دانلود رایگان مقاله انگلیسی مدل های حیوانی خشونت بیش از اندازه: پیامد هایی برای تجاوز و خشونت انسانی - الزویر 2018

Escalated interpersonal aggression and violence are common symptoms of multiple psychiatric disorders and represent a significant global health issue. Current therapeutic strategies are limited due to a lack of understanding about the neural and molecular mechanisms underlying the ‘vicious’ shift of normal adaptive aggression into violence, and the environmental triggers that cause it. Development of novel animal models that validly capture the salient features of human violent actions combined with newly emerging technologies for mapping, measuring, and manipulating neuronal activity in the brain significantly advance our understanding of the etiology, neuromolecular mechanisms, and potential therapeutic interventions of excessive aggressive behaviors in humans.

Synthesis and outlook

A large body of animal neurobehavioral research convincingly demonstrates that abnormal expressions of aggressive behavior principally find its origin in a dysregulation of the deeply rooted neuronal circuits and/or neurochemical pathways in the brain that mediate normal social affiliative-aggressive behaviors. The structural and functional properties of this social behavior brain network are established and constantly shaped by a dynamic interplay of genetic and environmental factors (stress, maltreatment, vicarious experiences, etc.) in particular during certain sensitive (i.e., perinatal and adolescent) developmental periods. Undisputedly, among the neurochemical systems that are considered key signaling molecules in this neurocircuitry controlling aggression are the canonical monoamines serotonin and dopamine, the ‘social’ neuropeptides oxytocin and vasopressin, the ‘stress’ neuropeptide CRF, the ‘stress’ HPA- and ‘sex’ HPG-axis’s steroid hormones (corticosterone, testosterone, estrogen), and their receptors. Particularly, from the viewpoint of targeting novel molecular sites for intervention, the intrinsic 5-HT autoregulatory mechanisms (i.e., the presynaptic 5-HT1A/B autoreceptors and 5-HT reuptake transporter), and extrinsic aminergic (DA), neuropeptidergic (i.e., OXT, AVP and CRF) and steroid receptor (i.e., MR and AR) modulatory influences on 5-HT signaling are emerging as important molecular determinants of escalated aggression regulation. This circuit-level knowledge of the neuromolecular underpinnings of escalated aggression has great potential to guide the rational development of effective therapeutic interventions for pathological social and aggressive behavior in humans.