Editorial: Information Processing and the Emotional Disorders

Abstract

It is shown that emotions can usefully be considered as states produced by reinforcing stimuli. The ways in which a wide variety of emotions can be produced, and the functions of emotion, are considered. There is evidence that the amygdala is involved in the formation of stimulus-reinforcement associations, and the orbitofrontal cortex with correcting behavioural responses when these are no longer appropriate because previous reinforcement contingencies change. This evidence comes from the effects of damage to these structures, and from recording the activity of single neurons in these structures in the monkey during the formation and disconnection of stimulus-reinforcement associations. In so far as emotions can be defined as states produced by reinforcing stimuli, then the amygdala and orbitofrontal cortex are seen to be of great importance for emotions, in that they are involved respectively in the elicitation of learned emotional responses, and in the correction or adjustment of these emotional responses as the reinforcing value of environmental stimuli alters. One of the theses advanced is that the changes in emotional behaviour produced by damage to the brain can be analysed and understood by considering how different parts of it function in reinforcement and in the formation and disconnection of stimulus-reinforcement connections. Another thesis is that there is a population of neurons in the amygdala and parts of the temporal lobe visual cortex specialised to respond to faces, and that these neurons may be involved in social and emotional resposes to faces.

Some of the outputs of the amygdala and orbitofrontal cortex are directed to the hypothalamus, which not only provides one route for these reinforcing environmental events to produce autonomic responses, but also is implicated in the utilisation of such stimuli in motivational responses, such as feeding and drinking, and in emotional behaviour. Other outputs of the amygdala and orbitofrontal cortex which may enable them to influence behaviour are directed to the striatum, and also back towards some of the cortical regions from which they receive inputs. It is suggested that these latter projections are important in the effects which mood states have on cognitive processing.     

Delta-sleep inducing peptide (DSIP) and ACTH (4-10) analogue influence fos-induction in the limbic structures of the rat brain under emotional stress

The effects of the ACTH (4-10) analogue, ACTH (4-7)-Pro-Gly-Pro, and delta-sleep inducing peptide (DSIP) on the induction of Fos immunoreactivity in the hypothalamic parvocellular paraventricular nucleus (pPVN) and limbic brain regions were studied in Wistar rats with high (resistant) or low (predisposed) resistance to emotional stress, predicted from differences in their open-field behaviour. Fos-immunoreactive (Fos-IR) cells were counted in brain sections automatically with a computer-based image analyser. Under basal conditions, Fos-IR cell numbers were greater in the pPVN in the predisposed rats, but were lower than in the resistant rats in the basolateral amygdala and medial and lateral septum. Intraperitoneal DSIP injection (30 μg/kg) increased basal Fos-IR cell number in the pPVN and lateral septum in resistant rats, with no effects in predisposed rats. ACTH (4-10) analogue (50 μg/kg)increased Fos expression in the pPVN in both resistant and predisposed rats, with essentially no effects in the basolateral amygdala or medial and lateral septum. Emotional stress (60 min restraint and intermittent subcutaneous electrical shocks) increased Fos expression in the pPVN and medial and lateral septum similarly in predisposed and resistant rats, but in the basolateral amygdala in only the predisposed rats. Intraperitoneal DSIP injection reduced the increases in Fos-IR cell number after emotional stress, particularly in predisposed rats. In predisposed rats DSIP decreased the number of Fos-IR cells in the pPVN and the medial and lateral septum, with no change in the basolateral amygdala. In resistant rats, DSIP decreased Fos expression only in the lateral septum. ACTH (4-10) analogue injection inhibited stress-induced Fos expression in the pPVN and the medial septum, but only in predisposed rats. The experiments indicate that DSIP and ACTH (4-10) analogue reduce pPVN and limbic neurone responses to emotional stress in the rats predisposed to emotional stress; the effects on Fos expression may play a role in the biological activities of these peptides.     

