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Featured researches published by Any Boehrer.


Epilepsy Research | 1995

Effects of levetiracetam, a novel antiepileptic drug, on convulsant activity in two genetic rat models of epilepsy

A.T. Gower; Edouard Hirsch; Any Boehrer; M. Noyer; Christian Marescaux

The anticonvulsant effects of levetiracetam were assessed in two genetic rat models. In the audiogenic-seizure prone rat, levetiracetam, 5.4 to 96 mg/kg i.p. dose-dependently inhibited both wild running and tonic-clonic convulsions. In the GAERS model of petit mal epilepsy, levetiracetam markedly suppressed spontaneous spike-and-wave discharge (SWD) but left the underlying EEG trace normal. The effects were already marked at 5.4 mg/kg and did not increase significantly up to 170 mg/kg although more animals were completely protected. Levetiracetam produced no observable effects on behaviour apart from slight reversible sedation at 170 mg/kg. In contrast, piracetam, a structural analogue of levetiracetam, significantly and consistently suppressed SWD in GAERS rats only at the high dose of 1000 mg/kg with some slight effects at lower doses. The effect of piracetam appeared to be due to increased sleeping rather than to a direct antiepileptic effect. The results with levetiracetam argue for a clinical application in both petit mal, absence epilepsy and in treating generalised tonic-clonic and partial seizures.


Epilepsia | 2005

Glutamate Receptor Antagonists and Benzodiazepine Inhibit the Progression of Granule Cell Dispersion in a Mouse Model of Mesial Temporal Lobe Epilepsy

Fumio Suzuki; Christophe Heinrich; Any Boehrer; Koichi Mitsuya; Kiyoshi Kurokawa; Masayuki Matsuda; Antoine Depaulis

Summary:  Purpose: Unilateral intrahippocampal injection of kainic acid (KA) in adult mice induces the progressive dispersion of dentate granule cells, one of the characteristic pathologic changes of mesial temporal lobe epilepsy. However, little is known about the mechanisms that trigger this dispersion. In this study, the possible involvement of glutamatergic and γ‐aminobutyric acid (GABA)ergic neurotransmissions in the development of granule cell dispersion (GCD) was examined in this model.


Epilepsy Research | 1996

Thalamic NMDA transmission in a genetic model of absence epilepsy in rats

C. Koerner; L. Danober; Any Boehrer; Christian Marescaux; Marguerite Vergnes

In the selected strain of GAERS Wistar rats (Genétic Absence Epilepsy Rats from Strasbourg), all animals present spontaneously recurrent absence seizures characterized by bilateral and synchronous generalized spike-and-wave discharges (SWD) accompanied by behavioural arrest. SWD depend on a thalamo-cortical network connecting the reticular and relay nuclei of the thalamus and their cortical projection areas. This loop involves both GABAergic and glutamatergic synapses. In the present study, we investigated the implication of NMDA transmission in the genesis of absence seizures in GAERS. Intra-peritoneal or intra-cerebroventricular injections of NMDA, the competitive NMDA antagonist CGP 40116, the non-competitive NMDA antagonist (+)-MK 801 and the antagonist of the glycine modulatory site 5,7-dichlorokynurenic acid dose-dependently suppressed SWD. Bilateral infusions of the same drugs in the lateral relay nuclei of the thalamus had similar suppressive effects. Intra-cerebroventricular or intrathalamic administration of D-serine, an agonist of the glycine modulatory site, had no effect on SWD. These data show that NMDA neurotransmission, especially within the thalamus, plays a major role in the control of absence seizures in GAERs. Disregulation of NMDA-mediated transmission by NMDA or antagonists, interacting with various sites of the receptor complex, may suppress the thalamo-cortical oscillatory activity which underlies SWD.


