Genetic mechanisms for impaired synaptic plasticity in schizophrenia revealed by computational modeling.

ABSTRACT: Schizophrenia phenotypes are suggestive of impaired cortical plasticity in the disease, but the mechanisms of these deficits are unknown. Genomic association studies have implicated a large number of genes that regulate neuromodulation and plasticity, indicating that the plasticity deficits have a genetic origin. Here, we used biochemically detailed computational modeling of postsynaptic plasticity to investigate how schizophrenia-associated genes regulate long-term potentiation (LTP) and depression (LTD). We combined our model with data from postmortem RNA expression studies (CommonMind gene-expression datasets) to assess the consequences of altered expression of plasticity-regulating genes for the amplitude of LTP and LTD. Our results show that the expression alterations observed post mo

SUBMITTER: Maki-Marttunen T 

PROVIDER: S-EPMC11348150 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature