Violence and Latin‐American preadolescents: A study of social brain function and cortisol levels

The present study investigated exposure to violence and its association with brain function and hair cortisol concentrations in Latin‐American preadolescents. Self‐reported victimization scores (JVQ‐R2), brain imaging (fMRI) indices for a social cognition task (the ‘eyes test’), and hair cortisol concentrations were investigated, for the first time, in this population. The eyes test is based on two conditions: attributing mental state or sex to pictures of pairs of eyes (Baron‐Cohen, Wheelwright, Hill, Raste, & Plumb, 2001). The results showed an association among higher victimization scores and (a) less activation of posterior temporoparietal right‐hemisphere areas, in the mental state condition only (including right temporal sulcus and fusiform gyrus); (b) higher functional connectivity indices for the Amygdala and Right Fusiform Gyrus (RFFG) pair of brain regions, also in the mental state condition only; (c) higher hair cortisol concentrations. The results suggest more exposure to violence is associated with significant differences in brain function and connectivity. A putative mechanism of less activation in posterior right‐hemisphere regions and of synchronized Amygdala: RFFG time series was identified in the mental state condition only. The results also suggest measurable effects of exposure to violence in hair cortisol concentrations, which contribute to the reliability of self‐reported scores by young adolescents. The findings are discussed in light of the effects of exposure to violence on brain function and on social‐cognitive development in the adolescent brain. A video abstract of this article can be viewed at https://www.youtube.com/watch?v=qHcXq7Y9PBk     

情绪大脑机制研究的进展

文章综述情绪大脑机制研究的最新进展。情绪的脑机制——大脑回路,包括前额皮层、杏仁核、海马、前部扣带回、腹侧纹状体等。前额皮层中的不对称性与趋近和退缩系统有关,左前额皮层与趋近系统和积极感情有关,右前额皮层与消极感情和退缩有关。杏仁核易被消极的感情刺激所激活,尤其是恐惧。海马在情绪的背景调节中起着重要作用。前额皮层和杏仁核激活不对称性的个体差异是情绪个体差异的生理基础。情绪的中枢回路有可塑性。     

Neurochemical mechanisms underlying amygdaloid modulation of aggressive behavior in the cat

Studies designed to determine the respective roles of substance P, excitatory amino acids, and enkephalins in amygdaloid modulation of defensive rage behavior in the cat are presented. The basic design of these studies involved three stages. In stage I, cannula electrodes for stimulation and drug infusion were implanted into medial hypothalamic or midbrain periaqueductal gray (PAG) sites from which defensive rage behavior could be elicited. Then, a stimulating electrode was implanted into a site within the medial, basal, or central nuclear complex from which modulation of the defensive rage response could be obtained. Amygdaloid modulation of defensive rage was determined in the following manner: it employed the paradigm of dual stimulation in which comparisons were made of response latencies between alternate trials of dual (i. e., amygdala = medial hypothalamus [or PAG]) and single stimulation of the hypothalamus or PAG alone. Thus, stage I established the baseline level ofmodulation (i. e., facilitation or suppression of defensive rage) in the predrug stimulation period. In stage II, a selective or nonselective receptor antagonist for a given transmitter system was administered either peripherally or intracerebrally at the defensive rage site, after which time the same dual stimulation paradigm was then repeated over the ensuing 180 min postinjection period in order to determine the effects of drug delivery upon amygdaloid modulation of defensive rage. Stage III of the study took place at the completion of the pharmacological testing phase. The retrograde axonal tracer, Fluoro-Gold, was microinjected into the defensive rage site within the medial hypothalamus or PAG, and following a 6-14 day survival period, animals were sacrificed and brains were processed for histological and immunocytochemical analyses for the neurotransmitters noted above. This procedure thus permitted identification of cells within the amygdala which were labeled retrogradely and which were also immunostained positively for substance P, excitatory amino acids, or enkephalin. For studies involving substance P, defensive rage was elicited from the medial hypothalamus and for studies examining the roles of excitatory amino acids and enkephalin, defensive rage was elicited from the PAG. In the first study, facilitation of hypothalamically elicited defensive rage was obtained with dual stimulation of the medial nucleus of the amygdala. In separate experiments, the selective NK₁ non-peptide antagonist, CP 96,345, was administered both peripherally as well as intracerebrally into the hypothalamic defensive rage sites in doses of 0.5-4.0 mg/kg (i. p.) and 0.5-2.5 nmol (i. c.). Following drug delivery, the facilitatory effects of medial amygdaloid stimulation were blocked in a dose- and time-dependent manner in which the effects were noted as early as 5 min postinjection. The maximum drug dose (4.0 mg/kg) employed for peripheral administration resulted in a 42% reduction in the facilitatory effects of the medical amygdala (P < 0.002). This drug, when microinjected directly into medial hypothalamic defensive rage sites at the maximum dose level of 2.5 nmol, resulted in an 84% reduction of the suppressive effects of amygdaloid stimulation (P < 0.5) at 5 min postinjection. In the next study, an N-methyl-D-aspartate (NMDA) antagonist, DL-α-amino-7-phosphonoheptanoic acid (AP-7), was administered either peripherally (0.1-1.0 mg/kg) or intracerebrally (0.2 and 2.0 nmol) into PAG defensive rage sites. Facilitation of defensive rage behavior, which was observed following dual stimulation of the basal amygdala and PAG, was significantly reduced by either route of drug administration in a dose- and time-dependent manner. At the maximum dose level of peripheral administration, AP-7 reduced amygdaloid facilitation of defensive rage by 63% (P < 0.001) for 60 min, postinjection. A smaller (i. e., 19%) but still significant (P < 0.05) reduction in facilitation was obtained following intracerebral administration of the drug. In a third study, the non-selective opioid receptor antagonist, naloxone (27.5 nmol), infused directly into PAG defensive rage sites, totally blocked the suppressive effects of central amygdaloid stimulation for a period of 30 min (P < 0.05) in a dose- and time-dependent manner. The anatomical phase of this study revealed the following relationships: 1) that large numbers of neurons projecting to the medial hypothalamus from the medial amygdala immunoreact positively for substance P; 2) that neurons projecting to the PAG from the basal complex of amygdala immunoreact positively for glutamate and aspartate; and 3) that neurons located within the central nucleus of the amygdala which project to the PAG immunoreact positively for met-enkephalin. Collectively, these observations provide new evidence which characterizes the likely neurotransmitters linked with specific amygdaloid pathways subserving the modulation of defensive rage behavior in the cat.     