Conditioned and unconditioned fear organized in the periaqueductal gray are differentially sensitive to injections of muscimol into amygdaloid nuclei

The lateral and basolateral nuclei of the amygdala (LaA and BLA, respectively) serve as a filter for unconditioned and conditioned aversive information that ascends to higher structures from the brainstem, whereas the central nucleus of the amygdala (CeA) is considered to be the main output for the defense reaction. It has been shown that the dorsal periaqueductal gray (dPAG) is activated by threatening stimuli and has important functional links with the amygdala through two-way anatomical connections. In this work, we examined the influence of chemical inactivation of these nuclei of amygdala on the freezing and escape responses induced by electrical stimulation through electrodes implanted in the dPAG of Wistar rats. Each rat also bore a cannula implanted in the LaA, BLA or CeA for injections of muscimol (0.5 microg/0.5 microL) or its vehicle. The duration of freezing behavior that outlasts electrical stimulation of the dPAG was also measured. On the following day, these animals were submitted to a contextual fear-conditioning using foot shocks as unconditioned stimulus. Conditioned freezing to contextual cues previously associated with foot shocks was also inhibited by injections of muscimol into these amygdaloid nuclei. The contextual conditioned freezing behavior is generated in the neural circuits of conditioned fear in the amygdala. The data obtained also show that injections of muscimol into the three amygdaloid nuclei did not change the aversive threshold of freezing, but disrupted the dPAG post-stimulation freezing. Previous findings that the latter freezing results directly from dPAG stimulation and that it is not sensitive to a context shift suggest that it is unconditioned in nature. Thus, the amygdala can affect some, but not all, aspects of unconditioned freezing. Post-stimulation freezing may reflect the process of transferring aversive information from dPAG to higher brain structures.     

情绪加工中杏仁核的效价特异性

杏仁核是情绪信息加工的关键脑区。近年来心理学和神经科学领域发现了杏仁核情绪加工的效价特异性现象,并且整体存在左侧杏仁核对正性情绪、右侧杏仁核对负性情绪以及双侧杏仁核负性偏好的特异性趋势,且受到材料突出特征、个体差异、任务条件的调节。未来可进一步探索注意对杏仁核情绪效价特异性的调节作用,探究动态情绪刺激加工时杏仁核的活动特点,考察心理障碍患者加工负性情绪时的杏仁核激活模式,并确定杏仁核的效价特异性在思维、计划、决策等高级认知过程中的表现。     

Norepinephrine infused into the basolateral amygdala posttraining enhances retention in a spatial water maze task

Recent evidence indicates that the amygdala plays a role in modulating memory processes in other brain regions. For example, posttraining intra-amygdala infusions of amphetamine enhanced memory in both spatial and cued training water maze tasks; these tasks are known to depend on the integrity of the hippocampus and caudate nucleus, respectively. To determine whether this modulation is dependent on noradrenergic activation within a subregion of the amygdala (the basolateral nucleus), the present study examined the effects of posttraining microinfusions (0.2 microl) of norepinephrine or propranolol into the basolateral amygdala immediately following training in a spatial version of the water maze task. Rats received a four-trial training session on each of 2 consecutive days. On the third day, rats were given a 60-s probe test in the absence of a platform. Retention latencies obtained on the second training day revealed that norepinephrine dose-dependently enhanced retention for the location of the hidden platform. In contrast, propranolol significantly impaired retention. Probe trial analysis revealed that rats treated with 0.25 microg norepinephrine demonstrated a selective spatial bias for the training platform location relative to all other groups. These findings are consistent with others and support the view that the basolateral amygdala has a role in modulating memory storage by interacting with other brain regions.     

Amygdala modulation of memory consolidation: interaction with other brain systems

There is a strong consensus that the amygdala is involved in mediating influences of emotional arousal and stress on learning and memory. There is extensive evidence that the basolateral amygdala (BLA) is a critical locus of integration of neuromodulatory influences regulating the consolidation of several forms of memory. Many drug and stress hormone influences converge in activating the release of norepinephrine (NE) within the BLA. Evidence from studies using in vivo microdialysis and high-performance liquid chromatography indicates that increases in amygdala NE levels assessed following inhibitory avoidance training correlate highly with subsequent retention. Other evidence indicates that NE influences on memory consolidation require muscarinic cholinergic activation within the BLA provided by projections from the nucleus basalis magnocellularis (NB). Evidence from several experiments indicates that activation of the BLA plays an essential role in modulating memory consolidation processes involving other brain regions. These findings provide strong support for the hypothesis that the BLA plays a critical role in regulating the consolidation of lasting memories of significant experiences.     

