Delaney K. Fischer

TL;DR: It is shown that mice harboring loss of cacna1c in excitatory glutamatergic neurons of the forebrain (fbKO) that have previously reported to exhibit anxiety-like behavior, displayed a social behavioral deficit and impaired learning and memory, and systemic treatment with ISRIB was sufficient to reverse the social deficit and elevated anxiety- like behavior in adult cacna 1c fbKO mice.

TL;DR: It is reported that viral vector-mediated deletion of cacna1c in the adult prefrontal cortex (PFC) of mice recapitulates the antidepressant-like effect observed in cacna 1c HET mice using the sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST).

TL;DR: It is reported that chronic stress leads to a delayed increase in Cav1.2 expression selectively within the prefrontal cortex (PFC), but not in other stress-sensitive brain regions such as the hippocampus or amygdala, and molecular studies find a delayed upregulation of the p25/Cdk5-glucocorticoid receptor (GR) pathway in the PFC when examined 8 days post-stress.

TL;DR: An essential role is demonstrated for the hippocampal Cav1.2 channels in extinction of contextual cocaine-associated memories in cocaine CPP extinction, providing a framework for further exploration of mechanisms underlying extinction of cocaine-seeking behavior.

TL;DR: It is identified that loss of Crbn results in learning, memory, and synaptic defects as a consequence of exaggerated AMPK activity, inhibition of mTORC1 signaling, and decreased glutamatergic synaptic proteins, which establishes the cereblon knock-out mouse as a model of pure ID without the confounding behavioral phenotypes associated with other current models of ID.