Serine racemase deletion alters adolescent social behavior and whole-brain cFos activation.

ABSTRACT:

Background

Neurodevelopmental disorders (NDDs) can cause debilitating impairments in social cognition and aberrant functional connectivity in large-scale brain networks, leading to social isolation and diminished everyday functioning. To facilitate the treatment of social impairments, animal models of NDDs that link N- methyl-D-aspartate receptor (NMDAR) hypofunction to social deficits in adulthood have been used. However, understanding the etiology of social impairments in NDDs requires investigating social changes during sensitive windows during development.

Methods

We examine social behavior during adolescence using a translational mouse model of NMDAR hypofunction (SR-/-) caused by knocking out serine racemase (SR), the enzyme needed to make D-serine, a key NMDAR coagoni

SUBMITTER: Brown SE 

PROVIDER: S-EPMC11228300 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature