Rescue of impaired sociability and anxiety-like behavior in adult cacna1c-deficient mice by pharmacologically targeting eIF2α.

ABSTRACT: CACNA1C, encoding the Ca_v1.2 subunit of L-type Ca²⁺ channels, has emerged as one of the most prominent and highly replicable susceptibility genes for several neuropsychiatric disorders. Ca_v1.2 channels play a crucial role in calcium-mediated processes involved in brain development and neuronal function. Within the CACNA1C gene, disease-associated single-nucleotide polymorphisms have been associated with impaired social and cognitive processing and altered prefrontal cortical (PFC) structure and activity. These findings suggest that aberrant Ca_v1.2 signaling may contribute to neuropsychiatric-related disease symptoms via impaired PFC function. Here, we show that mice harboring loss of cacna1c in excitatory glutamatergic neurons of the forebrain (f

SUBMITTER: Kabir ZD 

PROVIDER: S-EPMC5863913 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature