Abstract
In adult rats, kainic acid-induced status epilepticus markedly reduces GluR2 (the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid, AMPA subunit that limits Ca2+ permeability), receptor mRNA in the vulnerable CA3 and may contribute to delayed neurodegeneration. In rat pups resistant to kainate seizure-induced hippocampal neurodegeneration by silver impregnation, glutamate or GABA(A) alpha1-receptor mRNAs were unaltered in CA3 neurons 24 h after status epilepticus. In the dentate gyrus, GluR1 and GluR2 mRNAs were transiently increased in P14 but not P5 pups. Immunocytochemistry revealed no apparent differences in the distribution patterns of GluR1, GluR2, or GluR2/3 receptor proteins in the CA3 or dentate gyrus of P14 pups. Status epilepticus-induced alterations in receptor GluR2 and GABA(A) alphal mRNAs and AMPA protein expression vary with developmental age. Sustained expression at young ages may contribute to the resistance of developing hippocampal neurons to seizure-induced damage.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
