Social plasticity relies upon neuroplasticity (149). Essentially, every aspect of social communication may need a rapid evaluation of social signals and accurate working (online) responses to social demands (135). In a course of approximately three decades, research in social neuroscience has elucidated that cortical changes influenced by social information can provide elemental neural representations of social-environmental alterations during which a set of accurate computational processes (136) of time and social context is needed. On a neocortical level, the brain is also required to appropriately respond to the emotional climate and cues of the social interaction (150). More specifically, the cortical responsiveness to the emotional engagement in social interactions (137, 140) consists of an ongoing perceiving and a flexible integrating of emotional cues conveyed through, for example, facial, vocal, and gestural cues. It appears that the symmetry of information relayed from these interactive sources to the subcortical [e.g. amygdala; (151–153)] and cortical processing network determine the basis for understanding others. Using functional magnetic resonance imaging (fMRI) in studies for analysing grey matter volume and thickness as well as the strength of connections, it was shown that changes in emotional signals were associated with robust network variations and remodeling in the insular cortex (154), ventromedial prefrontal cortex (vmPFC) (155), and anterior cingulate cortex (ACC) and dorsomedial prefrontal cortex (dmPFC) (156). Also, an fMRI-based study recently indicated that alterations of one’s response to an emotional incident that can potentially be experienced in the daily social interaction was associated with an efficient functional remodeling in the frontoparietal (FPN) network (157).

To be able to make rapid decisions about the emotional contents in an ongoing communication, one should readily interpret facial features and the underlying emotions. This fundamental process seems to require a dedicated cortical computation. It is now well-known that primates including humans have evolved a specific cortical architecture in occipitotemporal cortex (OTC) (158) and orbitofrontal cortex (OFC) (159) where face selective neurons are used in facial-emotional processing. In this context, Barat, et al. (159) have recently shown that face cells within the OFT of rhesus monkeys specifically categorize photographs of conspecifics into emotion and social clusters. These neurons, however, do not respond to acoustic stimuli such as mere vocalizations and are poorly modulated by vocalizations added to faces. Therefore, it seems that the OFC face cells provide a neural substrate that dynamically codes physical attributes of faces and support a successful interpretation of the emotions conveyed by faces during social interaction.

Two interacting brains also require joint attention (JA) during which information in social interaction needs to be nonverbally transferred from one person (sender) to another (receiver). In humans’ social interaction, JA is a fundamental mechanism that is used to coordinate shared intentions and information, typically by eye gaze which results in nonverbal grasping of others’ attention (160). Using a novel neuroimaging approach by fMRI hyperscanning and interaction-based tasks, Bilek, et al. (161) found that interacting individuals show unique cross-brain connectivity components that restrict information flow only between the sender’s and receiver’s temporoparietal junction (TPJ). Beside a neural coupling that was found between the sender’s right TPJ (a key region for social interaction), mPFC and OFC, a neural coupling of the sender’s right TPJ with the receiver’s right TPJ was also found. As the right TPJ has been shown to be involved in two sets of functions related to JA (i.e., reorienting of attention and social cognitive functions), all these findings reveal the central role of human-specific cortical areas in the brain dynamics of dyadic interactions during which very short-time scales of adaptive responses are essential (161).

The idea of “two brains in interaction” leaves open many questions for future investigation. First and foremost, the sparsity of information on how genetics impacts cerebral (e.g., cortical) structures dedicated to social cognition and behaviours calls for more convergent studies in the social brain field. Genetic influences may profoundly impact the development of many cerebral areas (162–164) and social cognition through which humans are able to understand and respond to others’ social responses (165). If social brain function determines the extent of social fitness, sociality, and mutual social responsiveness, then one can speculate that the social brain network can also be influenced by genetic factors, thus assuming sociality is partially inherited or, at least, marginally influenced by social learning. Interestingly, measures of surface area and cortical thickness of social brain regions, especially mPFC, and TPJ and pSTS (see assumption II) have been recently shown to be remarkably determined by genetic influences (166). Such findings seem more important when one considers the profound within-species individual differences in, for example, the size of cerebral cortex in humans (167) and the geno-developmental cascade that causes such a vast cortical anatomical disparity. Therefore, greater detail provided by further genomic and multivariate studies will be required to better understand how genetic influences contribute to variations in structural measures of the social brain.