Involvement of amygdala in inhibitory control over aggression in the rat: A synopsis

An experimentally produced hyperreactivity facilitates initiation of mouse-killing in rats that did not previously develop any stable inhibition of interspecific aggression. Destruction of the corticomedial amygdala or interruption of the stria terminalis interferes with the development of such an inhibition on the basis of “social” influences, whereas lateral amygdaloid lesions have no effect on mouse-killing.     

Shock-induced aggression and pain sensitivity in the rat: Catecholamine involvement in the corticomedial amygdala

The possible role of amygdaloid catecholamines in the control of shock-induced aggression and pain sensitivity in the rat was investigated. Bilateral microinjections of chlorpromazine into the corticomedial amygdala resulted in decreased fighting and decreased sensitivity to the shock stimulus. Further analysis of this effect, using specific adrenergic antagonists, revealed that neither a- nor Padrenergic systems appeared to be responsible for the behavioral effect of chlorpromazine. Injections of haloperidol into the same region, however, yielded a reduction similar to that produced by chlorpromazine, while dopamine injections resulted in significant elevations in both fighting and pain sensitivity. No effect on any of these behavioral measures was obtained following injection of any of the agents into the basolateral amygdala. These results suggest that the observed effect of catecholamine injections in the corticomedial amygdala is related to changes in pain sensitivity mediated by dopamine.     

威胁性信息检测的脑机制

快速而准确地检测威胁性信息是进化过程中形成的一种重要能力,是有效应对危险的前提条件,对有机体的生存具有重要价值.威胁性信息的检测由不同的神经通路合作完成.在视觉通道中,皮层通路的精确检测和皮层下通路的快速检测在杏仁核得到整合.杏仁核能接受多感觉通道的信息输入,并接受额叶的调节,是威胁性信息加工中连通自上而下加工和自下而上加工的枢纽.将来的研究需要进一步关注杏仁核的功能以及不同的神经通路如何合作完成威胁性信息的检测.     

Structural and Functional Neuroplasticity in Relation to Traumatic Stress

ABSTRACT— The body's stress response is an essential adaptive and protective mechanism to cope with threatening situations. However, chronic or traumatic stress leads to structural and functional alterations in the traumatized brain. We argue for a building-block effect: Exposure to different types of traumatic events increases the probability of developing posttraumatic stress disorder (PTSD), via incremental enlargement of a fear network. We summarize evidence of brain changes in PTSD, including recent results from research on animal models of stress-related neuroplastic remodeling, with an emphasis on structural and functional changes in the hippocampus, the amygdala, and the medial prefrontal cortex.     

Negative Emotion Enhances Memory Accuracy: Behavioral and Neuroimaging Evidence

ABSTRACT— There have been extensive discussions about whether emotional memories contain more accurate detail than nonemotional memories do, or whether individuals simply believe that they have remembered emotional experiences more accurately. I review evidence that negative emotion enhances not only the subjective vividness of a memory but also the likelihood of remembering some (but not all) event details. I then describe neuroimaging evidence suggesting that engagement of emotion-processing regions (particularly the amygdala and orbitofrontal cortex) relates to the encoding and retrieval of details intrinsically linked to negative items.     

人类情绪记忆的行为遗传学与神经遗传学研究进展述评

情绪记忆及其增强效应存在广泛的个体差异,这种个体差异可能有其神经与遗传基础。近来的行为遗传学与神经遗传学证实人类ADRA2B基因缺失突变以及BDNF Val66Met基因的多态性与情绪记忆增强及其神经机制的个体差异相联系。本文重点介绍与人类情绪记忆相关的这两种基因,梳理了行为与神经遗传学研究的最新进展,指出未来应关注更多候选基因,并重视多个脑区之间的交互作用;还应使用情绪面孔刺激探索BDNF Val66Met基因多态性对情绪记忆编码和提取的影响等。