PubMed · 7163521
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B Pilecka. 1982. [Suicide and aggression].. https://pubmed.ncbi.nlm.nih.gov/7163521/
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OBJECTIVE: To evaluate fluoxetine for the treatment of owner-directed dominance aggression in dogs. DESIGN: Prospective study. ANIMALS: 9 dogs of various breeds, ages, and either sex determined to have owner-directed dominance aggression. PROCEDURE: Placebo and fluoxetine (1 mg/kg of body weight) were compared for the treatment of owner-directed dominance aggression in a single-blind crossover study. Owners were instructed to record aggressive and nonaggressive responses of their dogs daily on a canine-overt aggression chart for the 5-week duration of the study. Total aggression scores (linear and geometric) were calculated for each week of the study. The frequency of individual responses was also analyzed independently. RESULTS: Fluoxetine resulted in a significant (P = 0.01) reduction in owner-directed dominance aggression after 3 weeks of treatment. No particular aggressive response accounted for the overall reduction in aggression. CLINICAL IMPLICATIONS: Fluoxetine may be useful in the management of dominance aggression in dogs.
Enkephalins are endogenous opioid peptides that are derived from a pre-proenkephalin precursor protein. They are thought to be vital in regulating many physiological functions, including pain perception and analgesia, responses to stress, aggression and dominance. Here we have used a genetic approach to study the role of the mammalian opioid system. We disrupted the pre-proenkephalin gene using homologous recombination in embryonic stem cells to generate enkephalin-deficient mice. Mutant enk-/- animals are healthy, fertile, and care for their offspring, but display significant behavioural abnormalities. Mice with the enk-/- genotype are more anxious and males display increased offensive aggressiveness. Mutant animals show marked differences from controls in supraspinal, but not in spinal, responses to painful stimuli. Unexpectedly, enk-/- mice exhibit normal stress-induced analgesia. Our results show that enkephalins modulate responses to painful stimuli. Thus, genetic factors may contribute significantly to the experience of pain.
There are multiple pathways involved in the regulation of male typical aggression by T, and the functional pathway is determined by genotype. Target-tissue sensitivity to the aggression-promoting properties of T and its estrogenic and androgenic metabolites is determined by a complex sequence of events in which steroid receptors play a critical role. To date, it appears that the relative density of AR may be an important factor in the biobehavioral effects of androgens. Regarding sensitivity to estrogens, characterization of ER-NM interactions, and understanding of the contribution of the two activating functions within ER, appears to be necessary to comprehensively describe the cellular basis for responsiveness to the aggression-promoting effect of this T metabolite. In broader terms, these observations indicate that understanding the relationship between T and the expression of aggression in humans will require models that incorporate cellular aspects of steroid hormone action, including metabolism, receptor function, and gene regulation.