Induction of apoptosis in cerebellar granule neurons by low potassium: inhibition of death by insulin-like growth factor I and cAMP.
Open accessAbstract
High levels of extracellular K+ ensure proper development and prolong survival of cerebellar granule neurons in culture. We find that when switched from a culture medium containing high K+ (25 mM) to one containing a low but more physiological K+ concentration (5 mM), differentiated granule neurons degenerate and die. Death induced by low K+ is due to apoptosis (programmed cell death), a form of cell death observed extensively in the developing nervous system and believed to be necessary for proper neurogenesis. The death process is accompanied by cleavage of genomic DNA into internucleosome-sized fragments, a hallmark of apoptosis. Inhibitors of transcription and translation suppress apoptosis induced by low K+, suggesting the necessity for newly synthesized gene products for activation of the process. Death can be prevented by insulin-like growth factor I but not by several other growth/neurotrophic factors. cAMP but not the protein kinase C activator phorbol 12-myristate 13-acetate can also support survival in low K+. In view of the large numbers of granule neurons that can be homogeneously cultured, our results offer the prospect of an excellent model system to study the mechanisms underlying apoptosis in the central nervous system and the suppression of this process by survival factors such as insulin-like growth factor I.
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IGF-1 is neuroprotective in cerebellar granule neurons in vitro.
“and proved to be neuroprotective in cerebellar granule neurons in vitro (D’Mello et al. 1993).”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as D’Mello et al. 1993
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- Authors
- D'Mello, S. R., Galli, C., Ciotti, T., & Calissano, P.
- Affiliations
- Institute of Neurobiology, Consiglio Nazionale delle Ricerche, Rome, Italy.
- National Research Council (IT)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1993-12
- Volume
- 90
- Issue
- 23
- Pages
- 10989-10993
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC47907
- OpenAlex
- W2072286244
- Cited by
- 892
- References
- 0
- Citations by year
- 2026: 2 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 3 · 2020: 24 · 2019: 6 · 2018: 7 · 2017: 13 · 2016: 7 · 2015: 20 · 2014: 21 · 2013: 27 · 2012: 26
- FWCI
- 9.23
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- apoptosis, cerebellar granule cells, low potassium, neuronal cell death, insulin-like growth factor I, cyclic AMP, protein kinase C, DNA fragmentation, neurotrophic factors, neuronal survival, neurogenesis
- MeSH terms
- Cyclic AMP, Animals, Cells, Cultured, Cerebellum, DNA Damage, Insulin-Like Growth Factor I, Neurons, Phorbol Esters, Potassium, Proto-Oncogene Proteins, Time Factors, Rats, Wistar, Apoptosis, Receptors, Nerve Growth Factor, Receptor Protein-Tyrosine Kinases, Receptor, trkA, Rats, In Vitro Techniques
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