Target-Derived Neurotrophic Factors Regulate the Death of Developing Forebrain Neurons after a Change in their Trophic Requirements
Open accessAbstract
Many neurons die as the normal brain develops. How this is regulated and whether the mechanism involves neurotrophic molecules from target cells are unknown. We found that cultured neurons from a key forebrain structure, the dorsal thalamus, develop a need for survival factors including brain-derived neurotrophic factor (BDNF) from their major target, the cerebral cortex, at the age at which they innervate it. Experiments in vivo have shown that rates of dorsal thalamic cell death are reduced by increasing cortical levels of BDNF and are increased in mutant mice lacking functional BDNF receptors or thalamocortical projections; these experiments have also shown that an increase in the rates of dorsal thalamic cell death can be achieved by blocking BDNF in the cortex. We suggest that the onset of a requirement for cortex-derived neurotrophic factors initiates a competitive mechanism regulating programmed cell death among dorsal thalamic neurons.
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In the central nervous system, overproduction of neurons with ensuing neuronal death is a common mechanism employed by the developing brain to ensure that the appropriate balance of projection and receptive neurons is attained.
“in the central nervous system overproduction of neurons with ensuing neuronal death is a common mechanism employed by the developing brain to ensure that the appropriate balance of projection and receptive neurons is attained.19, 23, 24, 25”
From A role for synaptic plasticity in the adolescent development of executive function (2013) · cites this paper as [25]
The Abstract says many neurons die during normal brain development, and the Discussion links target-derived factors to cell death in the developing dorsal thalamus. The paper proposes that competition may help match neuron numbers to those in a target, but it does not establish neuronal overproduction and subsequent death as a common CNS mechanism that ensures this balance. (LLM, conf=0.86)
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- Authors
- Lotto, R. B., Asavaritikrai, P., Vali, L., & Price, D. J.
- Affiliations
- University of Edinburgh (GB)
- University of Strathclyde (GB)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2001-06-01
- Volume
- 21
- Issue
- 11
- Pages
- 3904-3910
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6207345
- OpenAlex
- W2131345268
- Cited by
- 44
- References
- 39
- Citations by year
- 2022: 1 · 2019: 2 · 2018: 1 · 2013: 5 · 2012: 3
- FWCI
- 1.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Amgen
- Bristol-Myers Squibb
- Wellcome Trust (065620)
- European Commission
- Genentech
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- brain-derived neurotrophic factor, dorsal thalamus, neuronal cell death, programmed cell death, thalamocortical connections, cerebral cortex, neurotrophic factors, BDNF receptor, forebrain development, neuronal survival
- MeSH terms
- PAX6 Transcription Factor, Animals, Antibodies, Cell Survival, Cells, Cultured, Cerebral Cortex, Eye Proteins, Nerve Growth Factors, Neural Pathways, Neurons, Repressor Proteins, Thalamic Nuclei, Thalamus, Prosencephalon, Culture Media, Conditioned, Apoptosis, Receptors, Nerve Growth Factor, Mice, Knockout, Homeodomain Proteins, Gene Expression Regulation, Developmental, Brain-Derived Neurotrophic Factor, In Situ Nick-End Labeling, Receptor, trkC, Receptor, trkB, Mice, Paired Box Transcription Factors
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