Enhancing excitatory projections from the ventral subiculum to the nucleus accumbens shell contribute to the MK-801-induced impairment of prepulse inhibition.

Prepulse inhibition (PPI), a measure of sensorimotor gating, has been shown to be disrupted in several animal models of neuropsychiatric disorders, such as schizophrenia. The neural circuits involving the hippocampus and nucleus accumbens (NAC) have been studied in rats to uncover the neurochemical and neuroanatomical substrates that regulate PPI. Majority of the studies of the hippocampus on PPI to date have been focused on CA1, CA2, and dentate gyrus (DG) area.

Mice Lacking the Transcriptional Coactivator PGC-1α Exhibit Hyperactivity.

Significant evidence from various sources suggests that structural alterations in mitochondrial function may play a role in both the pathogenesis of mood disorders and the therapeutic effects of available treatments. PGC-1α is a distinct transcriptional regulator designed to mediate the synchronous release of neurotransmitter in the brain and thereby to coordinate a number of gene expression pathways to promote mitochondrial biogenesis and oxidative phosphorylation. The role of PGC-1α in the context of affective disorder phenotypes and treatments has been suggested but not studied in depth.