GRM2 eta GRM3 geneen adierazpenaren ebaluazioa subjektu eskizofrenikoen garun postmortemeko kortex aurrefrontalean

Abstract

mGluR2/3ren farmako aktibatzaileak eskizofreniaren disfuntzio glutamatergikoa tratatzeko saiatu dira eraginkortasun eskasarekin, baliteke klozapinak edo beste antipsikotikok eragindako mGluR2ren murrizketagatik. mGluR2/3 kodetzen duten GRM2 eta GRM3ren gene-adierazpena qPCRz neurtu zen postmortem garuneko kortex aurrefrontalean. Tratamendu antipsikotikoaren, eta bereziki klozapinaren, eragina ebaluatu zen, tratatu eta ez-tratatutako subjektu eskizofrenikoetan. GRM2 eta GRM3ren gene-adierazpenean ez zen desberdintasunik aurkitu subjektu eskizofrenikoen eta kontrolen artean. Klozapinak ez zuen GRM2/3 gene-adierazpena esanguratsuki modulatu beste antipsikotikoekin konparatuz. GRM2ren transkripzio murriztuak ez du mGluR2ren dentsitate murriztua azaltzen.

mGluR2/3 activating drugs have been tested to treat glutamatergic dysfunction in schizophrenia with poor efficacy, possibly due to mGluR2 depletion caused by clozapine or other antipsychotics. Gene expression of GRM2 and GRM3, which encode mGluR2/3, was measured by qPCR in postmortem brain prefrontal cortex. The effect of antipsychotic treatment, and specially clozapine, was evaluated in schizophrenic subjects treated or not-treated with these drugs. No differences were found in the gene expression of GRM2 and GRM3 between schizophrenic and control subjects. Clozapine did not significantly modulate GRM2/3 gene expression compared to other antipsychotics. Reduced transcription of GRM2 does not explain reduced mGluR2 receptor density.