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Journal Article

Citation

Devine DP. Methods Mol. Biol. 2019; 2011: 41-60.

Affiliation

Behavioral and Cognitive Neuroscience Program, Department of Psychology, University of Florida, Gainesville, FL, USA. dpdevine@ufl.edu.

Copyright

(Copyright © 2019, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/978-1-4939-9554-7_3

PMID

31273692

Abstract

Although self-injurious behavior is a common comorbid behavior problem among individuals with neurodevelopmental disorders, little is known about its etiology and underlying neurobiology. Interestingly, it shows up in various forms across patient groups with distinct genetic errors and diagnostic categories. This suggests that there may be shared neuropathology that confers vulnerability in these disparate groups. Convergent evidence from clinical pharmacotherapy, brain imaging studies, postmortem neurochemical analyses, and animal models indicates that dopaminergic insufficiency is a key contributing factor. This chapter provides an overview of studies in which animal models have been used to investigate the biochemical basis of self-injury and highlights the convergence in findings between these models and expression of self-injury in humans.


Language: en

Keywords

Animal model; Dopamine; Lesch-Nyhan syndrome; Prader-Willi syndrome; Self-injurious behavior; Striatum

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