ArticleThe Journal of physiology2008
Network hyperexcitability within the deep layers of the pilocarpine-treated rat entorhinal cortex.
Article in The Journal of physiology, 2008. 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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16 citing papers in PubMed, 31 citations in OpenAlex.
- Voltage-Dependent Calcium Channels, Calcium Binding Proteins, and Their Interaction in the Pathological Process of Epilepsy.International journal of molecular sciences · 2018Review
- Disease Modifying Effects of the Spider Toxin Parawixin2 in the Experimental Epilepsy Model.Toxins · 2017Article
- Activation of specific neuronal networks leads to different seizure onset types.Annals of neurology · 2016Article
- Aggravation of seizure-like events by hydrogen sulfide: involvement of multiple targets that control neuronal excitability.CNS neuroscience & therapeutics · 2014Article
- Pathophysiogenesis of mesial temporal lobe epilepsy: is prevention of damage antiepileptogenic?Current medicinal chemistry · 2014Review
- Perirhinal cortex and temporal lobe epilepsy.Frontiers in cellular neuroscience · 2013Review
- Sequel of spontaneous seizures after kainic acid-induced status epilepticus and associated neuropathological changes in the subiculum and entorhinal cortex.Neuropharmacology · 2012Article
- Somatostatin and neuropeptide Y neurons undergo different plasticity in parahippocampal regions in kainic acid-induced epilepsy.Journal of neuropathology and experimental neurology · 2012Article
- GABAergic synchronization in the limbic system and its role in the generation of epileptiform activity.Progress in neurobiology · 2011Review
- Parvalbumin interneurons and calretinin fibers arising from the thalamic nucleus reuniens degenerate in the subiculum after kainic acid-induced seizures.Neuroscience · 2011Article
- Article
- High-frequency (80-500 Hz) oscillations and epileptogenesis in temporal lobe epilepsy.Neurobiology of disease · 2011Article
- Involvement of inward rectifier and M-type currents in carbachol-induced epileptiform synchronization.Neuropharmacology · 2011Article
- In vitro ictogenesis and parahippocampal networks in a rodent model of temporal lobe epilepsy.Neurobiology of disease · 2010Article
- Selective changes in inhibition as determinants for limited hyperexcitability in the insular cortex of epileptic rats.The European journal of neuroscience · 2010Article
- Minimal latency to hippocampal epileptogenesis and clinical epilepsy after perforant pathway stimulation-induced status epilepticus in awake rats.The Journal of comparative neurology · 2008Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study we report that in the presence of normal buffer, epileptiform discharges occur spontaneously (duration = 2.60 +/- 0.49 s) or can be induced by electrical stimuli (duration = 2.50 +/- 0.62 s) in the entorhinal cortex (EC) of brain slices obtained from pilocarpine-treated rats but not in those from age-matched, nonepileptic control (NEC) animals. These network-driven epileptiform events consist of field oscillatory sequences at frequencies greater than 200 Hz that most often initiate in the lateral EC and propagate to the medial EC with 4-63 ms delays. The NMDA receptor antagonist CPP depresses the rate of occurrence (P < 0.01) of these spontaneous epileptiform discharges but fails in blocking them. Paradoxically, stimulus-induced epileptiform responses are enhanced in duration during CPP application. However, concomitant application of NMDA and non-NMDA glutamatergic antagonists abolishes spontaneous and stimulus-induced epileptiform events. Intracellular recordings from lateral EC layer V cells indicate a lower frequency of spontaneous hyperpolarizing postsynaptic potentials in pilocarpine-treated tissue than in NEC (P < 0.002) both under control conditions and with glutamatergic receptor blockade; the reversal potential of pharmacologically isolated GABA(A) receptor-mediated inhibitory postsynaptic potentials has similar values in the two types of tissue. Finally, immunohistochemical analysis shows that parvalbumin-positive interneurons are selectively reduced in number in EC deep layers. Collectively, these results indicate that reduced inhibition within the pilocarpine-treated EC layer V may promote network epileptic hyperexcitability.
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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.