No abstract

Photothrombotic infarcts of the neocortex result in structural and functional alterations of cortical networks, including decreased GABAergic inhibition, and can generate epileptic seizures within one month of lesioning. In our study, we assessed the involvement and potential changes of cortical GABA A receptor (GABA A R) α 1 subunits at 1, 3, 7, and 30 days after photothrombosis. Quantitative competitive reverse transcription polymerase chain reaction (cRT-PCR) and semi-quantitative Western blot analysis were used to investigate GABA A R α 1 subunit mRNA and protein levels in proximal and distal regions of perilesional cortex and in homotopic areas of young adult SpragueDawley rats. GABA A R α 1 subunit mRNA levels were decreased ipsilateral and contralateral to the infarct at 7 days, but were increased bilaterally at 30 days. GABA A R α 1 subunit protein levels revealed no significant change in neocortical areas of both hemispheres of lesioned animals compared with protein levels of sham-operated controls at 1, 3, 7, and 30 days. At 30 days, GABA A R α 1 subunit protein expression was significantly increased in lesioned animals within proximal and distal regions of perilesional cortex compared with distal neocortical areas contralaterally (Student's t-test, p<0.05). Short-and long-term alterations of mRNA and protein levels of the GABA A R α 1 subunit ipsilateral and contralateral to the lesion may influence alterations in cell surface receptor subtype expression and GABA A R function following ischemic infarction and may be associated with formative mechanisms of poststroke epileptogenesis.