Influence of social setting on the induction of brain cyclic AMP in response to electric shock in the rat.
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Biomedical subjects
Publications and source records attributed to B Eichelman.
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Septal irritability and shock-induced aggression were suppressed by the administration of p-chlorophenylalanine (PCPA) to septal rats. The levels of septal irritability and shock-induced fighting were significantly lower in septal, PCPC-treated rats than in nontreated septal rats. Since both parameters of septal aggression were reduced by PCPA, and while PCPA has no effect on shock-induced fighting of unlesioned rats under similar parameters, it appears that both forms of aggression may function through a common neural mechanism.
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A significant increase in shock-induced aggression occurs in the rat 4 days after an intraventricular injection of 90 micrograms of 6-hydroxydopa. Both fluorescent histology and biochemical assay demonstrate that brain norepinephrine is reduced by 90 micrograms of 6-hydroxydopa, while brain dopamine remains unaltered. This suggests that one form of aggressive behavior (shock-induced aggression) is modulated through a central noradrenergic system.
Male Sprague-Dawley rats were subjected to 4 weeks of daily periods of immobilization stress. One of two experimental groups was allowed 1 month of recovery. After 4 weeks of stress, there was a significant increase in shockinduced fighting, in the activity of serum dopamine-beta-hydroxylase, and in the activity of hypothalamic tyrosine hydroxylase. The concentration of hypothalamic norepinephrine was not decreased. After 4 weeks of recovery, only serum dopamine-betahydroxylase activity returned to normal; it therefore appears that longterm stress may increase central catecholamine synthesis. possibly resulting in a persistent increase in aggressive behavior.
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A significant fall in tail blood pressure occurs in paired rats after shock-induced aggression. Pressure returns to baseline levels within 4 hours after fighting. Conversely, single rats subjected to jump threshold measurements or to shocks identical to those used in the aggression paradigm show significant elevations in tail blood pressure. The size of the pressure increase in rats shocked alone appears dependent on the intensity of the shocks, while the pressure fall in rats shocked in pairs occurs over a broad range of shock intensities.
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Rats were tested for changes in shock-induced fighting following treatment with antidepressants of both the dibenzazepine and monoamine oxidase inhibitor classes of drug. Rats were retested for shock-induced fighting 3, 4, and 5 days after initial injections of imipramine (10 mg/kg IP bid), or saline. All three dibenzazepine groups showed increased levels of shock-induced fighting (p less than 0-01). In addition, rats were retested for shock-induced fighting 6, 30. 54, and 78 hours following the initiation of treatment with daily injections of saline, or the monoamine oxidase inhibitors: nialamide (100 mg/kg/day), iproniazid (150 mg/kg/day), and pargyline (20 mg/kg/day). All three monoamine oxidase inhibitor groups showed increased levels of shock-induced fighting after 30 hr (p less than 0.001). There was no difference in the jump threshold of rats treated with pargyline or saline.
Affective aggression was studied in pairs of Flinders Sensitive Line hypercholinergic rats (FSL) and Flinders Resistant Line (FRL) rats in shock-induced and apomorphine-induced fighting tests. FSL rats were significantly more aggressive in both tests. They had higher pain threshold, assessed by the jump-flinch method, than FRL rats. It is concluded that genetically developed cholinergic system supersensitivity has resulted in enhanced responsiveness to stimuli eliciting affective aggression.