Citation

King BH, Cromwell HC, Lee HT, Behrstock SP, Schmanke T, Maidment NT. Dev. Neurosci. 1998; 20(2-3): 180-187.

Affiliation

UCLA Neuropsychiatric Institute, Los Angeles, CA 90024-1759, USA.

Copyright

(Copyright © 1998, Karger Publishers)

DOI

unavailable

PMID

9691192

Abstract

Self-injurious behavior occurring in persons with severe mental retardation is a clinically significant and poorly understood problem. Multiple neurotransmitter systems have been implicated in the pathogenesis of this behavior, particularly dopaminergic, opioidergic, and serotonergic systems. Pemoline, a central stimulant, administered systemically at high doses reliably produces self-biting behavior in the rat. The systemic bolus of pemoline produces sustained neostriatal levels of pemoline for over 24 h in a continuous infusion paradigm. Studies of the effect of cortical lesions on pemoline-mediated behaviors reveal that cortical damage, as is common in profound mental retardation, lowers the threshold for pemoline-induced self-biting behavior. Data from the corticostriatal slice suggests that sustained exposure to pemoline produces a shift in N-methyl-D-aspartate receptor-mediated responses rendering them more susceptible to dopaminergic enhancement. Thus, dopaminergic and glutamatergic interactions appear to play an important role in the development and expression of self-biting in the pemoline model.

Language: en