Experimental Neurology | 2000

Selective Susceptibility to Inhibitors of GABA Synthesis and Antagonists of GABAA Receptor in Rats with Genetic Absence Epilepsy

Marguerite Vergnes; Any Boehrer; Sophie Reibel; Simone Simler; Christian Marescaux

Thalamocortical spike-and-wave discharges characterize the nonconvulsive absence seizures that occur spontaneously in genetic absence epilepsy rats from Strasbourg (GAERS), a selected strain of Wistar rats. GABA is crucial in the generation of absence seizures. The susceptibility to convulsions induced by threshold doses of various GABA receptor antagonists and inhibitors of GABA synthesis, kainic acid and strychnine, was compared in GAERS and in nonepileptic rats from a selected control strain (NE). The brain structures involved in the drug-elicited convulsive seizures were mapped by c-Fos immunohistochemistry. Injection of various antagonists of the GABA(A) receptor, bicuculline and picrotoxin, and inverse agonists of the benzodiazepine site (FG 7142 and DMCM) induced myoclonic spike-and-wave discharges followed by clonic or tonic-clonic seizures with high paroxysmal activity on the cortical EEG. The incidence of the convulsions was dose-dependent and was higher in GAERS than in NE rats. Mapping of c-Fos expression showed that the frontoparietal cortex was constantly involved in the convulsive seizures elicited by a threshold convulsant dose, whereas limbic participation was variable. In contrast, GAERS were less susceptible than NE rats to the tonic-clonic convulsions induced by the inhibitors of glutamate decarboxylase, isoniazide and 3-mercaptopropionic acid. The GABA(B) receptor antagonist CGP 56999 and kainic acid induced a similar incidence of seizures in GAERS and NE rats and predominantly activated the hippocampus. No difference in the tonic seizures elicited by strychnine could be evidenced between the strains. These results suggest that an abnormal cortical GABAergic activity may underlie absence seizures in GAERS.


Epilepsia | 2003

Effects of topiramate in two models of genetically determined generalized epilepsy, the GAERS and the audiogenic Wistar AS

Marie-Aude Rigoulot; Any Boehrer; Astrid Nehlig

Summary:  Purpose: The antiepileptic effects of topiramate (TPM) were assessed in two models of genetically determined generalized epilepsy. The model of nonconvulsive epilepsy used was a model of absence seizures, the GAERS (Genetic Absence Epilepsy Rat from Strasbourg); and the model of convulsive seizures was an audiogenic rat model, the Wistar Audiogenic Sensitive (AS) rat.


Epilepsia | 2008

Effects of carisbamate (RWJ-333369) in two models of genetically determined generalized epilepsy, the GAERS and the audiogenic Wistar AS.

Jennifer François; Any Boehrer; Astrid Nehlig

Purpose: The antiepileptic effects of carisbamate were assessed in two models of genetic epilepsy, a model of absence seizures, the Genetic Absence Epilepsy Rat from Strasbourg (GAERS) and a model of convulsive seizures, the Wistar Audiogenic Sensitive (AS) rat.


Epilepsy Research | 2003

Effects of remacemide in two models of genetically determined generalized epilepsy, the GAERS and the audiogenic Wistar AS

Astrid Nehlig; Any Boehrer

The antiepileptic effects of remacemide were assessed in two models of genetically determined generalized epilepsy. The model of non-convulsive epilepsy used was a model of absence seizures, the GAERS (genetic absence epilepsy rats from Strasbourg), and the model of convulsive seizures was an audiogenic rat model, the Wistar AS. In the eight GAERS studied, the three doses of remacemide (20, 40, and 80 mg/kg) dose-dependently reduced the expression of spike-and-wave discharges (SWDs) that had almost totally disappeared at the highest dose used, 80 mg/kg. However, at the latter dose, the effect of remacemide may be partly due to a change in the vigilance level of the animals. In the Wistar AS, the dose of 20 mg/kg prolonged by twofold the latencies to wild running and tonic seizures, and prevented their expression in one rat out of the eight studied. At 40 mg/kg, the expression of wild running and tonic seizures was inhibited in seven and maintained in one of the eight rats studied. The present results support the effects of remacemide in tonic/clonic seizure, which was the first target of the drug, and confirm the effect of the anticonvulsant on absence seizures.


