16p11.2 duplication shows early male-biased impacts on reward learning, but NMDA receptor antagonism reduces optimal choice selection in both wildtypes and 16p11.2 duplication.

ABSTRACT:

Rationale

16p11.2 duplication is associated with numerous neuropsychiatric conditions at a genome-wide level, including psychosis. Mice modeling 16p11.2 duplication may provide important insights into cognitive risk factors, in particular in reward-guided decision making. NMDAR function has also been implicated in psychosis phenotypes, but whether these phenotypes differ by genetic risk factor is unknown.

Objectives

We aimed to: 1) identify sex and genotype differences in early operant training and two-arm spatial restless bandit task performance; 2) examine the effects of an NMDAR antagonist on task performance and strategy across genotypes.

Methods

16p11.2 duplication and wildtype mice completed a series of training schedules of escalating difficulty followed by ban

SUBMITTER: Mueller D 

PROVIDER: S-EPMC12262533 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature