Confronting the loss of trophic support.

Autor:	Hu HL; Department of Biochemistry and Molecular Pharmacology, New York University Langone School of Medicine, New York, NY, United States., Khatri L; Skirball Institute for Biomolecular Medicine, Neuroscience Institute, New York University Langone Medical Center, New York, NY, United States., Santacruz M; Department of Neuroscience, Pomona College, Claremont, CA, United States., Church E; Department of Neuroscience, Pomona College, Claremont, CA, United States., Moore C; Skirball Institute for Biomolecular Medicine, Neuroscience Institute, New York University Langone Medical Center, New York, NY, United States., Huang TT; Department of Biochemistry and Molecular Pharmacology, New York University Langone School of Medicine, New York, NY, United States., Chao MV; Skirball Institute for Biomolecular Medicine, Neuroscience Institute, New York University Langone Medical Center, New York, NY, United States.; Department of Cell Biology, New York Langone Medical Center, New York, NY, United States.; Department of Psychiatry, New York Langone Medical Center, New York, NY, United States.; Department of Neuroscience and Physiology, New York Langone Medical Center, New York, NY, United States.
Jazyk:	angličtina
Zdroj:	Frontiers in molecular neuroscience [Front Mol Neurosci] 2023 Jun 23; Vol. 16, pp. 1179209. Date of Electronic Publication: 2023 Jun 23 (Print Publication: 2023).
DOI:	10.3389/fnmol.2023.1179209
Abstrakt:	Classic experiments with peripheral sympathetic neurons established an absolute dependence upon NGF for survival. A forgotten problem is how these neurons become resistant to deprivation of trophic factors. The question is whether and how neurons can survive in the absence of trophic support. However, the mechanism is not understood how neurons switch their phenotype to lose their dependence on trophic factors, such as NGF and BDNF. Here, we approach the problem by considering the requirements for trophic support of peripheral sympathetic neurons and hippocampal neurons from the central nervous system. We developed cellular assays to assess trophic factor dependency for sympathetic and hippocampal neurons and identified factors that rescue neurons in the absence of trophic support. They include enhanced expression of a subunit of the NGF receptor (Neurotrophin Receptor Homolog, NRH) in sympathetic neurons and an increase of the expression of the glucocorticoid receptor in hippocampal neurons. The results are significant since levels and activity of trophic factors are responsible for many neuropsychiatric conditions. Resistance of neurons to trophic factor deprivation may be relevant to the underlying basis of longevity, as well as an important element in preventing neurodegeneration. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2023 Hu, Khatri, Santacruz, Church, Moore, Huang and Chao.)
Databáze:	MEDLINE
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