scholarly journals The p75 neurotrophin receptor is required for the survival of neuronal progenitors and normal formation of the basal forebrain, striatum, thalamus and neocortex

Development ◽  
2019 ◽  
Vol 146 (18) ◽  
pp. dev181933 ◽  
Author(s):  
Sonja Meier ◽  
Fabienne Alfonsi ◽  
Nyoman D. Kurniawan ◽  
Michael R. Milne ◽  
Maria A. Kasherman ◽  
...  
Keyword(s):  
Basal Forebrain ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor ◽  
Neuronal Progenitors

The p75 neurotrophin receptor has nonapoptotic antineurotrophic actions in the basal forebrain

2011 ◽  
Vol 90 (1) ◽  
pp. 278-287 ◽  
Author(s):  
Ursula Greferath ◽  
Jennifer Trieu ◽  
Graham L. Barrett
Keyword(s):  
Basal Forebrain ◽  
Neurotrophin Receptor ◽  
P75 Neurotrophin Receptor

scholarly journals Regulation of cholinergic basal forebrain development, connectivity, and function by neurotrophin receptors

2019 ◽  
Vol 3 (1) ◽  
Author(s):  
Zoran Boskovic ◽  
Sonja Meier ◽  
Yunpeng Wang ◽  
Michael R. Milne ◽  
Tessa Onraet ◽  
...  
Keyword(s):  
Basal Forebrain ◽  
Neuronal Development ◽  
Critical Role ◽  
Neurotrophin Receptor ◽  
Current Evidence ◽  
P75 Neurotrophin Receptor ◽  
Neurotrophin Receptors ◽  
Cortical Function ◽  
Cholinergic Basal Forebrain ◽  
And Function

Abstract Cholinergic basal forebrain (cBF) neurons are defined by their expression of the p75 neurotrophin receptor (p75NTR) and tropomyosin-related kinase (Trk) neurotrophin receptors in addition to cholinergic markers. It is known that the neurotrophins, particularly nerve growth factor (NGF), mediate cholinergic neuronal development and maintenance. However, the role of neurotrophin signalling in regulating adult cBF function is less clear, although in dementia, trophic signalling is reduced and p75NTR mediates neurodegeneration of cBF neurons. Here we review the current understanding of how cBF neurons are regulated by neurotrophins which activate p75NTR and TrkA, B or C to influence the critical role that these neurons play in normal cortical function, particularly higher order cognition. Specifically, we describe the current evidence that neurotrophins regulate the development of basal forebrain neurons and their role in maintaining and modifying mature basal forebrain synaptic and cortical microcircuit connectivity. Understanding the role neurotrophin signalling plays in regulating the precision of cholinergic connectivity will contribute to the understanding of normal cognitive processes and will likely provide additional ideas for designing improved therapies for the treatment of neurological disease in which cholinergic dysfunction has been demonstrated.

scholarly journals Proneurotrophin-3 promotes cell cycle withdrawal of developing cerebellar granule cell progenitors via the p75 neurotrophin receptor

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Juan Pablo Zanin ◽  
Elizabeth Abercrombie ◽  
Wilma J Friedman
Keyword(s):  
Cell Cycle ◽  
Granule Cell ◽  
Death Receptor ◽  
Cerebellar Granule Cell ◽  
Neurotrophin Receptor ◽  
Motor Deficits ◽  
P75 Neurotrophin Receptor ◽  
Cerebellar Granule ◽  
Neuronal Progenitors ◽  
Normal Period

Cerebellar granule cell progenitors (GCP) proliferate extensively in the external granule layer (EGL) of the developing cerebellum prior to differentiating and migrating. Mechanisms that regulate the appropriate timing of cell cycle withdrawal of these neuronal progenitors during brain development are not well defined. The p75 neurotrophin receptor (p75NTR) is highly expressed in the proliferating GCPs, but is downregulated once the cells leave the cell cycle. This receptor has primarily been characterized as a death receptor for its ability to induce neuronal apoptosis following injury. Here we demonstrate a novel function for p75NTR in regulating proper cell cycle exit of neuronal progenitors in the developing rat and mouse EGL, which is stimulated by proNT3. In the absence of p75NTR, GCPs continue to proliferate beyond their normal period, resulting in a larger cerebellum that persists into adulthood, with consequent motor deficits.

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