Amygdala and "emotional" modulation of the relative use of multiple memory systems

The basolateral amygdala modulates the cognitive and habit memory processes mediated by the hippocampus and caudate nucleus, respectively. The present experiments used a plus-maze task that can be acquired using either hippocampus-dependent "place" learning or caudate-dependent "response" learning to examine whether peripheral or intra-basolateral amygdala injection of anxiogenic drugs would bias rats towards the use of a particular memory system. In Experiment 1, adult male Long-Evans rats were trained to swim from the same start point to an escape platform located in a consistent goal arm, and received pre-training peripheral injections of the alpha(2)-adrenoceptor antagonists yohimbine (2.5 or 5.0 mg/kg), RS 79948-197 (0.05, 0.1, or 0.2 mg/kg), or vehicle. On a drug-free probe trial from a novel start point administered 24h following acquisition, vehicle treated rats predominantly displayed hippocampus-dependent place learning, whereas rats previously treated with yohimbine (2.5, 5.0 mg/kg) or RS 79948-197 (0.1 mg/kg) predominantly displayed caudate-dependent response learning. In Experiment 2, rats receiving pre-training intra-basolateral amygdala infusions of RS 79948-197 (0.1 microg/0.5 microl) also predominantly displayed response learning on a drug-free probe trial. The findings indicate (1) peripheral injections of anxiogenic drugs can influence the relative use of multiple memory systems in a manner that favors caudate-dependent habit learning over hippocampus-dependent cognitive learning, and (2) intra-basolateral amygdala infusion of anxiogenic drugs is sufficient to produce this modulatory influence of emotional state on the use of multiple memory systems.     

The functional neuroanatomy of emotion and affective style

Recently, there has been a convergence in lesion and neuroimaging data in the identification of circuits underlying positive and negative emotion in the human brain. Emphasis is placed on the prefrontal cortex (PFC) and the amygdala as two key components of this circuitry. Emotion guides action and organizes behavior towards salient goals. To accomplish this, it is essential that the organism have a means of representing affect in the absence of immediate elicitors. It is proposed that the PFC plays a crucial role in affective working memory. The ventromedial sector of the PFC is most directly involved in the representation of elementary positive and negative emotional states while the dorsolateral PFC may be involved in the representation of the goal states towards which these elementary positive and negative states are directed. The amygdala has been consistently identified as playing a crucial role in both the perception of emotional cues and the production of emotional responses, with some evidence suggesting that it is particularly involved with fear-related negative affect. Individual differences in amygdala activation are implicated in dispositional affective styles and increased reactivity to negative incentives. The ventral striatum, anterior cingulate and insular cortex also provide unique contributions to emotional processing.     

杏仁核对感觉刺激的情绪性加工:自动化过程和注意调控过程的整合

利用有限的认知资源应对多变的环境刺激,选择性注意和情绪加工一个重要的共同机制是优先化关键信息的加工。尽管情绪性刺激(特别是威胁刺激)能够影响注意资源的分配,但一些关键脑区(如杏仁核)的对情绪性刺激的加工是自动化过程还是受到注意调节一直是个有争议的问题。最新的结合高时间分辨率和高空间分辨率的神经生理记录研究表明,情绪加工的重要核团,杏仁核,对情绪性刺激的加工包含早期快速的不依赖于注意资源和认知加工负荷的自动化加工成分和晚期受到额-顶叶皮层自上而下的注意调控成分,这种功能整合证实杏仁核情绪性加工存在并行的皮层下和皮层通路。     

Variations in unconditioned stimulus processing in unblocking

Three experiments examined the mechanisms by which downward shifts in reinforcer value influence learning in appetitive unblocking procedures. The downward shift was accomplished by omitting the 2nd of a 2-reinforcer sequence (food-food or food-sucrose). Performance of normal rats was compared with that of rats with lesions of the central nucleus of the amygdala, which are thought to interfere with surprise-induced enhancements of event processing. The results suggested that, in normal rats, omission of the 2nd reinforcer enhanced processing of the 1st reinforcer rather than processing of the conditioned stimuli and that lesions of the central nucleus eliminated this enhancement. The roles of reinforcement error signals in conditioning are discussed.     

