Review
- Peripheral Nerve Regeneration Is Independent From Schwann Cell p75Frontiers in cellular neuroscience · 2019Article
- Exploring the Pathogenesis of Alzheimer Disease in Basal Forebrain Cholinergic Neurons: Converging Insights From Alternative Hypotheses.Frontiers in neuroscience · 2019Review
- Nerve Growth Factor Is Responsible for Exercise-Induced Recovery of Septohippocampal Cholinergic Structure and Function.Frontiers in neuroscience · 2018Article
- A novel inhibitor of p75-neurotrophin receptor improves functional outcomes in two models of traumatic brain injury.Brain : a journal of neurology · 2016Article
- Commentary: Impact of a deletion of the full-length and short isoform of p75NTR on cholinergic innervation and the population of postmitotic doublecortin positive cells in the dentate gyrus.Frontiers in neuroanatomy · 2016Article
- Reduced Anxiety-Like Behavior and Altered Hippocampal Morphology in Female p75NTR(exon IV-/-) Mice.Frontiers in behavioral neuroscience · 2016Article
- Regulation of Neurogenesis by Neurotrophins during Adulthood: Expected and Unexpected Roles.Frontiers in neuroscience · 2016Review
- Impact of a deletion of the full-length and short isoform of p75NTR on cholinergic innervation and the population of postmitotic doublecortin positive cells in the dentate gyrus.Frontiers in neuroanatomy · 2015Article
- The role of p75NTR in cholinergic basal forebrain structure and function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 in p75exonIII (partial p75NTR knock-out) and p75exonIV (complete p75NTR knock-out) mice, in their original genetic background and in congenic strains. At postnatal day 15, the p75exonIII 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 p75exonIV 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.
Indexed as
Identifiers
11923404PMC6758339W1540484053What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.