Amygdaloid function in the central cholinergic mediation of shock-induced aggression in the rat

A series of experiments was designed to examine the role of central cholinergic mechanisms in shock-induced aggression. Cholinergic blockade in the basolateral amygdala, ventral hippocampus, or dorsal hippocampus resulted in greatly reduced levels of fighting in response to footshock. However, while pain sensitivity remained unaltered in the amygdala group, both of the hippocampal groups exhibited decreased shock sensitivity. Further investigation of the amygdala revealed (1) increased fighting in response to increased cholinergic levels, (2) neuroanatomical specificity to the basolateral division of this complex, (3) that an intact basolateral amygdala is essential to the normal manifestation of shock-induced aggression, and (4) that social attraction remains unaltered by cholinergic blockade of the basolateral amygdala. Motor coordination and motor activity were not significantly affected in any treatment condition.     

情绪对注意功能网络的调制

情绪性注意是一种对具有情绪意义的刺激进行选择和加工的注意.由于刺激的情绪效价能调制人脑的感知和注意系统,因而,与对中性刺激的注意相比,情绪性注意的神经机制更加复杂.较早的研究显示,杏仁核对感知皮层的调制对情绪性注意起关键作用.近期的证据表明,杏仁核对注意功能网络的调制可能是其重要的神经机制.本文梳理了相关领域的研究证据,主要强调情绪性刺激对注意的警觉、定向和执行控制网络的调制,发现情绪性注意加工的认知神经机制可能涉及一个以杏仁核为核心的多重功能网络.     

Activation of cannabinoid CB1 receptors in the central amygdala impairs inhibitory avoidance memory consolidation via NMDA receptors

In the present study, we investigated the influence of bilateral intra-central amygdala (intra-CeA) microinjections of N-methyl-d-aspartate (NMDA) receptor agents on amnesia induced by a cannabinoid CB1 receptor agonist, arachydonilcyclopropylamide (ACPA). This study used a step-through inhibitory (passive) avoidance task to assess memory in adult male Wistar rats. The results showed that intra-CeA administration of ACPA (2 ng/rat) immediately after training decreased inhibitory avoidance (IA) memory consolidation as evidenced by a decrease in step-through latency on the test day, which was suggestive of drug-induced amnesia. Post-training intra-CeA microinjections of NMDA (0.0001, 0.001 and 0.01 μg/rat) did not affect IA memory consolidation. However co-administration of NMDA with ACPA (2 ng/rat) prevented the impairment of IA memory consolidation that was induced by ACPA. Although post-training intra-CeA administration of the NMDA receptor antagonist, d-(−)-2-amino-5-phosphonopentanoic acid (d-AP5; 0.01, 0.05 and 0.1 μg/rat) alone had no effect, its co-administration with an ineffective dose of ACPA (1 ng/rat) impaired IA memory consolidation. Post-training intra-CeA microinjection of an ineffective dose of d-AP5 (0.01 μg/rat) prevented an NMDA response to the impaired effect of ACPA. These results suggest that amnesia induced by intra-CeA administration of ACPA is at least partly mediated through an NMDA receptor mechanism in the Ce-A.     

The Structure of Emotion

ABSTRACT— One common point of debate in the study of emotion is whether the basic, irreducible elements of emotional life are discrete emotion categories, such as anger , fear , sadness , and so on, or dimensions such as approach and avoidance . Resolving this debate will identify the basic building blocks of emotional life that are the most appropriate targets of scientific inquiry. In this paper, we briefly review meta-analytic work on the neuroimaging of emotion and examine its potential for identifying "natural kinds" of emotion in the brain. We outline criteria for identifying such natural kinds, summarize the evidence to date on category and dimensional approaches, and suggest ways in which neuroimaging studies could more directly address fundamental questions about the nature of emotion.     

