Citation

Itohara S, Kobayashi Y, Nakashiba T. Curr. Opin. Behav. Sci. 2015; 2: 46-51.

Copyright

(Copyright © 2015, Elsevier Publishing)

DOI

10.1016/j.cobeha.2014.09.002

PMID

unavailable

Abstract

Increasing evidence suggests complex genetic factors for attention-deficit/hyperactivity disorder (ADHD). Animal models with definitive genetic characteristics are indispensable for gaining an understanding of the molecular, cellular, and neural circuit mechanisms underlying ADHD. Toward this aim, mice have several advantages because of their well-controlled genetic backgrounds and the relative ease with which functions of defined neuronal circuits can be manipulated. Dopamine signaling dysfunction was once the major pathogenic focus of interest in ADHD research, but hypotheses have expanded to include functionally distinct molecules. Forward and reverse genetic approaches have produced diverse mouse genetic models for genes involved in monoaminergic signaling, synaptic plasticity, and neuronal circuit formation. Data suggest crucial roles of gene-gene interactions and gene-environment interactions in the pathophysiology of ADHD.