PubMed · 6911814
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J Mercier, C Roche. 1980-07-01. [Normal aggressiveness].. https://pubmed.ncbi.nlm.nih.gov/6911814/
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To study the behavioral role of neurons containing the D1 dopamine receptor (D1+), we have used a genetic neurostimulatory approach. We generated transgenic mice that express an intracellular form of cholera toxin (CT), a neuropotentiating enzyme that chronically activates stimulatory G-protein (Gs) signal transduction and cAMP synthesis, under the control of the D1 promoter. Because the D1 promoter, like other CNS-expressed promoters, confers transgene expression that is regionally restricted to different D1+ CNS subsets in different transgenic lines, we observed distinct but related psychomotor disorders in different D1CT-expressing founders. In a D1CT line in which transgene expression was restricted to the following D1+ CNS regions-the piriform cortex layer II, layers II-III of somatosensory cortical areas, and the intercalated nucleus of the amygdala-D1CT mice showed normal CNS and D1+ neural architecture but increased cAMP content in whole extracts of the piriform and somatosensory cortex. These mice also exhibited a constellation of compulsive behavioral abnormalities that strongly resembled human cortical-limbic-induced compulsive disorders such as obsessive-compulsive disorder (OCD). These compulsive behaviors included episodes of perseverance or repetition of any and all normal behaviors, repetitive nonaggressive biting of siblings during grooming, and repetitive leaping. These results suggest that chronic potentiation of cortical and limbic D1+ neurons thought to induce glutamatergic output to the striatum causes behaviors reminiscent of those in human cortical-limbic-induced compulsive disorders.
Considerable evidence suggests that there is a relationship between pathologic aggressive behavior and low cerebrospinal fluid (CSF) concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in both humans and non-human primates. The purpose of this investigation is to examine the relationship between CSF concentrations of human newborn 5-HIAA and subsequent aggressive behavior observed at 30 months of age. Leftover portions of culture negative CSF drawn from febrile infants (age, birth to 3 months) were assayed for 5-HIAA. Family environment and child behavior were assessed at 30 months by parent report. Subjects with 5-HIAA levels below the median of the distribution had higher externalizing behavior scores at 30 months than did subjects whose 5-HIAA levels fell above the median (P = 0.02). While it is likely that serotonin mediates one component of genetic liability to antisocial outcome, the magnitude of that component may be less than what has been inferred from previously published reports.
Thirty-two permanently pseudopregnant bitches were treated with the anti-prolactin drug cabergoline. They had all been ovariohysterectomised up to five months after their last season, in some cases over two years previously, when most were reported as showing no signs of the condition. The clinical signs were mainly behavioural, the majority being aggressive, and a small number were lactating. The efficiency of the cabergoline therapy was classified by the owners as 'excellent' or 'good' in 50 per cent of the cases, and fair in 36 per cent. The rate of success was markedly better than in similar cases treated with reproductive steroids. In all but one of the bitches, the plasma prolactin concentrations were basal.