Neural cell-types and circuits linking thermoregulation and social behavior.

Understanding how social and affective behavioral states are controlled by neural circuits is a fundamental challenge in neurobiology. Despite increasing understanding of central circuits governing prosocial and agonistic interactions, how bodily autonomic processes regulate these behaviors is less resolved. Thermoregulation is vital for maintaining homeostasis, but also associated with cognitive, physical, affective, and behavioral states. Here, we posit that adjusting body temperature may be integral to the appropriate expression of social behavior and argue that understanding neural links between behavior and thermoregulation is timely. First, changes in behavioral states-including social interaction-often accompany changes in body temperature. Second, recent work has uncovered neural populations controlling both thermoregulatory and social behavioral pathways. We identify additional neural populations that, in separate studies, control social behavior and thermoregulation, and highlight their relevance to human and animal studies. Third, dysregulation of body temperature is linked to human neuropsychiatric disorders. Although body temperature is a "hidden state" in many neurobiological studies, it likely plays an underappreciated role in regulating social and affective states.

The "psychiatric" neuron: the psychic neuron of the cerebral cortex, revisited.

Nearly 25 years ago, Dr. Patricia Goldman-Rakic published her review paper, "The 'Psychic' Neuron of the Cerebral Cortex," outlining the circuit-level dynamics, neurotransmitter systems, and behavioral correlates of pyramidal neurons in the cerebral cortex, particularly as they relate to working memory. In the decades since the release of this paper, the existing literature and our understanding of the pyramidal neuron have increased tremendously, and research is still underway to better characterize the role of the pyramidal neuron in both healthy and psychiatric disease states. In this review, we revisit Dr. Goldman-Rakic's characterization of the pyramidal neuron, focusing on the pyramidal neurons of the prefrontal cortex (PFC) and their role in working memory. Specifically, we examine the role of PFC pyramidal neurons in the intersection of working memory and social function and describe how deficits in working memory may actually underlie the pathophysiology of social dysfunction in psychiatric disease states. We briefly describe the cortico-cortical and corticothalamic connections between the PFC and non-PFC brain regions, as well the microcircuit dynamics of the pyramidal neuron and interneurons, and the role of both these macro- and microcircuits in the maintenance of the excitatory/inhibitory balance of the cerebral cortex for working memory function. Finally, we discuss the consequences to working memory when pyramidal neurons and their circuits are dysfunctional, emphasizing the resulting social deficits in psychiatric disease states with known working memory dysfunction.

Effects of fluorene-9-bisphenol exposure on anxiety-like and social behavior in mice and protective potential of exogenous melatonin.

Fluorene-9-bisphenol (BHPF) is widely used in the manufacture of plastic products and potentially disrupts several physiological processes, but its biological effects on social behavior remain unknown. In this study, we investigated the effects of BHPF exposure on anxiety-like and social behavior in female mice and the potential mechanisms, thereby proposing a potential therapy strategy. We exposed female Balb/c mice to BHPF by oral gavage at different doses (0.5, 50 mg/kg bw/2-day) for 28 days, which were found BHPF (50 mg/kg) exposure affected motor activity in the open field test (OFT) and elevated cross maze (EPM), resulting in anxiety-like behaviors, as well as abnormal social behavioral deficits in the Social Interaction Test (SIT). Analysis of histopathological staining results showed that BHPF exposure caused damage to hippocampal neurons in the CA1/CA3/DG region and decreased Nissl pyramidal neurons in the CA1/CA3 regions of the hippocampus, as well as a decrease in parvalbumin neuron expression. In addition, BHPF exposure upregulated the expression of excitatory and inhibitory (E/I) vesicle transporter genes (Vglut1, Vglut2, VGAT, GAD67, Gabra) and axon growth gene (Dcc) in the mouse hippocampus. Interestingly, behavioral disturbances and E/I balance could be alleviated by exogenous melatonin (15 mg/kg bw/2-day) therapy. Our findings suggest that exogenous melatonin may be a potential therapy with protective potential for ameliorating or preventing BHPF-induced hippocampal neuronal damage and behavioral disturbances. This study provided new insight into the neurotoxicological effects on organisms exposed to endocrine-disrupting chemicals and aroused our vigilance in current environmental safety about chemical use.

Dissecting the long-term neurobehavioral impact of embryonic benz[a]anthracene exposure on zebrafish: Social dysfunction and molecular pathway activation.

Benz[a]anthracene (BaA), a prevalent environmental contaminant within the polycyclic aromatic hydrocarbon class, poses risks to both human health and aquatic ecosystems. The impact of BaA on neural development and subsequent social behavior patterns remains inadequately explored. In this investigation, we employed the zebrafish as a model to examine the persisting effects of BaA exposure on social behaviors across various developmental stages, from larvae, juveniles to adults, following embryonic exposure. Our findings indicate that BaA exposure during embryogenesis yields lasting neurobehavioral deficits into adulthood. Proteomic analysis highlights that BaA may impair neuro-immune crosstalk in zebrafish larvae. Remarkably, our proteomic data also hint at the activation of the aryl hydrocarbon receptor (AHR) and cytochrome P450 1A (CYP1A) pathway by BaA, leading to the hypothesis that this pathway may be implicated in the disruption of neuro-immune interactions, contributing to observable behavioral disruptions. In summary, our findings suggest that early exposure to BaA disrupts social behaviors, such as social ability and shoaling behaviors, from the larval stage through to maturity in zebrafish, potentially through the detrimental effects on neuro-immune processes mediated by the AHR-CYP1A pathway.

Dynamic skin behaviors in cephalopods.

The coleoid cephalopods (cuttlefish, octopus, and squid) are a group of soft-bodied mollusks that exhibit a wealth of complex behaviors, including dynamic camouflage, object mimicry, skin-based visual communication, and dynamic body patterns during sleep. Many of these behaviors are visually driven and engage the animals' color changing skin, a pixelated display that is directly controlled by neurons projecting from the brain. Thus, cephalopod skin provides a direct readout of neural activity in the brain. During camouflage, cephalopods recreate on their skin an approximation of what they see, providing a window into perceptual processes in the brain. Additionally, cephalopods communicate their internal state during social encounters using innate skin patterns, and create waves of pigmentation on their skin during periods of arousal. Thus, by leveraging the visual displays of cephalopods, we can gain insight into how the external world is represented in the brain and how this representation is transformed into a recapitulation of the world on the skin. Here, we describe the rich skin behaviors of the coleoid cephalopods, what is known about cephalopod neuroanatomy, and how advancements in gene editing, machine learning, optical imaging, and electrophysiological tools may provide an opportunity to explore the neural bases of these fascinating behaviors.

Cannabidiol improves maternal obesity-induced behavioral, neuroinflammatory and neurochemical dysfunctions in the juvenile offspring.

Maternal obesity is associated with an increased risk of psychiatric disorders such as anxiety, depression, schizophrenia and autism spectrum disorder in the offspring. While numerous studies focus on preventive measures targeting the mothers, only a limited number provide practical approaches for addressing the damages once they are already established. We have recently demonstrated the interplay between maternal obesity and treatment with cannabidiol (CBD) on hypothalamic inflammation and metabolic disturbances, however, little is known about this relationship on behavioral manifestations and neurochemical imbalances in other brain regions. Therefore, here we tested whether CBD treatment could mitigate anxiety-like and social behavioral alterations, as well as neurochemical disruptions in both male and female offspring of obese dams. Female Wistar rats were fed a cafeteria diet for 12 weeks prior to mating, and during gestation and lactation. Offspring received CBD (50 mg/kg) from weaning for 3 weeks. Behavioral tests assessed anxiety-like manifestations and social behavior, while neuroinflammatory and neurochemical markers were evaluated in the prefrontal cortex (PFC) and hippocampus. CBD treatment attenuated maternal obesity-induced anxiety-like and social behavioral alterations, followed by rescuing effects on imbalanced neurotransmitter and endocannabinoid concentrations and altered expression of glial markers, CB1, oxytocin and dopamine receptors, with important differences between sexes. Overall, the findings of this study provide insight into the signaling pathways for the therapeutic benefits of CBD on neuroinflammation and neurochemical imbalances caused by perinatal maternal obesity in the PFC and the hippocampus, which translates into the behavioral manifestations, highlighting the sexual dimorphism encompassing both the transgenerational effect of obesity and the endocannabinoid system.

Hearing loss in juvenile rats leads to excessive play fighting and hyperactivity, mild cognitive deficits and altered neuronal activity in the prefrontal cortex.

