Upstream regulators on the c-Jun amino-terminal kinase (JNK) pathway are associated with neuropsychiatric disorders such as schizophrenia, bipolar, and autism. However, the mechanism of action of the JNK pathway in the context of these diseases is unknown. We previously identified that inhibition of JNK in dentate gyrus granule cells of mouse hippocampus induces a low anxiety- and low depressive-like phenotype (Mohammad et al., Molecular Psychiatry, 2018). However, whether JNK pathway activity in other brain regions contributes to these behaviours is not known. Here we use cell restrictive expression of a JNK inhibitor peptide to suppress JNK activity in distinct neuronal subsets in the brain using systemic AAV vectors injected retro-orbitally to C57BL/6 mice. mRuby2-tagged nuclear-targeted JNK inhibitor peptide (JIP1a1-277) is expressed under the control of the CAG, hSyn1, or mDlx promoters and compared to empty vector mRuby2 alone. Systemic vectors AAV-PHP.eB and AAV.CAP-B10 are compared. The behaviour of the mice is assessed with the open field, elevated plus maze, novel object recognition, Y-maze, and forced swim tests. Our preliminary results show that inhibition of JNK with the hSyn1 promoter using the AAV-PHP.eB vector induces a low anxiety-like phenotype in the elevated plus maze, whereas inhibition with the hSyn1 and AAV.CAP-B10 increased depressive-like behaviour in the forced swim test. Ongoing work compares the spatial distribution of JNK inhibitor expression using these vectors in order to pinpoint the precise regions from where JNK inhibition evokes these behaviours.