Face processing in different brain areas,and critical band masking

Neurophysiological evidence is described showing that some neurons in the macaque inferior temporal visual cortex have responses that are invariant with respect to the position, size, view, and spatial frequency of faces and objects, and that these neurons show rapid processing and rapid learning. Critical band spatial frequency masking is shown to be a property of these face‐selective neurons and of the human visual perception of faces. Which face or object is present is encoded using a distributed representation in which each neuron conveys independent information in its firing rate, with little information evident in the relative time of firing of different neurons. This ensemble encoding has the advantages of maximizing the information in the representation useful for discrimination between stimuli using a simple weighted sum of the neuronal firing by the receiving neurons, generalization, and graceful degradation. These invariant representations are ideally suited to provide the inputs to brain regions such as the orbitofrontal cortex and amygdala that learn the reinforcement associations of an individual's face, for then the learning, and the appropriate social and emotional responses generalize to other views of the same face. A theory is described of how such invariant representations may be produced by self‐organizing learning in a hierarchically organized set of visual cortical areas with convergent connectivity. The theory utilizes either temporal or spatial continuity with an associative synaptic modification rule. Another population of neurons in the cortex in the superior temporal sulcus encodes other aspects of faces such as face expression, eye‐gaze, face view, and whether the head is moving. These neurons thus provide important additional inputs to parts of the brain such as the orbitofrontal cortex and amygdala that are involved in social communication and emotional behaviour. Outputs of these systems reach the amygdala, in which face‐selective neurons are found, and also the orbitofrontal cortex, in which some neurons are tuned to face identity and others to face expression. In humans, activation of the orbitofrontal cortex is found when a change of face expression acts as a social signal that behaviour should change; and damage to the human orbitofrontal and pregenual cingulate cortex can impair face and voice expression identification, and also the reversal of emotional behaviour that normally occurs when reinforcers are reversed.     

Microinfusions of flumazenil into the basolateral but not the central nucleus of the amygdala enhance memory consolidation in rats.

Extensive evidence indicates that benzodiazepine receptors in the amygdala are involved in regulating memory consolidation. Recent findings indicate that many other drugs and hormones influence memory through selective activation of the basolateral amygdala nucleus (BLA). This experiment examined whether the memory-modulatory effect of flumazenil, a benzodiazepine receptor antagonist, selectively involves the BLA. Bilateral microinfusions of flumazenil (12 nmol in 0.2 microl) into the BLA of rats administered immediately after training in an inhibitory avoidance task significantly enhanced 48-h retention performance whereas infusions into the central nucleus were ineffective. These findings indicate that the BLA is selectively involved in mediating flumazenil's influence on memory storage and are thus consistent with extensive evidence indicating that the BLA is involved in regulating memory consolidation.     

The central amygdala nucleus via corticotropin-releasing factor is necessary for time-limited consolidation processing but not storage of contextual fear memory

The central nucleus of the amygdala (CeA) is traditionally portrayed in fear conditioning as the key neural output that relays conditioned information established in the basolateral amygdala complex to extra-amygdalar brain structures that generate emotional responses. However, several recent studies have questioned this serial processing view of the amygdalar fear conditioning circuit by showing an influence of the CeA on memory consolidation. We previously reported that inhibition of endogenous CeA secretion of corticotropin-releasing factor (CRF) at the time of contextual training effectively impaired fear memory consolidation. However, the time-dependent range of CeA CRF secretion in facilitating consolidation processing has not been examined. Therefore, to address this issue, we performed CeA site-specific microinjections of CRF antisense oligonucleotides (CRF ASO) at several post-training time intervals. Rats microinjected with CRF ASO at post-training intervals up to 24-h subsequently exhibited significant impairments in contextual freezing retention in contrast to animals treated 96-h after training. To further establish the validity of the results, CeA fiber-sparing lesions were made at two distinct post-training periods (24-h and 96-h), corresponding respectively to the temporal intervals when CeA CRF ASO administration disrupted or had no significant effects on memory consolidation. Similar to the CeA CRF ASO results, CeA lesions made 24-h, but not 96-h, after training induced significant freezing deficits in the retention test. In conclusion, the current results demonstrate: (1) an extended involvement of CeA CRF in contextual memory consolidation and (2) that contextual fear memory storage is not dependent on a functional CeA.     

