ArticleNeuromolecular medicine2013
AMPA receptor properties are modulated in the early stages following pilocarpine-induced status epilepticus.
Article in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 37 citations in OpenAlex.
- The AMPA receptor life cycle: assembly, regulation and synaptic diversity.Nature reviews. Neuroscience · 2026Review
- Loose-patch recordings reveal differential Kv7-dependent effects on spontaneous excitatory activity in control and epileptic CA1.Frontiers in neurology · 2026Article
- Chemogenetic activation of Gq signaling modulates dendritic development of cortical neurons in a time- and layer-specific manner.Frontiers in cellular neuroscience · 2025Article
- Seizures exacerbate excitatory: inhibitory imbalance in Alzheimer's disease and 5XFAD mice.Brain : a journal of neurology · 2024Article
- Febrile Seizures Cause a Rapid Depletion of Calcium-Permeable AMPA Receptors at the Synapses of Principal Neurons in the Entorhinal Cortex and Hippocampus of the Rat.International journal of molecular sciences · 2023Article
- The Role of Glutamate Receptors in Epilepsy.Biomedicines · 2023Review
- Epileptiform activity influences theta-burst induced LTP in the adult hippocampus: a role for synaptic lipid raft disruption in early metaplasticity?Frontiers in cellular neuroscience · 2023Article
- Short-Term Epileptiform Activity Potentiates Excitatory Synapses but Does Not Affect Intrinsic Membrane Properties of Pyramidal Neurons in the Rat Hippocampus In Vitro.Biomedicines · 2021Article
- Increased immunoreactivity of glutamate receptors, neuronal nuclear protein and glial fibrillary acidic protein in the hippocampus of epileptic rats with fast ripple activity.Experimental brain research · 2021Article
- Transcriptome analysis of rat dorsal hippocampal CA1 after an early life seizure induced by kainic acid.Epilepsy research · 2020Article
- Chronic mild stress induces anhedonic behavior and changes in glutamate release, BDNF trafficking and dendrite morphology only in stress vulnerable rats. The rapid restorative action of ketamine.Neurobiology of stress · 2019Article
- The Good and the Bad of Glutamate Receptor RNA Editing.Molecular neurobiology · 2017Review
- Pilocarpine-induced seizures trigger differential regulation of microRNA-stability related genes in rat hippocampal neurons.Scientific reports · 2016Article
- Glutamatergic Mechanisms Associated with Seizures and Epilepsy.Cold Spring Harbor perspectives in medicine · 2015Review
- Article
- Altered intrathalamic GABAA neurotransmission in a mouse model of a human genetic absence epilepsy syndrome.Neurobiology of disease · 2015Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glutamate over-activation and the consequent neuronal excitotoxicity have been identified as crucial players in brain dysfunctions such as status epilepticus (SE). Owing to the central function of 2-amino-3-(hydroxyl-5-methylisoxazole-4-yl) propionic acid receptors (AMPARs) in fast excitatory neurotransmission, these receptors have been recognized to play a prominent role in the development and generation of epileptic seizure. This study was undertaken to investigate both the early changes that affect glutamatergic neurons in the rat cerebral cortex and hippocampus and the level and channel properties of AMPARs in response to SE. The results obtained after 3 h of pilocarpine (PILO)-induced SE showed a disorganization of glutamatergic neurons in the CA3 and a thinner neuronal cell layer in the dentate gyrus (DG) region as compared with controls. A significant increase in AMPAR GluA2 protein expression, a decrease in GluA1, GluA3, and GluA4 expression, and a reduction in the phosphorylation of Ser831-GluA1 and Ser880-GluA2 were also observed. In addition, we report a downregulation of R/G editing levels and of Flip splicing isoforms, with a prominent effect on the hippocampus of PILO-treated rats. Our results suggest the presence of an attenuation of AMPARs' post-synaptic excitatory response to glutamate after PILO treatment, thus conferring neuronal protection from the excitotoxic conditions observed in the SE. This study suggests a role for AMPARs in alterations of the glutamatergic pathway during the onset and early progression of epilepsy, thus indicating additional targets for potential therapeutic interventions.
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