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dc.contributor.author
Dasgupta, Srestha
dc.contributor.author
Montroull, Laura Ester
dc.contributor.author
Pandya, Mansi
dc.contributor.author
Zanin, Juan P.
dc.contributor.author
Wang, Wei
dc.contributor.author
Wu, Zhuhao
dc.contributor.author
Friedman, Wilma J
dc.date.available
2024-03-14T15:13:20Z
dc.date.issued
2023-08-09
dc.identifier.citation
Dasgupta, Srestha; Montroull, Laura Ester; Pandya, Mansi; Zanin, Juan P.; Wang, Wei; et al.; Cortical brain injury causes retrograde degeneration of afferent basal forebrain cholinergic neurons via the p75NTR; Society for Neuroscience; eNeuro; 10; 8; 9-8-2023; 1-38
dc.identifier.uri
http://hdl.handle.net/11336/230578
dc.description.abstract
Traumatic brain injury elicits neuronal loss at the site of injury and progressive neuronal loss in the penumbra. However, the consequences of TBI on afferent neurons projecting to the injured tissue from distal locations is unknown. Basal forebrain cholinergic neurons (BFCNs) extend long projections to multiple brain regions including the cortex, regulate many cognitive functions and are compromised in numerous neurodegenerative disorders. To determine the consequence of cortical injury on these afferent neurons, we used the Fluid Percussion Injury (FPI) model of traumatic brain injury and assessed the effects on BFCN survival and axon integrity in male and female mice. Survival or death of BF neurons can be regulated by neurotrophins or proneurotrophins, respectively. The injury elicited an induction of proNGF and proBDNF in the cortex, and a loss of BFCNs ipsilateral to the injury compared to sham uninjured mice. p75NTR knockout mice did not show loss of BFCN neurons, indicating a retrograde degenerative effect of the cortical injury on the afferent BFCNs mediated through p75NTR. In contrast, locus coeruleus (LC) neurons which also project throughout the cortex were unaffected by the injury, suggesting specificity in retrograde degeneration after cortical TBI. Proneurotrophins (proNTs) provided directly to basal forebrain axons in microfluidic cultures triggered retrograde axonal degeneration and cell death, which did not occur in the absence of p75NTR. This study shows that after traumatic brain injury, proNTs induced in the injured cortex promote BFCN axonal degeneration and retrograde neuron loss through p75NTR.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Society for Neuroscience
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
AXON DEGENERATION
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BASAL FOREBRAIN NEURONS
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P75NTR
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PRONEUROTROPHINS
dc.subject.classification
Biología Celular, Microbiología
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Ciencias Biológicas
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CIENCIAS NATURALES Y EXACTAS
dc.title
Cortical brain injury causes retrograde degeneration of afferent basal forebrain cholinergic neurons via the p75NTR
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2024-03-08T14:30:55Z
dc.identifier.eissn
2373-2822
dc.journal.volume
10
dc.journal.number
8
dc.journal.pagination
1-38
dc.journal.pais
Estados Unidos
dc.description.fil
Fil: Dasgupta, Srestha. Department Of Biological Sciences; Estados Unidos. Rutgers University; Estados Unidos
dc.description.fil
Fil: Montroull, Laura Ester. Department Of Biological Sciences; Estados Unidos. Rutgers University; Estados Unidos. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales. Centro de Biología Celular y Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Pandya, Mansi. Rutgers University; Estados Unidos. Department Of Biological Sciences; Estados Unidos
dc.description.fil
Fil: Zanin, Juan P.. Department Of Biological Sciences; Estados Unidos. Rutgers University; Estados Unidos
dc.description.fil
Fil: Wang, Wei. Weill Cornell Medical College; Estados Unidos
dc.description.fil
Fil: Wu, Zhuhao. Weill Cornell Medical College; Estados Unidos
dc.description.fil
Fil: Friedman, Wilma J. Rutgers University; Estados Unidos. Department Of Biological Sciences; Estados Unidos
dc.journal.title
eNeuro
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.eneuro.org/lookup/doi/10.1523/ENEURO.0067-23.2023
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1523/ENEURO.0067-23.2023
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