Interactions between knockout of schizophrenia risk factor Dysbindin-1 and copper metabolism in mice.

ABSTRACT:

Background and purpose

DTNBP1 gene variation and lower dysbindin-1 protein are associated with schizophrenia. Previous evidence suggests that downregulated dysbindin-1 expression results in lower expression of copper transporters ATP7A (intracellular copper transporter) and SLC31A1 (CTR1; extracellular copper transporter), which are required for copper transport across the blood brain barrier. However, whether antipsychotic medications used for schizophrenia treatment may modulate these systems is unclear.

Experimental approach

The current study measured behavioral indices of neurological function in dysbindin-1 functional knockout (KO) mice and their wild-type (WT) littermates with or without quetiapine treatment. We assessed serum and brain copper levels, ATP7A and CTR1 mR

SUBMITTER: Schoonover KE 

PROVIDER: S-EPMC7554113 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature