The DOI matches its Crossref record; 71 of the 71 references it cites were found in a registry or an index.
Rapamycin Reverses Status Epilepticus-Induced Memory Deficits and Dendritic Damage
Open accessAbstract
Cognitive impairments are prominent sequelae of prolonged continuous seizures (status epilepticus; SE) in humans and animal models. While often associated with dendritic injury, the underlying mechanisms remain elusive. The mammalian target of rapamycin complex 1 (mTORC1) pathway is hyperactivated following SE. This pathway modulates learning and memory and is associated with regulation of neuronal, dendritic, and glial properties. Thus, in the present study we tested the hypothesis that SE-induced mTORC1 hyperactivation is a candidate mechanism underlying cognitive deficits and dendritic pathology seen following SE. We examined the effects of rapamycin, an mTORC1 inhibitor, on the early hippocampal-dependent spatial learning and memory deficits associated with an episode of pilocarpine-induced SE. Rapamycin-treated SE rats performed significantly better than the vehicle-treated rats in two spatial memory tasks, the Morris water maze and the novel object recognition test. At the molecular level, we found that the SE-induced increase in mTORC1 signaling was localized in neurons and microglia. Rapamycin decreased the SE-induced mTOR activation and attenuated microgliosis which was mostly localized within the CA1 area. These findings paralleled a reversal of the SE-induced decreases in dendritic Map2 and ion channels levels as well as improved dendritic branching and spine density in area CA1 following rapamycin treatment. Taken together, these findings suggest that mTORC1 hyperactivity contributes to early hippocampal-dependent spatial learning and memory deficits and dendritic dysregulation associated with SE.
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“Consistent with these results, in models of temporal lobe epilepsy there is a reduction in the expression of voltage-gated ion channels including Kv1.1 (30,31,36).”
From Analysis of proteins that rapidly change upon mechanistic/mammalian target of rapamycin complex 1 (mTORC1) repression identifies parkinson protein 7 (PARK7) as a novel protein aberrantly expressed in tuberous sclerosis complex (TSC) (2016) · cites this paper as [30]
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“Furthermore, epilepsy, which is common in AD and ASD, has enhanced mTORC1 activity (28 -32).”
From Analysis of proteins that rapidly change upon mechanistic/mammalian target of rapamycin complex 1 (mTORC1) repression identifies parkinson protein 7 (PARK7) as a novel protein aberrantly expressed in tuberous sclerosis complex (TSC) (2016) · cites this paper as [30]
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Metadata
- Authors
- Brewster, A. L., Lugo, J. N., Patil, V. V., Lee, W. L., Qian, Y., Vanegas, F., & Anderson, A. E.
- Affiliations
- Baylor College of Medicine (US)
- Corresponding author
- Anderson, Anne E.
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-03-11
- Volume
- 8
- Issue
- 3
- Pages
- e57808
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3594232
- OpenAlex
- W2014962014
- Cited by
- 112
- References
- 71
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 7 · 2023: 6 · 2022: 5 · 2021: 13 · 2020: 11 · 2019: 5 · 2018: 10 · 2017: 14 · 2016: 14 · 2015: 11 · 2014: 5 · 2013: 2
- FWCI
- 7.58
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- National Institutes of Health (T32 NS, R01 NS, 43124)
- National Institute of Neurological Disorders and Stroke (T32 NS 43124, F32NS056664, R01 NS 39943, T32NS043124, F32 NS 56664, R01 NS49427, R01NS039943, R01NS049427)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- status epilepticus, rapamycin, mTORC1 signaling, cognitive impairment, spatial memory impairment, hippocampus, CA1, microglial activation, pilocarpine-induced seizures, dendritic spine density, MAP2, ion channels, neuroprotection
- MeSH terms
- Mechanistic Target of Rapamycin Complex 1, Animals, Dendrites, Disease Models, Animal, Electroencephalography, Gliosis, Hippocampus, Ion Channels, Male, Memory Disorders, Neurons, Phosphorylation, Pilocarpine, Status Epilepticus, Microglia, Maze Learning, Ribosomal Protein S6 Kinases, Sirolimus, Multiprotein Complexes, Dendritic Spines, Rats, TOR Serine-Threonine Kinases
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