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     

情感风格及其神经基础

情感风格是个体在情绪反应与情绪调节等方面表现出的稳定的、一致性差异。情感风格的两个主要成分是情绪反应与情绪调节差异。情感风格与情绪恢复性、趋近——退缩系统、精神疾病的易感性等密切相关。前额皮层、前扣带皮层、杏仁核等及其构成的神经回路的结构与机能差异是情感风格的神经基础。     

Beyond family‐level adversities: Exploring the developmental timing of neighborhood disadvantage effects on the brain

A growing literature suggests that adversity is associated with later altered brain function, particularly within the corticolimbic system that supports emotion processing and salience detection (e.g., amygdala, prefrontal cortex [PFC]). Although neighborhood socioeconomic disadvantage has been shown to predict maladaptive behavioral outcomes, particularly for boys, most of the research linking adversity to corticolimbic function has focused on family‐level adversities. Moreover, although animal models and studies of normative brain development suggest that there may be sensitive periods during which adversity exerts stronger effects on corticolimbic development, little prospective evidence exists in humans. Using two low‐income samples of boys (n = 167; n = 77), Census‐derived neighborhood disadvantage during early childhood, but not adolescence, was uniquely associated with greater amygdala, but not PFC, reactivity to ambiguous neutral faces in adolescence and young adulthood. These associations remained after accounting for several family‐level adversities (e.g., low family income, harsh parenting), highlighting the independent and developmentally specific neural effects of the neighborhood context. Furthermore, in both samples, indicators measuring income and poverty status of neighbors were predictive of amygdala function, suggesting that neighborhood economic resources may be critical to brain development.     

Somatic Markers and Response Reversal: Is There Orbitofrontal Cortex Dysfunction in Boys with Psychopathic Tendencies?

This study investigated the performance of boys with psychopathic tendencies and comparison boys, aged 9 to 17 years, on two tasks believed to be sensitive to amygdala and orbitofrontal cortex functioning. Fifty-one boys were divided into two groups according to the Psychopathy Screening Device (PSD, P. J. Frick & R. D. Hare, in press) and presented with two tasks. The tasks were the gambling task (A. Bechara, A. R. Damasio, H. Damasio, & S. W. Anderson, 1994) and the Intradimensional/Extradimensional (ID/ED) shift task (R. Dias, T. W. Robbins, & A. C. Roberts, 1996). The boys with psychopathic tendencies showed impaired performance on the gambling task. However, there were no group differences on the ID/ED task either for response reversal or extradimensional set shifting. The implications of these results for models of psychopathy are discussed.     

The Limbic System and the Soul: Evolution and the Neuroanatomy of Religious Experience

The evolutionary neurological foundations of religious experience are detailed. Human beings have been burying and preparing their dead for the Hereafter for more than 100,000 years. These behaviors and beliefs are related to activation of the amygdala, hippocampus, and temporal lobe, which are responsible for religious, spiritual, and mystical trancelike states, dreaming, astral projection, near-death and out-of-body experiences, and the hallucination of ghosts, demons, angels, and gods. Abraham, Moses, Muhammad, and Jesus Christ, and others who have communed with angels or gods display limbic system hyperactivity, whereas patients report religious hallucinations or out-of-body experiences when limbic structures are stimulated or excessively activated. It is postulated that limbic and temporal lobe structures account for the sexual and violent aspects of religious behavior and also serve as a "transmitter to God," and that the evolution of these structures made spiritual experience possible.     

Is There Savings for Pavlovian Fear Conditioning after Neurotoxic Basolateral Amygdala Lesions in Rats?

Considerable evidence indicates an important role for amygdaloid nuclei in both the acquisition and expression of Pavlovian fear conditioning. Recent reports from my laboratory have focused on the impact of neurotoxic lesions of the basolateral complex of the amygdala (BLA) on conditional freezing behavior in rats. In these studies, I have observed severe effects of posttraining BLA lesions on the expression of conditional freezing even after extensive presurgical overtraining (25-75 trials). Moreover, I have found no evidence for sparing of fear memory (i.e., savings) in these rats when I assess their rate of reacquisition relative to BLA rats receiving minimal training (1 trial). In these experiments, freezing behavior was assessed using a conventional time-sampling procedure and expressed as a response probability. Although this measure is well established in the literature, it is conceivable that it is not sensitive to spared memory in rats with BLA lesions. To address this issue, I present a more detailed analysis of freezing behavior that quantifies latency to freeze, the number of freezing bouts, the duration of freezing bouts, and the probability distribution of bout lengths. I also include control data from untrained (no-shock) rats. Consistent with my earlier reports, I find no evidence of savings of fear memory in rats with neurotoxic BLA lesions using several measures of freezing behavior. These results reiterate the conclusion that fear memory, as it is expressed in freezing behavior, requires neurons in the BLA.