Background: In children, hearing loss has been associated with hyperactivity, disturbed social interaction, and risk of cognitive disturbances. Mechanistic explanations of these relations sometimes involve language. To investigate the effect of hearing loss on behavioral deficits in the absence of language, we tested the impact of hearing loss in juvenile rats on motor, social, and cognitive behavior and on physiology of prefrontal cortex. Methods: Hearing loss was induced in juvenile (postnatal day 14) male Sprague-Dawley rats by intracochlear injection of neomycin under general anesthesia. Sham-operated and non-operated hearing rats served as controls. One week after surgery auditory brainstem response (ABR) measurements verified hearing loss or intact hearing in sham-operated and non-operated controls. All rats were then tested for locomotor activity (open field), coordination (Rotarod), and for social interaction during development in weeks 1, 2, 4, 8, 16, and 24 after surgery. From week 8 on, rats were trained and tested for spatial learning and memory (4-arm baited 8-arm radial maze test). In a final setting, neuronal activity was recorded in the medial prefrontal cortex (mPFC). Results: In the open field deafened rats moved faster and covered more distance than sham-operated and non-operated controls from week 8 on (both p < 0.05). Deafened rats showed significantly more play fighting during development (p < 0.05), whereas other aspects of social interaction, such as following, were not affected. Learning of the radial maze test was not impaired in deafened rats (p > 0.05), but rats used less next-arm entries than other groups indicating impaired concept learning (p < 0.05). In the mPFC neuronal firing rate was reduced and enhanced irregular firing was observed. Moreover, oscillatory activity was altered, both within the mPFC and in coherence of mPFC with the somatosensory cortex (p < 0.05). Conclusions: Hearing loss in juvenile rats leads to hyperactive behavior and pronounced play-fighting during development, suggesting a causal relationship between hearing loss and cognitive development. Altered neuronal activities in the mPFC after hearing loss support such effects on neuronal networks outside the central auditory system. This animal model provides evidence of developmental consequences of juvenile hearing loss on prefrontal cortex in absence of language as potential confounding factor.

Evolution of laughter from play.

In this hypothesis, I discuss how laughter from physical play could have evolved to being induced via visual or even verbal stimuli, and serves as a signal to highlight incongruity that could potentially pose a threat to survival. I suggest how laughter's induction could have negated the need for physical contact in play, evolving from its use in tickling, to tickle-misses, and to taunting, and I discuss how the application of deep learning neural networks trained on images of spectra of a variety of laughter types from a variety of individuals or even species, could be used to determine such evolutionary pathways via the use of latent space exploration.

Suppression of Cofilin function in the somatosensory cortex alters social contact behavior in the BTBR mouse inbred line.

Sensory differences are a core feature of autism spectrum disorders (ASD) and are predictive of other ASD core symptoms such as social difficulties. However, the neurobiological substrate underlying the functional relationship between sensory and social functioning is poorly understood. Here, we examined whether misregulation of structural plasticity in the somatosensory cortex modulates aberrant social functioning in BTBR mice, a mouse model for autism spectrum disorder-like phenotypes. By locally expressing a dominant-negative form of Cofilin (CofilinS3D; a key regulator of synaptic structure) in the somatosensory cortex, we tested whether somatosensory suppression of Cofilin activity alters social functioning in BTBR mice. Somatosensory Cofilin suppression altered social contact and nest-hide behavior of BTBR mice in a social colony, assessed for seven consecutive days. Subsequent behavioral testing revealed that altered social functioning is related to altered tactile sensory perception; CofilinS3D-treated BTBR mice showed a time-dependent difference in the sensory bedding preference task. These findings show that Cofilin suppression in the somatosensory cortex alters social functioning in BTBR mice and that this is associated with tactile sensory processing, a critical indicator of somatosensory functioning.

A gut (microbiome) feeling about addiction: Interactions with stress and social systems.

In recent years, an increasing attention has given to the intricate and diverse connection of microorganisms residing in our gut and their impact on brain health and central nervous system disease. There has been a shift in mindset to understand that drug addiction is not merely a condition that affects the brain, it is now being recognized as a disorder that also involves external factors such as the intestinal microbiota, which could influence vulnerability and the development of addictive behaviors. Furthermore, stress and social interactions, which are closely linked to the intestinal microbiota, are powerful modulators of addiction. This review delves into the mechanisms through which the microbiota-stress-immune axis may shape drug addiction and social behaviors. This work integrates preclinical and clinical evidence that demonstrate the bidirectional communication between stress, social behaviors, substance use disorders and the gut microbiota, suggesting that gut microbes might modulate social stress having a significance in drug addiction.