Amygdala and “emotional” modulation of the relative use of multiple memory systems

The basolateral amygdala modulates the cognitive and habit memory processes mediated by the hippocampus and caudate nucleus, respectively. The present experiments used a plus-maze task that can be acquired using either hippocampus-dependent “place” learning or caudate-dependent “response” learning to examine whether peripheral or intra-basolateral amygdala injection of anxiogenic drugs would bias rats towards the use of a particular memory system. In Experiment 1, adult male Long–Evans rats were trained to swim from the same start point to an escape platform located in a consistent goal arm, and received pre-training peripheral injections of the α₂-adrenoceptor antagonists yohimbine (2.5 or 5.0 mg/kg), RS 79948-197 (0.05, 0.1, or 0.2 mg/kg), or vehicle. On a drug-free probe trial from a novel start point administered 24 h following acquisition, vehicle treated rats predominantly displayed hippocampus-dependent place learning, whereas rats previously treated with yohimbine (2.5, 5.0 mg/kg) or RS 79948-197 (0.1 mg/kg) predominantly displayed caudate-dependent response learning. In Experiment 2, rats receiving pre-training intra-basolateral amygdala infusions of RS 79948-197 (0.1 μg/0.5 μl) also predominantly displayed response learning on a drug-free probe trial. The findings indicate (1) peripheral injections of anxiogenic drugs can influence the relative use of multiple memory systems in a manner that favors caudate-dependent habit learning over hippocampus-dependent cognitive learning, and (2) intra-basolateral amygdala infusion of anxiogenic drugs is sufficient to produce this modulatory influence of emotional state on the use of multiple memory systems.     

Cortico-limbic-striatal circuits subserving different forms of cost-benefit decision making

Research on the neural basis that underlies decision making in humans has revealed that these processes are mediated by distributed neural networks that incorporate different regions of the frontal lobes, the amygdala, the ventral striatum, and the dopamine system. In the present article, we review recent studies in rodents investigating the contribution of these systems to different forms of cost-benefit decision making and focus on evaluations related to delays, effort, or risks associated with certain rewards. Anatomically distinct regions of the medial and orbital prefrontal cortex make dissociable contributions to different forms of decision making, although lesions of these regions can induce variable effects, depending on the type of tasks used to assess these functions. The basolateral amygdala and the nucleus accumbens play a more fundamental role in these evaluations, helping an organism overcome different costs to obtain better rewards. Dopamine activity biases behavior toward more costly yet larger rewards, although abnormal increases in dopamine transmission can exert opposing actions on different types of decision making. The fact that similar neural circuits are recruited to solve these types of problems in both humans and animals suggests that animal models of decision making will prove useful in elucidating the mechanisms mediating these processes.     

Altered emotional and motivational processing in the transgenic rat model for Huntington's disease

Huntington disease (HD) is caused by an expansion of CAG repeat in the Huntingtin gene. Patients demonstrate a triad of motor, cognitive and psychiatric symptoms. A transgenic rat model (tgHD rats) carrying 51 CAG repeats demonstrate progressive striatal degeneration and polyglutamine aggregates in limbic structures. In this model, emotional function has only been investigated through anxiety studies. Our aim was to extend knowledge on emotional and motivational function in symptomatic tgHD rats. We subjected tgHD and wild-type rats to behavioral protocols testing motor, emotional, and motivational abilities. From 11 to 15 months of age, animals were tested in emotional perception of sucrose using taste reactivity, acquisition, extinction, and re-acquisition of discriminative Pavlovian fear conditioning as well as reactivity to changes in reinforcement values in a runway Pavlovian approach task. Motor tests detected the symptomatic status of tgHD animals from 11 months of age. In comparison to wild types, transgenic animals exhibited emotional blunting of hedonic perception for intermediate sucrose concentration. Moreover, we found emotional alterations with better learning and re-acquisition of discriminative fear conditioning due to a higher level of conditioned fear to aversive stimuli, and hyper-reactivity to a negative hedonic shift in reinforcement value interpreted in term of greater frustration. Neuropathological assessment in the same animals showed a selective shrinkage of the central nucleus of the amygdala. Our results showing emotional blunting and hypersensitivity to negative emotional situations in symptomatic tgHD animals extend the face validity of this model regarding neuropsychiatric symptoms as seen in manifest HD patients, and suggest that some of these symptoms may be related to amygdala dysfunction.     