Experimental Neurology | 2009

Neurobehavioral maturation of offspring from epileptic dams: study in the rat lithium-pilocarpine model.

Emmanuel Raffo; Anne Pereira de Vasconcelos; Any Boehrer; Didier Desor; Astrid Nehlig

In the present study, we explored the consequences of epilepsy on the neurobehavioral development of the offspring in a rat model of spontaneous epilepsy, the lithium-pilocarpine model of temporal lobe epilepsy not dependent on genetic factors and in animals not receiving any antiepileptic treatment. Status epilepticus was induced by lithium-pilocarpine in female rats. After the occurrence of spontaneous seizures the rats were mated and the neurobehavioral development of the offspring was explored. Rat pups were cross-fostered early after birth. We hence obtained pups born from or raised by epileptic or non-epileptic dams. On the dams, we performed a follow-up of maternal care during pregnancy. On the pups, we performed a follow-up of classical parameters of development such as body weight and eyelid opening, and subjected the pups to various tests representative of neurobehavioral maturation extending from postnatal day 4 (PD4) to PD30 (righting reflex, suspension time, negative geotaxis, open field, locomotor coordination and eight arm maze). Altogether our data show that rat pups born from or raised by epileptic dams develop as well as control pups raised by control dams. Intriguingly, pups born from lithium-pilocarpine exposed dams and raised by control mothers tend to have better scores than the two other groups in all tests. This indicates that the exposure to seizures during pregnancy is not harmful for the development of the fetus.


Neuroscience | 1999

Susceptibility to focal and generalized seizures in Wistar rats with genetic absence-like epilepsy

Simón Brailowsky; Teresa Montiel; Any Boehrer; Christian Marescaux; Marguerite Vergnes

The susceptibility to develop cortically induced focal and generalized seizures was examined in Genetic Absence Epilepsy Rats from Strasbourg (GAERS), an inbred strain of Wistar rats with absence epilepsy. A GABA-withdrawal syndrome induced after suppression of a 2-h intracortical GABA infusion was used as a model of focal epileptogenesis: localized cortical discharges appear at the infusion site within 1 h. GAERS were more prone to develop a GABA-withdrawal syndrome than non-epileptic inbred controls and non-selected Wistar rats. After a transient suppression of absence seizures following GABA infusion in GAERS, generalized spike-and-wave discharges and focal spikes were recorded simultaneously in the cortex. GAERS also showed a higher incidence of systemic pentylenetetrazol-induced convulsions at the dose of 25 mg/kg. Higher doses had similar convulsant effects in all groups. In conclusion, the results confirm a genetic susceptibility in GAERS and/or resistance in inbred non-epileptic rats to focal and generalized seizures involving the cortex. Rats with absence epilepsy appear to be more prone to seizures elicited by cortical GABA deficiency.


Experimental Neurology | 2003

Developmental characteristics of picrotoxin-induced convulsions in rats with genetic absence epilepsy

Marguerite Vergnes; Any Boehrer; Astrid Nehlig

Adult rats with genetic absence epilepsy (GAERS) were shown to be hyperresponsive to convulsions induced by picrotoxin compared to nonepileptic controls (NERs). In contrast, young GAERS aged 22-26 days were less responsive than NERs to picrotoxin-induced convulsions. Around 30 days of age, when spontaneous spike-wave discharges develop in GAERS, the sensitivity of both strains did no longer differ. After 40 days of age, GAERS appeared definitely more prone than NERs to convulse in response to picrotoxin injection. A developmental imbalance in excitation/inhibition may parallel the occurrence of SWDs.

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Simón Brailowsky

National Autonomous University of Mexico

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Teresa Montiel

National Autonomous University of Mexico

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Didier Desor

Institut national de la recherche agronomique

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Edouard Hirsch

University of Strasbourg

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Fumio Suzuki

Shiga University of Medical Science

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Kiyoshi Kurokawa

Shiga University of Medical Science

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