Glial glutamate transporter mRNAs in the genetically absence epilepsy rat from Strasbourg

• Published in: Brain research. Molecular brain research. 2000-01, Vol.75 (1), p.96-104
• Main Authors: Ingram, Esther M, Tessler, Shoshi, Bowery, Norman G, Emson, Piers C
• Format: Article
• Language: English
• Subjects: Amino Acid Transport System X-AG; Animals; aspartic acid transporter; ATP-Binding Cassette Transporters - genetics; Biological and medical sciences; Brain - metabolism; Disease Models, Animal; Epilepsy; Epilepsy, Absence - genetics; GAERS; GLAST; GLT-1; Glutamate; Glutamic Acid - metabolism; glutamic acid transporter; glutamic acid/aspartic acid transporter; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Humans; Male; Medical sciences; mRNA; Nervous system (semeiology, syndromes); Neuroglia - metabolism; Neurology; Oligonucleotide Probes; Rats; Rats, Mutant Strains; Rats, Wistar; Reference Values; RNA, Messenger - analysis; RNA, Messenger - genetics; Seizures - genetics; Subthalamic Nucleus - metabolism; Transcription, Genetic; Transporter; Ventral Thalamic Nuclei - metabolism
• ISSN: 0169-328X; 1872-6941
• DOI: 10.1016/S0169-328X(99)00301-0

Recent studies support a critical role for the glutamatergic system and glutamate transporters in the pathogenesis of epilepsy. The glial glutamate transporters GLT-1 ( l-glutamate transporter) and GLAST ( l-glutamate/ l-aspartate transporter) are known to be responsible for the majority of glutamate reuptake from the synaptic cleft and constitute one mechanism by which extracellular glutamate levels may be controlled. The present study therefore compared GLT-1 and GLAST mRNA levels in the genetically absence epilepsy rat from Strasbourg (GAERS) with those of age-matched non-epileptic controls. The GAERS rat has been proposed as an animal model of inherited human absence epilepsy, displaying recurrent, generalised, non-convulsive seizures that originate from thalamic and cortical structures. In situ hybridisation with 35 S -labelled oligonucleotide probes demonstrated substantial and significant increases in GLT-1 mRNA levels in the ventromedial nucleus of the thalamus (VM) and the subthalamic nucleus (STN) of GAERS rats. Increases in GLAST mRNA were found in the primary somatosensory cortex (SS1) and temporal cortex (Te) of GAERS. These data, along with previous studies, suggest that regional imbalances in GABAergic and glutamatergic systems may be associated with the pathogenesis of absence seizures in GAERS.