Deletion of Glycogen Synthase Kinase-3β in D₂ Receptor-Positive Neurons Ameliorates Cognitive Impairment via NMDA Receptor-Dependent Synaptic Plasticity.

ABSTRACT:

Background

Cortical dopaminergic systems are critically involved in prefrontal cortex (PFC) functions, especially in working memory and neurodevelopmental disorders such as schizophrenia. GSK-3β (glycogen synthase kinase-3β) is highly associated with cAMP (cyclic adenosine monophosphate)-independent dopamine D₂ receptor (D₂R)-mediated signaling to affect dopamine-dependent behaviors. However, the mechanisms underlying the GSK-3β modulation of cognitive function via D₂Rs remains unclear.

Methods

This study explored how conditional cell-type-specific ablation of GSK-3β in D₂R+ neurons (D₂R-GSK-3β^-/-) in the brain affects synaptic function in the medial PFC (mPFC). Both male and female (postnatal days 60-90) mice

SUBMITTER: Li YC 

PROVIDER: S-EPMC7103512 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature