ArticleFrontiers in cell and developmental biology2021
Heat-Shock Induces Granule Cell Dispersion and Microgliosis in Hippocampal Slice Cultures.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 6 citations in OpenAlex.
- Review
- Insulin-like growth factor 1 in heat stress-induced neuroinflammation: novel perspective about the neuroprotective role of chromium.Stress biology · 2023Review
- The long-term neurodevelopmental outcomes of febrile seizures and underlying mechanisms.Frontiers in cell and developmental biology · 2023Review
- Adult-Onset Neuronal Ceroid Lipofuscinosis With a NovelFrontiers in aging neuroscience · 2022Article
- Considering the Role of Extracellular Matrix Molecules, in Particular Reelin, in Granule Cell Dispersion Related to Temporal Lobe Epilepsy.Frontiers in cell and developmental biology · 2022Review
- Tetrodotoxin prevents heat-shock induced granule cell dispersion in hippocampal slice cultures.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
Granule cell dispersion (GCD) has been found in the dentate gyrus (dg) of patients with temporal lobe epilepsy (TLE) and a history of febrile seizures but was also recently observed in pediatric patients that did not suffer from epilepsy. This indicates that GCD might not always be disease related, but instead could reflect normal morphological variation. Thus, distribution of newborn granule cells within the hilar region is part of normal dg development at early stages but could be misinterpreted as pathological GCD. In turn, pathological GCD may be caused, for example, by genetic mutations, such as the reeler mutation. GCD in the reeler mutant goes along with an increased susceptibility to epileptiform activity. Pathological GCD in combination with epilepsy is caused by experimental administration of the glutamate receptor agonist kainic acid in rodents. In consequence, the interpretation of GCD and the role of febrile seizures remain controversial. Here, we asked whether febrile temperatures alone might be sufficient to trigger GCD and used hippocampal slice cultures as
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