Modulation of apoptosis controls inhibitory interneuron number in the cortex
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Abstract
Cortical networks are composed of excitatory projection neurons and inhibitory interneurons. Finding the right balance between the two is important for controlling overall cortical excitation and network dynamics. However, it is unclear how the correct number of cortical interneurons (CIs) is established in the mammalian forebrain. CIs are generated in excess from basal forebrain progenitors, and their final numbers are adjusted via an intrinsically determined program of apoptosis that takes place during an early postnatal window. Here, we provide evidence that the extent of CI apoptosis during this critical period is plastic and cell-type specific and can be reduced in a cell-autonomous manner by acute increases in neuronal activity. We propose that the physiological state of the emerging neural network controls the activity levels of local CIs to modulate their numbers in a homeostatic manner.
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Cell-autonomous manipulation of cortical interneuron excitability influences their survival.
“Second, cell-autonomous manipulation of the excitability of cortical interneurons influence their survival.”
From Development and Functional Diversification of Cortical Interneurons (2018) · cites this paper as Denaxa et al., 2018
Programmed cell death appears to affect all classes of interneurons.
“This process seems to impact all classes of interneurons (Denaxa et al., 2018; Priya et al., 2018; Wong et al., 2018) (Figure 6A).”
From Development and Functional Diversification of Cortical Interneurons (2018) · cites this paper as Denaxa et al., 2018
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- Authors
- Denaxa, M., Neves, G., Rabinowitz, A., Kemlo, S., Liodis, P., Burrone, J., & Pachnis, V.
- Affiliations
- The Francis Crick Institute (GB)
- King's College London (GB)
- National Institute for Medical Research (GB)
- Corresponding author
- Denaxa, Myrto
- Neves, Guilherme
- Burrone, Juan
- Pachnis, Vassilis
- Venue
- Cell Reports
- Publisher
- Elsevier BV
- Published
- 2018-02
- Volume
- 22
- Issue
- 7
- Pages
- 1710-1721
- ISSN
- 2211-1247 (ISSN-L)
- PMC
- PMC6230259
- OpenAlex
- W2787132038
- Cited by
- 112
- References
- 65
- Citations by year
- 2026: 10 · 2025: 9 · 2024: 8 · 2023: 17 · 2022: 13 · 2021: 15 · 2020: 17 · 2019: 14 · 2018: 9
- FWCI
- 5.07
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cell Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Figshare (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Research Portal (King's College London) (submittedVersion, cc-by)
- The Francis Crick Institute (cc-by)
- Funders
- Cancer Research UK
- Wellcome Trust (095589/Z/11/Z)
- European Research Council (282047)
- Francis Crick Institute
- Lister Institute of Preventive Medicine
- Biotechnology and Biological Sciences Research Council (BB/L022974/1)
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- inhibitory interneurons, apoptosis, neuronal activity, postnatal development, cortical excitation, homeostatic regulation, neural network development
- MeSH terms
- Animals, Cell Count, Cell Survival, Cerebral Cortex, Interneurons, Median Eminence, Mice, Transgenic, Mutation, Nerve Tissue Proteins, Neural Inhibition, Transcription Factors, Up-Regulation, Apoptosis, Cell Lineage, Transcriptome, Cellular Microenvironment, LIM-Homeodomain Proteins
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