Metabolic approach of absence seizures in a genetic model of absence epilepsy, the GAERS: Study of the leucine-glutamate cycle

2001 ◽  
Vol 66 (5) ◽  
pp. 923-930 ◽  
Author(s):  
Franck Dufour ◽  
Katarzyna A. Nalecz ◽  
Maciej J. Nalecz ◽  
Astrid Nehlig
Keyword(s):  
Genetic Model ◽  
Absence Epilepsy ◽  
Absence Seizures

scholarly journals Nucleus-Specific Abnormalities of GABAergic Synaptic Transmission in a Genetic Model of Absence Seizures

2006 ◽  
Vol 96 (6) ◽  
pp. 3074-3081 ◽  
Author(s):  
Thomas Bessaïh ◽  
Laurence Bourgeais ◽  
Carmen I. Badiu ◽  
David A. Carter ◽  
Tibor I. Toth ◽  
...  
Keyword(s):  
Genetic Model ◽  
Molecular Genetic ◽  
Experimental Studies ◽  
Protein S ◽  
Absence Epilepsy ◽  
Pathophysiological Mechanism ◽  
Full Spectrum ◽  
Genetic Changes ◽  
Absence Seizures ◽  
Thalamocortical Network

Human and experimental studies indicate that molecular genetic changes in GABAA receptors may underlie the expression of spike-and-waves discharges (SWDs) occurring during absence seizures. However, the full spectrum of the genetic defects underlying these seizures has only been partially elucidated, the expression and functional profiles of putative abnormal protein(s) within the thalamocortical network are undefined, and the pathophysiological mechanism(s) by which these proteins would lead to absence paroxysms are poorly understood. Here we investigated GABAA inhibitory postsynaptic currents (IPSCs) in key thalamocortical areas, i.e., the somatosensory cortex, ventrobasal thalamus (VB) and nucleus reticularis thalami (NRT), in preseizure genetic absence epilepsy rats from Strasbourg (GAERS), a well-established genetic model of typical absence seizures that shows no additional neurological abnormalities, and compared their properties to age-matched non-epileptic controls (NECs). Miniature GABAA IPSCs of VB and cortical layers II/III neurons were similar in GAERS and NEC, whereas in GAERS NRT neurons they had 25% larger amplitude, 40% faster decay. In addition, baclofen was significantly less effective in decreasing the frequency of NRT mIPSCs in GAERS than in NEC, whereas no difference was observed for cortical and VB mIPSCS between the two strains. Paired-pulse depression was 45% smaller in GAERS NRT, but not in VB, and was insensitive to GABAB antagonists. These results point to subtle, nucleus-specific, GABAA receptor abnormalities underlying SWDs of typical absence seizures rather than a full block of these receptors across the whole thalamocortical network, and their occurrence prior to seizure onset suggests that they might be of epileptogenic significance.

Finasteride inhibits the progesterone-induced spike-wave discharges in a genetic model of absence epilepsy

2003 ◽  
Vol 75 (4) ◽  
pp. 889-894 ◽  
Author(s):  
Gilles van Luijtelaar ◽  
Bogusława Budziszewska ◽  
Magdalena Tetich ◽  
Władysław Lasoń
Keyword(s):  
Genetic Model ◽  
Absence Epilepsy ◽  
Spike Wave Discharges ◽  
Spike Wave

Thalamic low threshold calcium current in a genetic model of absence epilepsy

Neuroreport ◽  
1993 ◽  
Vol 4 (11) ◽  
pp. 1231-1234 ◽  
Author(s):  
Alice Guyon ◽  
Marguerite Vergnes ◽  
Nathalie Leresche
Keyword(s):  
Calcium Current ◽  
Genetic Model ◽  
Absence Epilepsy ◽  
Low Threshold

scholarly journals Cortical Glutamate Metabolism is Enhanced in a Genetic Model of Absence Epilepsy

2006 ◽  
Vol 26 (12) ◽  
pp. 1496-1506 ◽  
Author(s):  
Torun M Melø ◽  
Ursula Sonnewald ◽  
Monique Touret ◽  
Astrid Nehlig
Keyword(s):  
Genetic Model ◽  
Absence Epilepsy ◽  
Glutamate Metabolism

scholarly journals Reduced GABAB receptor subunit expression and paired-pulse depression in a genetic model of absence seizures

2007 ◽  
Vol 25 (3) ◽  
pp. 631-641 ◽  
Author(s):  
D. Merlo ◽  
C. Mollinari ◽  
Y. Inaba ◽  
A. Cardinale ◽  
A.M. Rinaldi ◽  
...  
Keyword(s):  
Genetic Model ◽  
Gabab Receptor ◽  
Receptor Subunit ◽  
Absence Seizures ◽  
Paired Pulse ◽  
Subunit Expression ◽  
Paired Pulse Depression

scholarly journals Seizure Exacerbation by Antiepileptic Drugs

2005 ◽  
Vol 5 (5) ◽  
pp. 192-193 ◽  
Author(s):  
Jacqueline A. French
Keyword(s):  
Antiepileptic Drugs ◽  
De Novo ◽  
Focal Epilepsy ◽  
Juvenile Myoclonic Epilepsy ◽  
Absence Epilepsy ◽  
Absence Seizures ◽  
Incorrect Diagnosis ◽  
Juvenile Absence Epilepsy ◽  
Generalized Epilepsy

Worsening of Seizures by Oxcarbazepine in Juvenile Idiopathic Generalized Epilepsies Gelisse P, Genton P, Kuate C, Pesenti A, Baldy-Moulinier M, Crespel A Epilepsia 2004;45:1282–1286 Purpose Several studies have shown that carbamazepine (CBZ) may aggravate idiopathic generalized epilepsy (IGE). Oxcarbazepine (OXC) is a new drug chemically related to CBZ. We report six cases of juvenile IGE with a clear aggravation by OXC. Methods We retrospectively studied all patients with IGE first referred to our epilepsy department between January 2001 and June 2003 and treated with OXC. Results During this period, six patients were identified. All had an aggravation of their epilepsy in both clinical and EEG activities. OXC had been used because of an incorrect diagnosis of focal epilepsy or generalized tonic–clonic seizures (GTCSs) of undetermined origin (no syndromic classification of the epilepsy). Before OXC, only one patient had experienced a worsening of seizures with an inadequate drug (carbamazepine; CBZ). Four had juvenile myoclonic epilepsy, one had juvenile absence epilepsy, and one had IGE that could not be classified into a precise syndrome. OXC (dosage range, 300–1,200 mg/day) was used in monotherapy in all of them except for one patient. Aggravation consisted of a clear aggravation of myoclonic jerks (five cases) or de novo myoclonic jerks (one case). Three patients had exacerbation of absence seizures. One patient had worsened dramatically and had absence status, and one had de novo absences after OXC treatment. The effects of OXC on GTCSs were less dramatic, with no worsening in frequency in three and a slight increase in three. Conclusions OXC can be added to the list of antiepileptic drugs that can exacerbate myoclonic and absence seizures in IGE.

Sign in / Sign up

Export Citation Format

Share Document