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Initiation of network bursts by Ca2+‐dependent intrinsic bursting in the rat pilocarpine model of temporal lobe epilepsy
TLDR
The dramatic up‐regulation of intrinsic bursting in CA1 pyramidal cells, particularly the de novo appearance of Ca2+‐dependent bursting, may contribute to the epileptogenicity of the hippocampus in the pilocarpine model of TLE. Expand
Stimulus and Potassium-Induced Epileptiform Activity in the Human Dentate Gyrus from Patients with and without Hippocampal Sclerosis
TLDR
In granule cell populations of hippocampal slices from TLE patients, high K+-induced seizure-like activity and ictal spiking coincide with basic electrophysiological abnormalities, hippocampal sclerosis, and mossy fiber sprouting, suggesting that network reorganization could play a crucial role in determining type and threshold of such activity. Expand
Evidence That ATP Participates in the Pathophysiology of Pilocarpine‐Induced Temporal Lobe Epilepsy: A Fluorimetric, Immunohistochemical, and Western Blot Studies
TLDR
The role of adenosine triphosphate (ATP) in the brain of pilocarpine‐induced chronic epileptic rats and its role in the development of epilepsy was studied. Expand
Mitogen-activated protein kinase is increased in the limbic structures of the rat brain during the early stages of status epilepticus
TLDR
Findings are consistent with a spatial and time-dependent MAPK expression in selected limbic structures, and its activation could represent an initial trigger for neuronal modifications that may take part in the mechanism underlying acute epileptogenesis and in long-lasting neuropathological changes of the PILO model of epilepsy. Expand
Growth-associated phosphoprotein expression is increased in the supragranular regions of the dentate gyrus following pilocarpine-induced seizures in rats
TLDR
Growth-associated phosphoprotein levels increased following status epilepticus and remained elevated at the later time-points, both during the silent period and during the period of chronic recurring seizures, indicating that status epileptus is important to induce growth-associatedosphoprotein overexpression. Expand
GCP II (NAALADase) inhibition suppresses mossy fiber-CA3 synaptic neurotransmission by a presynaptic mechanism.
TLDR
The results suggest that NAAG suppresses synaptic transmission at mossy fiber-CA3 synapses through presynaptic activation of group II mGluRs. Expand
Physical training reverts hippocampal electrophysiological changes in rats submitted to the pilocarpine model of epilepsy
TLDR
The results indicate that physical training reduces CA1 hyperresponsiveness and can modify synaptic plasticity in rats submitted to the pilocarpine model of limbic epilepsy. Expand
Septal GABAergic neurons are selectively vulnerable to pilocarpine-induced status epilepticus and chronic spontaneous seizures
TLDR
Overall, data indicate that septal GABAergic neurons are selectively vulnerable to hippocampal hyperexcitability, and suggest that the processing of information in septohippocampal networks may be altered in chronic epilepsy. Expand
Alterations of the neocortical GABAergic system in the pilocarpine model of temporal lobe epilepsy: Neuronal damage and immunocytochemical changes in chronic epileptic rats
TLDR
Altered expression of PV, GAD65, and GAT1 pointed out specific neocortical disturbances in GABAergic inhibition, which could play a crucial role in seizure generation and expression. Expand
Glutamic acid decarboxylase isoforms are differentially distributed in the septal region of the rat
TLDR
Differences found between medial and lateral septal GABAergic neuronal populations are in agreement with the concept that medial and medial septum are brain structures with highly different connectivity and function despite anatomical proximity. Expand
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