Biomedical subjects
Publications and source records attributed to B Eichelman.
This paper reviews the clinical literature relevant to the association between aggressive behavior and the limbic system in humans. Specific areas of review include aggressive behavior related to: (1) naturally occurring and iatrogenic brain lesions; (2) electrical disturbances; (3) pharmacologic intervention; and (4) central neurochemical concentrations which may implicate limbic lobe involvement.
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Using a 15-s intershock interval, an increase in shock-induced fighting was observed following intraventricular 96 microgram 5,7-dihydroxytryptamine (5,7-DHT) and 90 microgram 6-hydroxydopa (6-OHdopa). The incidence of predatory mouse killing was enhanced by 5,7-DHT, but was not affected by 6-OHdopa. Pain sensitivity was increased by 6-OHdopa, but both neurotoxins produced hyperreactivity to footshock. Specific serotonin depletion was produced by 5,7-DHT and norepinephrine depletion by 6-OHdopa. The increase in shock-induced fighting could not be predicted on the basis of monoamine depletion alone, since a long intershock interval was necessary to observe this increase.
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Using two procedures known to enhance shock-induced defensive fighting (SIF) and mouse-killing--septal lesions and 5,7-DHT lesions--we determined if a 5% tryptophan-loaded diet could reverse the lesion effects. The results indicated that SIF, but not mouse-killing, could be maintained at normal levels following dietary tryptophan loading in both septally lesioned and 5,7-DHT lesioned rats. This behavioral reversal was independent of pain sensitivity, feeding, drinking and body weight levels. Regional brain analysis of monoamines and metabolites indicated that the lesions produced substantial depletions in 5-HT and 5-HIAA with minimal reduction or no change in catecholamines. Dietary tryptophan loading elevated 5-HT and 5-HIAA in unlesioned animals and partially restored 5-HT and 5-HIAA levels in lesioned animals. These patterns of depletion and repletion were confined to the hippocampus following septal lesions and distributed throughout the brain following 5,7-DHT lesions. The results are discussed in terms of a possible hippocampal mediation of the dietary tryptophan reversal in shock-induced defensive fighting following lesioning.
Cyclic nucleotides, particularly cyclic AMP, have been implicated as second messengers in neuronal activity. Attempts to demonstrate an association between endogenous cAMP or cGMP levels and rodent aggressive behavior have been only partially successful. Low levels of cAMP in rodent brain appear associated with lower levels of affective aggression. Consistent with this possible relationship is our finding that the infusion of dibutyryl cAMP into rodent cerebroventricles decreases aggressive behavior. The infusion of dibutyryl cyclic GMP, conversely, facilitates shock-induced fighting in the rat.
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The effects of a tryptophan-free diet on isolation-induced fighting and predatory cricket killing in mice were examined. The results demonstrated that consumption of a tryptophan-free diet for 18-20 days decreased both the number of fighters and duration of isolation-induced fighting; increased the number of cricket-killing mice and decreased the latencies to attack and the latencies to kill crickets; reduced brain serotonin 27%; increased water intake 38%; and decreased body weight 27% without affecting food intake. To determine if these effects were due specifically to the lack of dietary tryptophan, other groups of mice were fed a 5% tryptophan load in the standard chow; a 0.15% tryptophan supplement in the tryptophan-free diet; or a 3 grams/day restricted chow diet. The lack of tryptophan in the diet produced the marked inhibition in isolation-induced fighting, the reduction in brain serotonin, and the large decrease in body weight. The other non-specific effects appeared to be related to general factors such as dietary need for the cricket killing or diet composition (other than the lack of tryptophan) for the water intake.
The effects of dietary excesses of tryptophan, histidine, tyrosine or choline and of a tryptophan-free diet were examined on shock-induced fighting, muricide and jump-flinch thresholds. Following the tryptophan-free diet, shock-induced fighting and pain sensitivity were specifically increased. The increased incidence of muricide was not specific to the lack of tryptophan in the diet. Groups of rats which were pair fed chow or had 0.15% L-tryptophan added to the tryptophan-free diet increased muricide as well. Brain 5-HT levels were 41% depleted following the tryptophan-free diet and reduced 13% with the 0.15% tryptophan supplement. In addition body weights were reduced in the three groups compared to control. None of the excess diets affected shock-induced fighting, muricide and jump-flinch thresholds. Body weights were decreased in the excess tryptophan, histidine, tyrosine and choline groups. These data indicate that the expression of different forms of aggression appears to be influenced by a tryptophan deficiency in the diet, but not by excesses of tryptophan, tyrosine, histidine and choline.
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The methylxanthines caffeine and aminophylline, in daily doses of 100 mg/kg, facilitated shock-induced aggression in the rat. Under the limited parameters of this study, there was no induction of mouse-killing behavior or alteration of jump thresholds. Additional studies showed the optimal dose and time course for the facilitation of shock-induced aggression by caffeine to be 50 mg/kg administered i.p. 4 h prior to testing. Facilitation of a central adrenergic system may be the mechanism of action.
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Alkali metal cations were given in varying doses over 14 days to CF-1, male mice, isolated for 4 weeks prior to testing for isolation-induced fighting. Lithium and cesium in doses of 4.5 and 6.0 meq/kg reduced the duration of isolation-induced aggression in a 15 min test period when compared with controls. Toxicity was evident in the cesium-treated, but not the lithium-treated mice. No enhancement of aggression was seen in the rubidium-treated group.
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