Increased brain VDAC1 protein levels correlate with behavioural performance in a ketamine murine model of schizophrenia and are attenuated by the mGluR2 modulator JNJ-46356479.
Schizophrenia research June 16, 2026 David Olivares-Berjaga, Natàlia Rodríguez, Albert Martínez-pinteño et al.
In a mouse model of schizophrenia induced by postnatal ketamine exposure, the mitochondrial protein VDAC1 was elevated in the prefrontal cortex, and this increase was partially reversed by treatment with JNJ-46356479, a modulator of metabotropic glutamate receptors. Higher VDAC1 levels correlated with a greater Bax/Bcl-2 ratio—indicating apoptotic imbalance—and with worse performance on tests of memory and social behavior. VDAC1 may serve as a marker of apoptotic dysfunction in schizophrenia, and glutamatergic modulation could represent a therapeutic strategy targeting mitochondrial pathology.