44 research outputs found
Testosterone, cortisol, and serotonin as key regulators of social aggression: A review and theoretical perspective
In human and non-human animals the steroid hormones cortisol and testosterone are involved in social aggression and recent studies suggest that these steroids might jointly regulate this behavior. It has been hypothesized that the imbalance between cortisol and testosterone levels is predictive for aggressive psychopathology, with high testosterone to cortisol ratio predisposing to a socially aggressive behavioral style. In this review, we focus on the effects of cortisol and testosterone on human social aggression, as well as on how they might modulate the aggression circuitry of the human brain. Recently, serotonin is hypothesized to differentiate between impulsive and instrumental aggression, and we will briefly review evidence on this hypothesis. The aim of this article is to provide a theoretical framework for the role of steroids and serotonin in impulsive social aggression in humans
Recommended from our members
Glucocorticoids and agonistic responding in male golden hamsters: A behavioral, neuroanatomical and neurochemical analysis
This thesis research was designed to study the role of glucocorticoids in the central regulation of aggressive, submissive, and communicative behavior in male golden hamsters (Mesocricetus auratus). It represents the first time that site-, context-, dose-, and steroid-specific actions of glucocorticoids in behavioral regulation have been systematically examined within the central nervous system. Chronic implants of cortisol exerted site-specific and context-dependent effects on agonistic responding within the hypothalamus. In paired encounters with aggressive opponents, submissive responding was induced by cortisol implants in the medial preoptic area, anterior hypothalamus, and ventromedial hypothalamus; aggressive responding by implants in the paraventricular nucleus and third ventricle. Cortisol implants in the anterior hypothalamus induced submissive responding in paired encounters with aggressive opponents, aggressive responding in paired encounters with submissive opponents, and aggressive responding in territorial aggression tests with juvenile intruders. Acute microinjections of cortisol in the anterior hypothalamus exerted dose-dependent and steroid-specific effects on agonistic responding. High (10\sp{-2}M) doses of cortisol induced submissive responding; low (10\sp{-6}M) doses induced aggressive responding. The direction of these biphasic effects were unique to cortisol. High doses of deoxycorticosterone induced aggressive responding, while both high and low doses of testosterone, dihydrotestosterone, progesterone and estradiol had no effect. Low doses of deoxycorticosterone also had no effect. Acute peripheral administration of cortisol induced aggressive responding, as did chronic administration of the glucocorticoid synthesis inhibitor cyanoketone. In contrast, central and peripheral administration of the antiglucocorticoid RU486, had significant site- and dose-dependent effects hypothalamic-pituitary-adrenal axis function, but no effect on agonistic responding. In all cases, the effects of cortisol on flank marking behavior appeared to relate more to the social status of the cortisol-treated animal than a direct effect on the neural substrates of flank marking. Dominant animals flank marked at higher, and subordinate animals at lower levels than their opponents. In conclusion, glucocorticoids are prepotent modulators of agonistic responding within the medial hypothalamus. Both acute and chronic neuroendocrine regulation of agonistic responding by adrenal steroids appear to serve the function of promoting adaptive behavioral responses that minimize the risk of serious injury during competitive interactions
Recommended from our members
Developing Generative Dispositions Towards Writing Through Micro-Coaching: Results from a Dispositions Awareness Study
University Writing Cente
Associations of genotypes at the apolipoprotein AI-CIII-AIV, apolipoprotein B and lipoprotein lipase gene loci with coronary atherosclerosis and high density lipoprotein subclasses
Association studies were carried out in a sample of 86 patients from Sweden who had survived a myocardial infarction (MI) at a young age and 93 age-matched healthy individuals, to compare the impact of polymorphisms at the apolipoprotein (apo) AI-CIII-AIV gene cluster on among-individual differences in plasma lipid and lipoprotein traits, the five high density lipoprotein (HDL) subclasses (2b to 3c), lipoprotein lipase (LPL) activity and presence and progression of atherosclerosis. Individuals were genotyped for four polymorphisms; 5'apoAI (G/A-75), 3'apoAI (PstI; P +/-), apoCIII (C/T1100) and apoCIII (PvuII; V +/-), using PCR-based techniques. Allele frequencies were similar in healthy individuals and patients (frequencies of alleles in combined population: 5'apoAI-A-75 = 0.14, 3'apoAI-P- = 0.05, apoCIII-T1100 = 0.27 and apoCIII-V- = 0.18). In the healthy individuals, levels of low density lipoprotein (LDL) triglycerides were significantly associated with genotypes of the apoCIII-PvuII polymorphism (p = 0.02), but no other associations were found between lipids or HDL subclasses and single polymorphisms in the apoAI-CIII-AIV gene cluster. Levels of triglycerides and very low density lipoprotein (VLDL) triglycerides were significantly higher in the presence of the haplotype defined by the presence of apoCIII-T1100 and common alleles of the other three polymorphisms, explaining 5.8% and 7.8% (p = 0.03 and 0.01), respectively, of sample variance. In the patients, no associations were found between lipids or HDL subclasses and variation at the apoAI-CIII-AIV gene cluster. Associations were also examined between levels of HDL subclasses and variation at the apoE (common isoforms), apoB (signal peptide and XbaI polymorphisms) and lipoprotein lipase (PvuII, HindIII and Serine447/Stop polymorphisms) gene loci. In the patient group only, levels of protein in HDL2b, HDL2a and HDL3b subclasses were significantly associated with genotypes of the LPL-HindIII polymorphism (22.1, 19.3 and 11.4%, respectively, of sample variance; p < 0.05). Finally, associations were examined between genotypes at the apoAI-CIII-AIV gene cluster and the extent of coronary atherosclerosis. Global severity of atherosclerosis at the first angiography was weakly associated with genotypes of the apoCIII-C/T1100 polymorphism, presence of the T1100 allele being associated with 53% lower median score (1.6 vs 0.75; p = 0.09).(ABSTRACT TRUNCATED AT 400 WORDS