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Results for “Epilepsy, Absence”

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At least 127 records · Page 7Linked to original sources
PubMed1990

Genetics of absence epilepsy in rats.

All rats of the WAG inbred strain show electrophysiological and behavioral phenomena reminiscent of human absence epilepsy. To study the genetic architecture of this kind of epilepsy, WAG rats were cross bred with inbred ACI rats which show no signs of epilepsy. Number and duration of spike-wave discharges per hour were determined from 24-h recordings of cortical EEG in parental strains and reciprocal F1 hybrids. All hybrids showed spike-wave discharges, indicating complete dominance for occurrence, but different genetic backgrounds were suggested for number and duration of the phenomena. These results imply that more than one gene is involved in absence epilepsy. Some genes determine the occurrence, while others may manipulate the actual number and duration of the epileptic phenomena.

Animals↗
PubMedDate not supplied

Single locus mutations in mice expressing generalized spike-wave absence epilepsies.

Studies in mutant mice are beginning to reveal important general principles regarding the heredity of the spike-wave cortical synchronization trait. First, a defect at a single gene locus is sufficient to produce a generalized spike-wave seizure disorder. Second, the EEG pattern itself is genetically heterogeneous, and can arise from mutations in at least five independent loci. Third, the intervening cellular excitability mechanisms underlying the generation of spike-wave cortical discharges are not identical. Fourth, each of the mutant genes gives rise to syndromes that can differ in their seizure frequency, sensitivity to antiepileptic drugs, and severity of the associated neurological phenotype. Fifth, primary defects can be distinguished from secondary cellular alterations resulting from pathological neuronal synchronization. The patterns of these secondary changes vary according to the specific mutant allele, and may give rise to distinctive secondary phenotypes. The reproducibility of these defined genetic models may facilitate age-dependent antiepileptic drug discovery by defining novel targets for therapy at different developmental stages of the seizure disorder.

Action Potentials↗
PubMed1994

Proenkephalin and prodynorphin mRNA level in brain of rats with absence epilepsy.

An in situ hybridization method was used to estimate the proenkephalin (PENK) and prodynorphin (PDYN) mRNA levels in the brain of epileptic 6-month-old WAG/Rij rats in comparison with non-epileptic: 3-month-old WAG/Rij rats, 3-month-old ACI rats and 6-month-old ACI rats. The epileptic rats had a significantly higher level of PENK mRNA in the striatum as compared to non-epileptic controls. The PDYN mRNA level was significantly elevated only in the hippocampus of epileptic rats, whereas age- or strain-related changes in the striatal and cortical PDYN mRNA levels were found in both epileptic and non-epileptic rats. The changes in the biosynthetic activity of endogenous opioid peptide systems may be important for the occurrence of epileptic discharges in these animals.

Aging↗
PubMedDate not supplied

Circadian rhythmicity in absence epilepsy in rats.

In order to study putative time of day effects upon the number and mean duration of spike-wave complexes, 19 rats of the WAG/Rij strain were equipped with cortical EEG electrodes. The EEGs were recorded continuously for 48 h. A cosinor analysis was applied to both the data on each subject and the mean scores of all rats. A definite 24 h rhythm was found for the number of spike-wave complexes occurring each hour. The acrophase appeared during the early hours of the dark period, while the minimum was found to take place immediately after the onset of light. A 24 h rhythm was less prominent for the mean duration of the spike-wave complexes. Finally, there were no differences found between the 2 days of the 48 h registration period, suggesting that the number and duration of the spike-wave complexes found on a given day are representative for the following day.

Animals↗
PubMed1993

GABAA receptor impairment in the genetic absence epilepsy rats from Strasbourg (GAERS): an immunocytochemical and receptor binding autoradiographic study.

Some aspects of the GABA and cholinergic systems have been investigated in the cortex and thalamus of GAERS Wistar rats, a model of petit-mal epilepsy, and in a non-epileptic control strain. GABA and its synthetic enzyme, glutamic acid decarboxylase (GAD), were located by immunocytochemistry; the GABAA receptors were evaluated by autoradiography of GABA-enhanced 3H-flunitrazepam binding and by immunocytochemistry using specific antibodies against the beta 2-beta 3 subunits of GABAA receptor protein. GABA and GAD immunocytochemistry did not show up any difference in density or distribution of immunoreactive elements (fibers, terminals and neurons) between epileptic and control animals, but autoradiographic and immunocytochemical studies showed a decreased enhancement of 3H-flunitrazepam binding and of beta 2-beta 3 subunits of GABAA receptor in the sensorimotor cortex and anterior thalamic areas of the epileptic strain. No differences were found in benzodiazepine receptors in the two strains. GABAB receptors were measured as 3H-baclofen binding in a crude synaptic membrane preparation and there was no difference between epileptic and control animals. Choline acetyltransferase, the synthetic enzyme for acetylcholine, and muscarinic receptor subtypes (M1 and M2), visualized respectively by an immunocytochemical procedure and binding autoradiography, did not differ in epileptic and normal rats. The data suggest an impairment of the 'GABAA system' in restricted brain regions of epileptic rats, due to a reduction of receptor beta 2-beta 3 subunits and coupling to benzodiazepine receptors despite the normal synthesis and location of the neurotransmitter.

Acetylcholine↗
PubMed1987

Concepts of absence epilepsies: discrete syndromes or biological continuum?

There are two current approaches to the clinical conceptualization of the generalized epilepsies. The syndromic approach attempts to subdivide the patient population into relatively homogeneous groups, largely on the basis of clinical and EEG criteria. In contrast, the neurobiological approach aims to formulate a unique profile for each patient by incorporating particulars of the patient onto the background of knowledge regarding the etiologic factors important in generalized epilepsy. The value of these two approaches is discussed with regard to the dual aims of, first, improving the understanding of generalized epilepsy, and second, providing a precise diagnosis, an accurate prognosis, and optimal treatment for the patient.

Adolescent↗