ArticleProceedings of the National Academy of Sciences of the United States of America2004
Evidence that injury-induced changes in hippocampal neuronal calcium dynamics during epileptogenesis cause acquired epilepsy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 120 citations in OpenAlex.
- SUR1-TRPM4 is expressed in human epilepsy and promotes neuron hyperactivity and seizures in rodents.Brain : a journal of neurology · 2026Article
- Pathophysiology of Status Epilepticus Revisited.International journal of molecular sciences · 2025Review
- Excitotoxic glutamate levels cause the secretion of resident endoplasmic reticulum proteins.Journal of neurochemistry · 2024Article
- Insights into epileptogenesis from post-traumatic epilepsy.Nature reviews. Neurology · 2024Review
- Effects of L-Type Voltage-Gated Calcium Channel (LTCC) Inhibition on Hippocampal Neuronal Death after Pilocarpine-Induced Seizure.Antioxidants (Basel, Switzerland) · 2024Article
- Erythropoietin regulates signaling pathways associated with neuroprotective events.Experimental brain research · 2022Review
- Ellagic acid and allopurinol decrease HExperimental brain research · 2022Article
- Proteomic profiling of the rat hippocampus from the kindling and pilocarpine models of epilepsy: potential targets in calcium regulatory network.Scientific reports · 2021Article
- Neurodegenerative pathways as targets for acquired epilepsy therapy development.Epilepsia open · 2020Review
- Novel therapeutics for treating organophosphate-induced status epilepticus co-morbidities, based on changes in calcium homeostasis.Neurobiology of disease · 2020Review
- Targeting Intracellular Calcium Stores Alleviates Neurological Morbidities in a DFP-Based Rat Model of Gulf War Illness.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Calpain activation and neuronal death during early epileptogenesis.Neurobiology of disease · 2019Article
- In search of antiepileptogenic treatments for post-traumatic epilepsy.Neurobiology of disease · 2019Review
- The Paroxysmal Depolarization Shift: Reconsidering Its Role in Epilepsy, Epileptogenesis and Beyond.International journal of molecular sciences · 2019Review
- A Comparative Study of Cell Specific Effects of Systemic and Volatile Anesthetics on Identified Motor Neurons and Interneurons ofFrontiers in physiology · 2019Article
- Amelioration of Pentylenetetrazole-Induced Seizures by Modulators of Sigma, N-Methyl-D-Aspartate, and Ryanodine Receptors in Mice.Iranian journal of medical sciences · 2018Article
- Hypothermia Reduces Mortality, Prevents the Calcium Plateau, and Is Neuroprotective Following Status Epilepticus in Rats.Frontiers in neurology · 2018Article
- Zebrafish is a predictive model for identifying compounds that protect against brain toxicity in severe acute organophosphorus intoxication.Archives of toxicology · 2017Article
- Alterations in Properties of Glutamatergic Transmission in the Temporal Cortex and Hippocampus Following Pilocarpine-Induced Acute Seizures in Wistar Rats.Frontiers in cellular neuroscience · 2017Article
- The role of oxidative stress in organophosphate and nerve agent toxicity.Annals of the New York Academy of Sciences · 2016Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Alterations in hippocampal neuronal Ca(2+) and Ca(2+)-dependent systems have been implicated in mediating some of the long-term neuroplasticity changes associated with acquired epilepsy (AE). However, there are no studies in an animal model of AE that directly evaluate alterations in intracellular calcium concentration ([Ca(2+)](i)) and Ca(2+) homeostatic mechanisms (Ca(2+) dynamics) during the development of AE. In this study, Ca(2+) dynamics were evaluated in acutely isolated rat CA1 hippocampal, frontal, and occipital neurons in the pilocarpine model by using [Ca(2+)](i) imaging fluorescence microscopy during the injury (acute), epileptogenesis (latency), and chronic-epilepsy phases of the development of AE. Immediately after status epilepticus (SE), hippocampal neurons, but not frontal and occipital neurons, had significantly elevated [Ca(2+)](i) compared with saline-injected control animals. Hippocampal neuronal [Ca(2+)](i) remained markedly elevated during epileptogenesis and was still elevated indefinitely in the chronic-epilepsy phase but was not elevated in SE animals that did not develop AE. Inhibiting the increase in [Ca(2+)](i) during SE with the NMDA channel inhibitor MK801 was associated in all three phases of AE with inhibition of the changes in Ca(2+) dynamics and the development of AE. Ca(2+) homeostatic mechanisms in hippocampal neurons also were altered in the brain-injury, epileptogenesis, and chronic-epilepsy phases of AE. These results provide evidence that [Ca(2+)](i) and Ca(2+)-homeostatic mechanisms are significantly altered during the development of AE and suggest that altered Ca(2+) dynamics may play a role in the induction and maintenance of AE and underlie some of the neuroplasticity changes associated with the epileptic phenotype.
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Registered trials
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.