Also, sex differences in the brain structure including cortical maturation and function (168) is still an unappreciated model for variables that affect how male and female brains evaluate, for example, the emotional contents of social encounters. Also, concerning the sex differences in network efficiency (169), and the finding that women have greater overall cortical connectivity (170), one can expect that such structural disparities between males and females can result in robust behavioural bias during social information processing. Moreover, because sexual differentiation of the brain (e.g., brain masculinization) follows a fundamental sex/gender-specific developmental process (171, 172), sufficient consideration over the effect of sex and/or gender is a crucial necessity in social neuroscience. Practically, it can broadly inform us about how these differences in central processing determine males’ and females’ responses to social demands, and why males and females, for instance, are differentially vulnerable to prenatal and postnatal events with regard to social impacts, stressors, pathogens, and diseases (173, 174). This appears more important when findings show that prenatal maternal psychological disturbance is associated with altered brain connectivity and higher externalizing symptoms that can induce social conflicts in a sex-specific manner in young children (175).

Social inputs and interactions with the social environment are critical in early prenatal brain development, particularly for cortical circuits that later develop specialized roles in social cognition, a high order process that is involved in processing information about self, other people, and social interactions (183). Even from early childhood, human social cognition is special compared to other social animals, likely because children can fully imitate others, successfully follow the social learning rules and use a set of sophisticated cognitive skills. Interestingly, these inter-species differences are absent when children and chimpanzees are required to interact with the physical world or perform non-social tasks (6, 184).

Infants are also able to evaluate others based on their social behaviours during early developmental stages. They can make precise decisions about who is friend (or an appropriate social partner) and who is foe in social encounters (181). When assessed for how children evaluate others based on their social behaviours, 6- and 10-month-old infants showed that they prefer helpers to neutral individuals and hinders. An individual seen hindering another, however, was negatively evaluated compared to a neutral individual (181). Such developmental trajectory toward early capacity for social cognition supports the view that social evaluative bias in human development is a biological adaptation (181). Interestingly, this selective response to the nature of social interaction or socially significant stimuli was also recently shown in adults. A strong selective response in the posterior superior temporal sulcus (pSTS) was seen when participants were exposed to positive (helping) or negative (hindering) social interactions (180).

Despite elemental differences between the “two-person neuroscience (2PN)” (182) and the “second-person neuroscience” (140, 185), to elaborate the psychoneurophysiological nature of human social interaction both approaches provide important conceptual frameworks about how human brain development is rooted in the context of early social inputs. Additionally, both concepts emphasize that stimulatory function of social interaction during brain development relies upon the active-reciprocal participation of “self and other” or “sender and receiver” in the social discourse during which the reactions of one person stimulate the other person, and vice versa.

Prosody, faces, gestures and eye gaze of immediate household members (e.g., mother or caregiver) in early life are key components of the early perceptual world and social cognition and form the most principal attributes of human perception later in life through the direct involvement of cortical networks. For example, for decades, it was believed that the ToM emerged by approximately 3–4 years of age (179, 186). Yet, to address the questions of when the developmental onset of the mature adult ToM occur and what the cortical correlates (cortical thickness and surface area) of the early ToM are, Wiesmann and others (187) have recently indicated by MRI that infants display action (nonverbal) expectations consistent with others’ beliefs before the age of 2 years. More importantly, they found that there are two independent cortical networks for early nonverbal action expectations and explicit verbal ToM; while the former is supported by the cortical surface area and thickness of the supramarginal gyrus (SMG), the latter is supported by the cortical network of the precuneus (PC) and TPJ. The cortical functional organization localized in TPJ, which is relevant to high-level social cognition in preverbal infants, was also indicated with the use of functional near-infrared spectroscopy (fNIRS) by around 7 months of age (177). Interestingly, this robust developmental curve of cortical specialization for social stimuli in early life appears free of environmental and cultural influences. When responses to social versus non-social stimuli in infants from two contrasting environments (rural Gambian and urban United Kingdom) was investigated with fNIRS, results showed similar localized and socially selective cortical responses from 9 to 24 months of life to visual and auditory stimuli (145).

Longitudinal evidence recently reported by Ulmer Yaniv and others (153) has also shown that mother–child social synchrony in human early childhood provides a mechanism by which the brain is tuned to the social world across development. This level of influential lifelong plasticity allows both cortical (e.g., insula and ventromedial prefrontal cortex; vmPFC) and subcortical (e.g., amygdala) systems for being highly sensitive and adaptable to emotion-specific inputs underlying social interactions later in life (see assumption III). