背外侧前额叶对主动遗忘负性社会反馈的作用：针对抑郁症的TMS研究

抑郁症患者的负性心境可能源于其抑制功能障碍。患者在主动遗忘负性材料时无法有效调用背外侧前额叶(the dorsolateral prefrontal cortex, DLPFC)等负责抑制控制的额叶脑网络。同时, 患者对社会信息的加工比对非社会信息的加工存在更明显的认知神经障碍, 很难主动遗忘对自己不利的社会反馈信息。为了提高抑郁症患者对负性社会反馈的主动遗忘能力, 本研究采用经颅磁刺激技术(transcranial magnetic stimulation, TMS), 考察抑郁症患者在左侧(n = 32)或右侧DLPFC (n = 30)被激活后其记忆控制能力的改变。结果表明, 当患者的DLPFC被TMS激活时, 他们对社会拒绝的回忆正确率与健康对照组(n = 31)无差异, 且TMS激活右侧DLPFC还改善了患者对他人的社会态度。本研究是采用TMS提高抑郁症患者主动遗忘能力的首次尝试, 研究结果不但支持了DLPFC与记忆控制功能的因果关系, 还为临床治疗抑郁症、创伤后应激障碍、药物成瘾等患者的记忆控制缺陷提供了明确的神经靶点。     

EVidence for dorsolateral and orbital prefrontal cortical involvement in the expression of aggressive behavior

Numerous studies have implicated the role of the prefrontal cortex in the expression of aggressive behavior. However, the nature of this relationship remains poorly understood. As such, the purpose of this article is to review both the animal and human literature pertaining to prefrontal cortical functioning and aggression in an attempt to help clarify this relationship. Particular attention is paid to differentiating the functions of the dorsolateral and the orbital regions of the prefrontal cortex in the expression of aggression. Evidence was garnered from four different types of studies: 1) those examining aggressive behavior in animals following ablations to the prefrontal cortex; 2) those examining aggressive behavior in humans following surgical and accidental lesions to the prefrontal cortex; 3) those examining prefrontal cortical functioning in individuals with psychiatric disorders characterized by aggression; and 4) those relating prefrontal cortical functioning to human aggressive behavior in laboratory situations. The general conclusion of this article is that the dorsolateral region of the prefrontal cortex is more likely to be involved in the expression of physical aggression whereas the orbital region is more likely to be involved in the expression of what is termed herein “disinhibited-nonaggressive” behavior. © 1995 Wiley-Liss, Inc.     

Dopamine regulation of human speech and bird song: a critical review

To understand the neural basis of human speech control, extensive research has been done using a variety of methodologies in a range of experimental models. Nevertheless, several critical questions about learned vocal motor control still remain open. One of them is the mechanism(s) by which neurotransmitters, such as dopamine, modulate speech and song production. In this review, we bring together the two fields of investigations of dopamine action on voice control in humans and songbirds, who share similar behavioral and neural mechanisms for speech and song production. While human studies investigating the role of dopamine in speech control are limited to reports in neurological patients, research on dopaminergic modulation of bird song control has recently expanded our views on how this system might be organized. We discuss the parallels between bird song and human speech from the perspective of dopaminergic control as well as outline important differences between these species.     

Neural processing of intentional biological motion in unaffected siblings of children with autism spectrum disorder: An fMRI study

Despite often showing behaviorally typical levels of social cognitive ability, unaffected siblings of children with autism spectrum disorder have been found to show similar functional and morphological deficits within brain regions associated with social processing. They have also been reported to show increased activation to biological motion in these same regions, such as the posterior superior temporal sulcus (pSTS), relative to both children with autism and control children. It has been suggested that this increased activation may represent a compensatory reorganization of these regions as a result of the highly heritable genetic influence of autism. However, the response patterns of unaffected siblings in the domain of action perception are unstudied, and the phenomenon of compensatory activation has not yet been replicated. The present study used functional magnetic resonance imaging to determine the neural responses to intentional biological actions in 22 siblings of children with autism and 22 matched controls. The presented actions were either congruent or incongruent with the actor’s emotional cue. Prior studies reported that typically developing children and adults, but not children with autism, show increased activation to incongruent actions (relative to congruent), within the pSTS and dorsolateral prefrontal cortex. We report that unaffected siblings did not show a compensatory response, or a preference for incongruent over congruent trials, in any brain region. Moreover, interaction analyses revealed a sub-region of the pSTS in which control children showed an incongruency preference to a significantly greater degree than siblings, which suggests a localized deficit in siblings. A sample of children with autism also did not show differential activation in the pSTS, providing further evidence that it is an area of selective disruption in children with autism and siblings. While reduced activation to both conditions was unique to the autism sample, lack of differentiation to incongruent and congruent intentional actions was common to both children with ASD and unaffected siblings.     

A cross-sectional and longitudinal analysis of reward-related brain activation: Effects of age,pubertal stage,and reward sensitivity

Neurobiological models suggest that adolescents are driven by an overactive ventral striatum (VS) response to rewards that may lead to an adolescent increase in risk-taking behavior. However, empirical studies showed mixed findings of adolescents’ brain response to rewards. In this study, we aimed to elucidate the relationship between reward-related brain activation and risky decision-making. In addition, we examined effects of age, puberty, and individuals’ reward sensitivity. We collected two datasets: Experiment 1 reports cross-sectional brain data from 75 participants (ages 10–25) who played a risky decision task. Experiment 2 presents a longitudinal extension in which a subset of these adolescents (n = 33) was measured again 2 years later. Results showed that (1) a reward-related network including VS and medial PFC was consistently activated over time, (2) the propensity to choose the risky option was related to increased reward-related activation in VS and medial PFC, and (3) longitudinal comparisons indicated that self-reported reward sensitivity was specifically related to VS activation over time. Together, these results advance our insights in the brain circuitry underlying reward processing across adolescence.     

The amygdalostriatal and corticostriatal effective connectivity in anticipation and evaluation of facial attractiveness

Decision-making consists of several stages of information processing, including an anticipation stage and an outcome evaluation stage. Previous studies showed that the ventral striatum (VS) is pivotal to both stages, bridging motivation and action, and it works in concert with the ventral medial prefrontal cortex (vmPFC) and the amygdala. However, evidence concerning how the VS works together with the vmPFC and the amygdala came mainly from neuropathology and animal studies; little is known about the dynamics of this network in the functioning human brain. Here we used fMRI combined with dynamic causal modeling (DCM) to investigate the information flow along amygdalostriatal and corticostriatal pathways in a facial attractiveness guessing task. Specifically, we asked participants to guess whether a blurred photo of female face was attractive and to wait for a few seconds (“anticipation stage”) until an unblurred photo of feedback face, which was either attractive or unattractive, was presented (“outcome evaluation stage”). At the anticipation stage, the bilateral amygdala and VS showed higher activation for the “attractive” than for the “unattractive” guess. At the outcome evaluation stage, the vmPFC and the bilateral VS were more activated by feedback faces whose attractiveness was congruent with the initial guess than by incongruent faces; however, this effect was only significant for attractive faces, not for unattractive ones. DCM showed that at the anticipation stage, the choice-related information entered the amygdalostriatal pathway through the amygdala and was projected to the VS. At the evaluation stage, the outcome-related information entered the corticostriatal pathway through the vmPFC. Bidirectional connectivities existed between the vmPFC and VS, with the VS-to-vmPFC connectivity weakened by unattractive faces. These findings advanced our understanding of the reward circuitry by demonstrating the pattern of information flow along the amygdalostriatal and corticostriatal pathways at different stages of decision-making.     

Open field habituation learning is improved by nicotine and attenuated by mecamylamine administered posttrial into the nucleus accumbens

Using the paradigm of habituation learning in the open field, we tested the effects of unilateral microinjections of the agonist nicotine (8.0, 40.0, and 80.0 microg) and the nicotine receptor antagonist mecamylamine (0.1, 1.0, 10.0 microg) into the core of the nucleus accumbens. When injected posttrial, that is, immediately after the first exposure to the open field, nicotine dose-dependently enhanced behavioral habituation during the test on the following day, indicating a facilitation of memory, whereas mecamylamine impaired habituation at the highest dose, but not at the two lower doses. When injected 5 h after the learning trial, nicotine (40 microg) and mecamylamine (10 microg) impaired habituation on the subsequent day. A control experiment did not provide evidence for possible proactive effects of mecamylamine. These findings are discussed with respect to the possible behavioral functions of cholinergic, and especially nicotinic, mechanisms in the nucleus accumbens. They may also be relevant for understanding cholinergic-linked psychopathologies such as Alzheimer's disease, since the nucleus accumbens is one of the sites where cholinergic neurons are lost in this neurodegenerative disease.     

第三方惩罚的神经机制：来自经颅直流电刺激的证据

第三方惩罚既是社会规范在群体得以维系的基石, 也是个体维护社会规范的体现。当前关注社会规范的神经研究大多基于第二方惩罚的独裁者或最后通牒实验框架, 缺乏对第三方维护社会规范过程中相关脑区活动的探索, 对这一过程的内在神经机制也不清楚。本文基于第三方惩罚的独裁者博弈框架, 对右侧背外侧前额叶区域(DLPFC)进行不同极性的经颅直流电刺激(tDCS), 同时依据第三方是否需要为其惩罚付出成本设计了零成本和有成本两个实验任务。结果发现, 第三方在零成本任务的情绪反应和惩罚显著受到tDCS设置的影响, 且阴极刺激显著提升了第三方的惩罚值, 这表明情绪机制对第三方惩罚有着重要影响。另外, 第三方在零成本和有成本任务中的惩罚差异在不同tDCS设置之间也存在显著差异, 这与第三方惩罚还受到自利机制影响的观点相符。本文率先为右侧DLPFC活动影响第三方惩罚提供了神经层面的证据, 且支持了第三方对社会规范的遵从与其负性情绪反应和自利加工密切相关的机制解释。     

Evidence for the substantia nigra pars compacta as an essential component of a memory system independent of the hippocampal memory system

The aim of the present study was to test if the nigrostriatal pathway is an essential component for a water maze cued task learning and if it works independently of the hippocampal memory system. This hypothesis was tested using an animal model of Parkinson's disease in which male Wistar rats were lesioned in the substantia nigra pars compacta (SNc) by the intranigral infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), thus causing a partial depletion of striatal dopamine. SNc-lesioned and sham-operated animals were implanted bilaterally with guide cannulae above the dorsal hippocampus in order to be tested after the administration of 0.4 microl 2% lidocaine or saline into this structure. The animals were tested in a spatial or in a cued version of the water maze, memory tasks previously reported to model hippocampal-dependent spatial/relational and striatal-dependent S-R learning, respectively. Hippocampal inactivation, but not SNc lesion, impaired learning and memory in the spatial version of the water maze. An opposite situation was observed with the cued version. No significant interaction was observed between the SNc lesion and hippocampal inactivation conditions affecting scores in the spatial or in the cued version of the water maze. These results suggest that the nigrostriatal pathway is an essential part of the memory system that processes S-R learning and that it works independently of the hippocampal memory system that processes spatial/relational memories.