Quinic Acid Alleviates Behavior Impairment by Reducing Neuroinflammation and MAPK Activation in LPS-Treated Mice.

Compared to other organs, the brain has limited antioxidant defenses. In particular, the hippocampus is the central region for learning and memory and is highly susceptible to oxidative stress. Glial cells are the most abundant cells in the brain, and sustained glial cell activation is critical to the neuroinflammation that aggravates neuropathology and neurotoxicity. Therefore, regulating glial cell activation is a promising neurotherapeutic treatment. Quinic acid and its derivatives possess anti-oxidant and anti-inflammatory properties. Although previous studies have evidenced quinic acid's benefit on the brain, in vivo and in vitro analyses of its anti-oxidant and anti-inflammatory properties in glial cells have yet to be established. This study investigated quinic acid's rescue effect in lipopolysaccharide (LPS)-induced behavior impairment. Orally administering quinic acid restored social impairment and LPS-induced spatial and fear memory. In addition, quinic acid inhibited proinflammatory mediator, oxidative stress marker, and mitogen-activated protein kinase (MAPK) activation in the LPS-injected hippocampus. Quinic acid inhibited nitrite release and extracellular signal-regulated kinase (ERK) phosphorylation in LPS-stimulated astrocytes. Collectively, quinic acid restored impaired neuroinflammation-induced behavior by regulating proinflammatory mediator and ERK activation in astrocytes, demonstrating its potential as a therapeutic agent for neuroinflammation-induced brain disease treatments.

Population parameters of Drosophila larval cooperative foraging.

Cooperative foraging behavior can be advantageous when there is a common exploitable resource. By cooperating, members of the group can take advantage of the potential of increased efficiency of working together as well as equitable distribution of the product. An experimental signature of cooperative foraging is an Allee effect where at a certain number of individuals, there is a peak of fitness. What happens when there are intruders especially ones that do not contribute to any work required for foraging? Drosophila larvae secrete digestive enzymes and exodigest food. Under crowded conditions in liquid food these larvae form synchronized feeding clusters which provides a fitness benefit. A key for this synchronized feeding behavior is the visually guided alignment between adjacent larvae in a feeding cluster. Larvae who do not align their movements are excluded from the groups and subsequently lose the benefit. This may be a way of editing the group to include only known members. To test the model, the fitness benefit from cooperative behavior was further investigated to establish an Allee effect for a number of strains including those who cannot exodigest or cluster. In a standard lab vial, about 40 larvae is the optimal number for fitness. Combinations of these larvae were also examined. The expectation was that larvae who do not contribute to exodigestion are obligate cheaters and would be expelled. Indeed, obligate cheaters gain greatly from the hosts but paradoxically, so do the hosts. Clusters that include cheaters are more stable. Therefore, clustering and the benefits from it are dependent on more than just the contribution to exodigestion. This experimental system should provide a rich future model to understand the metrics of cooperative behavior.

Conducting head-mounted eye-tracking research with young children with autism and children with increased likelihood of later autism diagnosis.

BACKGROUND: Over the past years, researchers have been using head-mounted eye-tracking systems to study young children's gaze behaviors in everyday activities through which children learn about the world. This method has great potential to further our understanding of how millisecond-level gaze behaviors create multisensory experiences and fluctuate around social environments. While this line of work can yield insight into early perceptual experiences and potential learning mechanisms, the majority of the work is exclusively conducted with typically-developing children. Sensory sensitivities, social-communication difficulties, and challenging behaviors (e.g., disruption, elopement) are common among children with developmental disorders, and they may represent potential methodological challenges for collecting high-quality data. RESULTS: In this paper, we describe our research practices of using head-mounted eye trackers with 41 autistic children and 17 children with increased likelihood of later autism diagnosis without auditory or visual impairments, including those who are minimally or nonspeaking and/or have intellectual disabilities. The success rate in gathering data among children with autism was 92.68%. 3 of 41 children failed to complete the play-session, resulting in an 86.36% success rate among 1-4-year-olds and a 100.00% success rate among 5-8-year-olds. 1 of 17 children with increased likelihood of later autism diagnosis failed to complete the play-session, resulting in a success rate of 94.11%. There were numerous "challenging" behaviors relevant to the method. The most common challenging behaviors included taking the eye-tracking device off, elopement, and becoming distressed. Overall, among children with autism, 88.8% of 1-4-year-olds and 29.4% of 5-8-year-olds exhibited at least one challenging behavior. CONCLUSIONS: Research capitalizing on this methodology has the potential to reveal early, socially-mediated gaze behaviors that are relevant for autism screening, diagnosis, and intervention purposes. We hope that our efforts in documenting our study methodology will help researchers and clinicians effectively study early naturally-occuring gaze behaviors of children during non-experimental contexts across the spectrum and other developmental disabilities using head-mounted eye-tracking. Ultimately, such applications may increase the generalizability of results, better reflect the diversity of individual characteristics, and offer new ways in which this method can contribute to the field.

