RAPID COMMUNICATION Reduction of Zolpidem Sensitivity in a Freeze Lesion Model of Neocortical Dysgenesis
نویسندگان
چکیده
DeFazio, R. Anthony and John J. Hablitz. Reduction of zolpiazepine receptor (BZ1) agonist zolpidem on miniature inhibdem sensitivity in a freeze lesion model of neocortical dysgenesis. itory postsynaptic currents (mIPSCs). Preliminary results J. Neurophysiol. 81: 404–407, 1999. Early postnatal freeze lesions from this study have appeared in abstract form (DeFazio in rat neocortex produce anatomic abnormalities resembling those and Hablitz 1997). observed in human patients with seizure disorders. Although in
منابع مشابه
Reduction of zolpidem sensitivity in a freeze lesion model of neocortical dysgenesis.
Early postnatal freeze lesions in rat neocortex produce anatomic abnormalities resembling those observed in human patients with seizure disorders. Although in vitro brain slices containing the lesion are hyperexcitable, the mechanisms of this alteration have yet to be elucidated. To test the hypothesis that changes in postsynaptic inhibitory receptors may underlie this hyperexcitability, we exa...
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Induction of a focal freeze lesion to the skullcap of a 1-day-old rat pup leads to the formation of microgyria similar to those identified postmortem in human dyslexics. Rats with microgyria exhibit rapid auditory processing deficits similar to those seen in language-impaired (LI) children, and infants at risk for LI and these effects are particularly marked in juvenile as compared to adult sub...
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OBJECTIVE Malformations of cortical development are frequent causes of human refractory epilepsy. The freeze-lesion model in rats shows histopathological features similar to those found in human polymicrogyria. Previous studies reported in vitro hyperexcitability in this model, but in vivo epileptogenicity has not been confirmed. METHODS Neocortical freeze lesions were induced in Sprague-Dawl...
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