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Epileptic Animals (epileptic + animals)

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Medical Sciences	100%

Selected Abstracts

Glutamine induces epileptiform discharges in superficial layers of the medial entorhinal cortex from pilocarpine-treated chronic epileptic rats in vitro

EPILEPSIA, Issue 4 2009
Nora Sandow
Summary Purpose:, Glutamine (GLN) is a precursor for synthesis of glutamate and ,-aminobutyric acid (GABA) and has been found in the cerebrospinal fluid (CSF) at mean concentrations of 0.6 mM. Experiments on slices are usually performed in artificial CSF (aCSF) kept free of amino acids. Therefore, the role of glutamine, particularly in tissue of epileptic animals, remains elusive. Methods:, Using extracellular recordings we studied effects of GLN on field potentials and stimulus-evoked field responses in the medial entorhinal cortex (MEC) of combined entorhinal cortex hippocampal slices from pilocarpine-treated chronic epileptic rats and age-matched saline-injected control rats. Results:, In presence of GLN (0.5 and 2 mM) recurrent epileptiform discharges (REDs) were observed in slices from epileptic rats (64% and 80%, respectively), but not in slices from control rats. REDs were restricted to the superficial MEC, suppressed by the ,-Amino-3-hydroxy-5-methyl-4-isoxazol-propionate (AMPA)/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (30 ,M), attenuated by the inhibitor of neuronal glutamine transporters methylamino-isobutyric acid (10 mM), and apparently augmented and prolonged by the GABAA receptor antagonist bicuculline-methiodide (5 ,M). In contrast, amplitudes of stimulus evoked nonsynaptic and synaptic field responses increased in slices from control rats (+23% and +12% of the reference values) and insignificantly less or not in those of epileptic rats (+6.5% and ,0.25%, respectively). Notably, stimulus-evoked slow negative transients confined to slices of epileptic animals were reduced in amplitude (,18%). Discussion:, In combined entorhinal hippocampal slices from chronic epileptic animals, GLN induces glutamatergic REDs via neuronal uptake in superficial layers of the MEC where inhibitory function seemed to be partially preserved. [source]

Carbamazepine Enhances Discriminative Memory in a Rat Model of Epilepsy

EPILEPSIA, Issue 11 2004
Rosane B. Bernardi
Summary:,Purpose:,Seizures and antiepileptic drugs (AEDs) are the main causes for cognitive impairment in persons with epilepsy. It is still a matter of debate whether carbamazepine (CBZ) improves cognition because of its own psychotropic effects or because it is more effective to treat temporal epilepsy. Our objective was to analyze the performance of CBZ-treated or nontreated pilocarpine epileptic rats in an object-recognition test. Methods:,Twelve chronic pilocarpine-induced epileptic rats were treated with CBZ, 40 mg/kg, or saline, t.i.d. for 8 days. Twenty-one nonepileptic controls were treated with CBZ or saline. On day 8 of treatment, all rats were tested with an object-recognition paradigm. Results:,No locomotor impairment was detected in chronic epilepsy or CBZ treatment, as exploration during training was not affected. Exploratory behaviors during the choice session were not decreased in rats treated with CBZ; therefore CBZ does not compromise procedural memory. Epileptic rats showed a nonsignificant change in the discrimination performance, and prolonged treatment with CBZ in epileptic rats induced a significant increase in object discrimination during the choice session. Conclusions:,Even though pilocarpine-induced epileptic animals do not show compromised performance in the spontaneous object-recognition test, prolonged CBZ treatment has a positive effect on a simple object-discrimination task. These results may be associated with the psychotropic effects of CBZ. [source]

Endogenous neurosteroid synthesis modulates seizure frequency

ANNALS OF NEUROLOGY, Issue 5 2010
Courtney Lawrence
Inhibitory neurosteroids, molecules generated in glia from circulating steroid hormones and de novo from cholesterol, keep seizures in check in epileptic animals. They can enhance inhibitory transmission mediated by gamma-aminobutyric acid receptors and have anticonvulsant action. ANN NEUROL 2010;67:689,693 [source]