Operant social self-administration in male CD1 mice.

RATIONALE AND OBJECTIVE: We recently introduced a model of operant social reward in which female CD1 mice lever press for access to affiliative social interaction with a cagemate peer mouse of the same sex and strain. Here we determined the generality of the operant social self-administration model to male CD1 mice who, under certain conditions, will lever press to attack a subordinate male mouse. METHODS: We trained male CD1 mice to lever press for food and social interaction with a same sex and strain cagemate peer under different fixed-ratio (FR) schedule response requirements (FR1 to FR6). We then tested their motivation to seek social interaction after 15 days of isolation in the presence of cues previously paired with social self-administration. We also determined the effect of housing conditions on operant social self-administration and seeking. Finally, we determined sex differences in operant social self-administration and seeking, and the effect of housing conditions on unconditioned affiliative and antagonistic (aggressive) social interactions in both sexes. RESULTS: Male CD1 mice lever pressed for access to a cagemate peer under different FR response requirements and seek social interaction after 15 isolation days; these effects were independent of housing conditions. There were no sex differences in operant social self-administration and seeking. Finally, group-housed CD1 male mice did not display unconditioned aggressive behavior toward a peer male CD1 mouse. CONCLUSIONS: Adult socially housed male CD1 mice can be used in studies on operant social reward without the potential confound of operant responding to engage in aggressive interactions.

Identification of hippocampal area CA2 in hamster and vole brain.

Prairie voles (Microtus ochrogaster) and Syrian, or golden, hamsters (Mesocricetus auratus) are closely related to mice (Mus musculus) and are commonly used in studies of social behavior including social interaction, social memory, and aggression. Hippocampal area CA2 is known to play a key role in these behaviors in mice and responds to social stimuli in rats, but CA2 has yet to be characterized in hamsters or voles, which are also used in studies of social behaviors. Here, we used immunofluorescence to determine whether CA2 could be molecularly identified in tissue from voles and hamsters. We found that  staining for many CA2 markers was similar in these three species, with labeling seen in neurons at the distal end of the mossy fibers . In contrast, although perineuronal nets (PNNs) surround CA2 cells in mice, PNN staining differed across species. In voles, both CA2 and CA3 were labeled, whereas in hamsters, labeling was seen primarily in CA3. These results demonstrate that CA2 can be molecularly distinguished from neighboring CA1 and CA3 areas in voles and hamsters with several antibodies commonly used in mice. However, PNN staining is not useful for identifying CA2 in voles or hamsters, suggestive of differing roles for either PNNs or for the hippocampal subregions in social behavior. These findings reveal commonalities across species in the molecular profile of CA2 and should facilitate future studies of CA2 in these species.

Parental brain through time: The origin and development of the neural circuit of mammalian parenting.

This review consolidates current knowledge on mammalian parental care, focusing on its neural mechanisms, evolutionary origins, and derivatives. Neurobiological studies have identified specific neurons in the medial preoptic area as crucial for parental care. Unexpectedly, these neurons are characterized by the expression of molecules signaling satiety, such as calcitonin receptor and BRS3, and overlap with neurons involved in the reproductive behaviors of males but not females. A synthesis of comparative ecology and paleontology suggests an evolutionary scenario for mammalian parental care, possibly stemming from male-biased guarding of offspring in basal vertebrates. The terrestrial transition of tetrapods led to prolonged egg retention in females and the emergence of amniotes, skewing care toward females. The nocturnal adaptation of Mesozoic mammalian ancestors reinforced maternal care for lactation and thermal regulation via endothermy, potentially introducing metabolic gate control in parenting neurons. The established maternal care may have served as the precursor for paternal and cooperative care in mammals and also fostered the development of group living, which may have further contributed to the emergence of empathy and altruism. These evolution-informed working hypotheses require empirical validation, yet they offer promising avenues to investigate the neural underpinnings of mammalian social behaviors.

