GRM2 eta GRM3 geneen adierazpenaren ebaluazioa subjektu eskizofrenikoen postmortem garuneko kortex aurrefrontalean
- Jon Ander Santas Martín
- Alfredo Ramos Miguel
- Luis Felipe Callado Hernando
- José Javier Meana Martínez
- Guadalupe Rivero Calera
- Olatz Arbelaitz Gallego (ed. lit.)
- Ainhoa Latatu (ed. lit.)
- Elixabete Pérez Gaztelu (ed. lit.)
Publisher: Udako Euskal Unibertsitatea, UEU = Universidad Vasca de Verano
ISBN: 978-84-8438-862-3, 978-84-8438-866-1
Year of publication: 2023
Pages: 29-36
Congress: Ikergazte. Nazioarteko Ikerketa Euskaraz (5. 2023. Donostia)
Type: Conference paper
Abstract
mGluR2/3 activating drugs have been tested to treat glutamatergic dysfunction in schizophrenia with poor ejjicacy, possibly due to mGluR2 depletion caused by clozapine or oiher 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 modu/ate GRM2/3 gene expression compared to other antipsychotics. Reduced transcription of GRM2 does not explain reduced mGluR2 receptor density.