ArticlePloS one2013
Rapamycin reverses status epilepticus-induced memory deficits and dendritic damage.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 110 citations in OpenAlex.
- Temporal profiling of hippocampal astrocyte reactivity reveals persistent GFAP cleavage and complement C3 association after status epilepticus.Brain structure & function · 2026Article
- Severity-dependent proteomic alterations in the rat hippocampus following pilocarpine-induced status epilepticus.Molecular and cellular neurosciences · 2026Article
- Rapamycin and Minocycline Treatment Does Not Rescue Behavioral and Molecular Changes Induced by Early-Life Seizures in Female Mice.NeuroSci · 2026Article
- Cell-Intrinsic Regulation of Epilepsy-Associated Pathology by mTORC1 and mTORC2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Severity-dependent proteomic alterations in the rat hippocampus following pilocarpine-induced status epilepticus.bioRxiv : the preprint server for biology · 2026Article
- Sex-specific proteomic analysis of epileptic brain tissues from Pten knockout mice and human refractory epilepsy.Experimental neurology · 2025Article
- Interictal network dysfunction and cognitive impairment in epilepsy.Nature reviews. Neuroscience · 2025Review
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- Acute depletion of complement C3 with cobra venom factor attenuates memory deficits induced by status epilepticus.Epilepsia open · 2024Article
- NS-Pten knockout mice exhibit sex and hippocampal subregion-specific increases in microglia/macrophage density.Epilepsy research · 2024Article
- mTOR and neuroinflammation in epilepsy: implications for disease progression and treatment.Nature reviews. Neuroscience · 2024Review
- Potential roles of voltage-gated ion channel disruption in Tuberous Sclerosis Complex.Frontiers in molecular neuroscience · 2024Article
- Cognitive comorbidities in the rat pilocarpine model of epilepsy.Frontiers in neurology · 2024Article
- Assessment of tau phosphorylation and β-amyloid pathology in human drug-resistant epilepsy.Epilepsia open · 2023Article
- Mice deficient in complement C3 are protected against recognition memory deficits and astrogliosis induced by status epilepticus.Frontiers in molecular neuroscience · 2023Article
- The role of dendritic spines in epileptogenesis.Frontiers in cellular neuroscience · 2023Review
- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Constitutively active microglial populations limit anorexia induced by the food contaminant deoxynivalenol.Journal of neuroinflammation · 2022Article
- The role of mTORC1 activation in seizure-induced exacerbation of Alzheimer's disease.Brain : a journal of neurology · 2022Article
- Pilot study evaluating everolimus molecular mechanisms in tuberous sclerosis complex and focal cortical dysplasia.PloS one · 2022Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.