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While the origins and developmental course of self-injurious behavior (SIB) remain relatively unknown, recent studies suggest a biological imbalance may potentiate or provoke the contagious recurrence of SIB patterns in individuals with severe developmental disabilities (DD). Evidence from several laboratories indicates that functioning, relations, and processing of a stress-related molecule, proopiomelanocortin, (POMC), may be perturbed among certain subgroups of individuals exhibiting SIB. The current investigation employed a unique time-pattern analysis program (THEME) to examine whether recurrent temporal patterns (T-patterns) of SIB were related to morning levels of two POMC-derived hormones: β-endorphin (βE) and adrenocorticotropic hormone (ACTH). THEME was used to quantify highly significant (nonrandom) T-patterns that included SIB within a dataset of in-situ observational recordings spanning 8 days (~40 hours) in 25 subjects with DD. Pearson's product-moment analyses revealed highly significant correlations between the percentage of T-patterns containing SIB and basal levels of both βE and ACTH, which were not found with any other "control" T-patterns. These findings support the hypothesis that the recurrent temporal patterning of SIB represents a unique behavioral phenotype directly related to perturbed levels of POMC-derived stress hormones in certain individuals with severe DD.

Rats and mice were exposed to several different stress situations to investigate whether brain benzodiazepine receptors were sensitive to altered external or internal environmental circumstances. All stresses were applied for several days. Electrical foot shock and post-natal isolation of newborn pups resulted in small (7--25%; P less than 0.05--0.001) decreases in benzodiazepine receptor binding in some cerebral cortex or hippocampal areas while immobilization stress resulted in a small (9%; P less than 0.05) increase in frontal cortex. Other brain areas (i.e., striatum, cerebellum, pons-medulla, and occipital cortex) and other stress forms (isolation of male mice, forced swimming in cold water, or chronic amphetamine intoxication) did not change receptor binding. The effect of prolonged stress on benzodiazepine receptors is complex and not very pronounced.

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