Activation of amygdaloid PKC pathway is necessary for conditioned cues-provoked cocaine memory performance

Drug-associated cues are critical in reinstating the drug taking behavior even during prolonged abstinence and thus are thought to be a key factor to induce drug craving and to cause relapse. Amygdaloid complex has been known for its physiological function in mediating emotional experience storage and emotional cues-regulated memory retrieval. This study was undertaken to examine the role of basolateral nuclei of amygdala and the intracellular signaling molecule in drug cues-elicited cocaine memory retrieval. Systemic anisomycin treatment prior to the retrieval test abolished the cues-provoked cocaine conditioned place preference (CPP) memory. Likewise, a similar blockade of cues-provoked cocaine CPP performance was achieved by infusion of anisomycin and cycloheximide into the basolateral nuclei of amygdala before the test. Intra-amygdaloid infusion of H89, a protein kinase A inhibitor, or U0126, a MEK inhibitor, did not affect retrieval of the cues-elicited cocaine CPP memory. In contrast, intra-amygdaloid infusion of NPC 15437, a PKC inhibitor, abolished the cues-elicited cocaine CPP expression, while left the memory per se intact. Intra-amygdaloid infusion of NPC 15437 did not seem to affect locomotor activity or exert observable aversive effect. Taken together, our results suggest that activation of PKC signaling pathway and probably downstream de novo protein synthesis in the basolateral nuclei of amygdala is required for the cues-elicited cocaine memory performance. However, temporary inhibition of this signaling pathway does not seem to affect cocaine CPP memory per se.     

The role of neuropeptide Y in the amygdala on corticotropin-releasing factor receptor-mediated behavioral stress responses in the rat

Neuropeptide Y (NPY) is one of the most abundant peptides in the brain and has been shown to be a critical regulator of emotionality, most notably for its effect in decreasing anxiety-like behaviors. The stress response in both humans and animals has been shown to involve a cascade of biological events initiated by corticotropin releasing factor (CRF), another centrally acting peptide. Interestingly, NPY and CRF are present in similar brain regions mediating stress responses and may act in an opposing fashion. The basolateral nucleus of the amygdala (BLA) is a distinct division of the amygdala and contains CRF receptors and the highest concentration of NPY neurons. The current study investigates the behavioral effects in rodents when NPY is injected directly into the BLA prior to the pharmacological stressor, urocortin I (Ucn; a CRF receptor agonist) or the emotional stressor, restraint. The animals that underwent restraint were evaluated in the social interaction (SI) test, while those injected with Ucn into the BLA were assessed in the two floor choice test, a modified version of the conditioned-place avoidance paradigm. The results showed that injections of NPY into the BLA prior to Ucn significantly blocked the development of the avoidance behavior in the two floor choice test and the decrease in SI time that is usually seen following restraint stress. These results provide further support that an interaction between NPY and CRF within the BLA may be critical for maintaining a normal homeostatic emotional state.     

Automaticity and the Amygdala: Nonconscious Responses to Emotional Faces

The human face is an evolved adaptation for social communication. This implies that humans are genetically prepared to produce facial gestures that are automatically decoded by observers. Psychophysiological data demonstrate that humans respond automatically with their facial muscles, with autonomic responses, and with specific regional brain activation of the amygdala when exposed to emotionally expressive faces. Attention is preferentially and automatically oriented toward facial threat. Neuropsychological data, as well as a rapidly expanding brain-imaging literature, implicate the amygdala as a central structure for responding to negative emotional faces, and particularly to fearful ones. However, the amygdala may not be specialized for processing emotional faces, but may instead respond to faces because they provide important information for the defense appraisal that is its primary responsibility.     

从个体关系的角度看文化对社会脑功能的塑造

摘 要 尽管社会认知的内容丰富多样,但其核心在于人们对“自我”、“他人”及两者关系的理解。文化作为一种独特的社会现象,对社会认知有着广泛影响,这一点集中体现在文化对“自我” 与“他人” 信息加工及其大脑机制的影响上。文化神经科学的研究表明：文化显著影响自我相关记忆、自我表征、自我觉知等自我认知过程。这可能主要来源于不同文化人群自我建构方式的不同。上述差异的神经机制主要体现为不同文化人群自我相关加工时,其内侧前额叶功能性变化的不同。与此相对应的是,文化同样显著影响人们对他人,尤其是对他人情绪的认知。这一点集中表现为表情认知的文化优势效应及共情过程的文化差异。在神经机制上这一差异主要体现为杏仁核功能的文化可塑性。文化神经科学的未来研究,可继续探讨主流文化、区域文化、宗教文化等各种形式的文化差异：1）对自我认知与情绪认知相互作用的影响与神经基础;2）对共情（empathy）、社会比较（social comparison）、心理理论（theory of mind）与协同行为（joint action）等多种社会认知过程的影响及其神经机制。 关键词 自我建构 文化神经科学 情绪认知 自我表征 共情