The first study investigated mPFC–hippocampal synchrony in the Df (16)A+/− strain of transgenic mice, which models a human chromosomal abnormality that is associated with a ~30 fold greater risk of developing schizophrenia [25•]. Compared to wild-type mice, the mutant mice exhibited significantly reduced hippocampal theta phase-locking of mPFC neurons and decreased theta coherence between the hippocampus and mPFC. The mutants also showed significant deficits on a delayed non-match-to-sample spatial working memory task that correlated with reductions in hippocampal–prefrontal theta coherence. These results raise the possibility that deficient theta phase-locking between the regions contributes to working memory deficits associated with schizophrenia.