Ecological variation in adult social play reveals a hidden cost of motherhood for wild chimpanzees.

Though common among humans, social play by adults is an uncommon occurrence in most animals, even between parents and offspring.1,2,3 The most common explanation for why adult play is so rare is that its function and benefits are largely limited to development, so that social play has little value later in life.3,4,5,6 Here, we draw from 10 years of behavioral data collected by the Kibale Chimpanzee Project to consider an alternative hypothesis: that despite its benefits, adult play in non-humans is ecologically constrained by energy shortage or time limitations. We further hypothesized that, since they may be the only available partners for their young offspring, mother chimpanzees pay greater costs of play than other adults. Our analysis of nearly 4,000 adult play bouts revealed that adult chimpanzees played both among themselves and with immature partners. Social play was infrequent when diet quality was low but increased with the proportion of high-quality fruits in the diet. This suggests that adults engage in play facultatively when they have more energy and/or time to do so. However, when diet quality was low and most adult play fell to near zero, play persisted between mothers and offspring. Increased use of play by adult chimpanzees during periods of resource abundance suggests that play retains value as a social currency beyond development but that its costs constrain its use. At the same time, when ecological conditions constrain opportunities for young to play, play by mothers fills a critical role to promote healthy offspring development.

Social competence in autism: A structural equation modeling approach.

Autistic individuals present with difficulties in social competence (e.g., navigating social interactions and fostering relationships). Clinical interventions widely target social cognition and social behavior, but there is inconsistent understanding of the underlying components of social competence. The present study used structural equation modeling to examine social cognition and social behavior and explore the relationship between these latent constructs. Autistic youth (ages 10-17; n = 219) and their caregivers participated in this study. Constructs of social cognition and social behavior were captured using caregiver-report and self-report rating scales, as well as observational measures and direct clinical assessments (e.g., NEPSY-II). Measurement models of social cognition and social behavior demonstrated adequate to good fit. Correlational models demonstrated adequate to poor fit, indicating latent constructs of social cognition and social behavior are not closely related in autistic youth. Exploratory examination of a subsample of male youth (n = 157) evidenced improved model fit of social behavior, specifically. Findings tease apart social cognition and social behavior as cohesive and separable constructs; results do not support a structural relationship between social cognition and social behavior. Noted treatment implications include consideration of how targeting social cognition and social behavior together or separately may support autistic youth's progress toward reaching their identified therapeutic goals and supporting their self-directed social development.

Children's Social Behaviors: Developmental Mechanisms and Implications.

During the socialization process in family and school contexts, children display a wide variety of social behaviors with parents and peers. Yet the developmental trajectory, the predictors and outcomes, and the neural basis of those social behaviors are largely under-investigated. To address these problems, we invited experts in the field to submit their latest findings to tell this story. The current Special Issue is a collection of papers highlighting the complexity for various social behaviors, with a focus on the complex mechanisms that link social behaviors to child socio-emotional adjustment and mediating/moderating factors among the associations. Thirteen papers illustrate empirical work in the field, two papers present new methodological concerns, and one paper that provides a comprehensive review of the literature.

The Neural Mechanism Underlying Differentiated In-Group Versus Out-Group Face Recognition and Memory, Identification, Empathy and Pro-social Behavior: Evidence from fMRI and ERP Studies.

In the context of perceiving individuals within and outside of social groups, there are distinct cognitive processes and mechanisms in the brain. Extensive research in recent years has delved into the neural mechanisms that underlie differences in how we perceive individuals from different social groups. To gain a deeper understanding of these neural mechanisms, we present a comprehensive review from the perspectives of facial recognition and memory, intergroup identification, empathy, and pro-social behavior. Specifically, we focus on studies that utilize functional magnetic resonance imaging (fMRI) and event-related potential (ERP) techniques to explore the relationship between brain regions and behavior. Findings from fMRI studies reveal that the brain regions associated with intergroup differentiation in perception and behavior do not operate independently but instead exhibit dynamic interactions. Similarly, ERP studies indicate that the amplitude of neural responses shows various combinations in relation to perception and behavior.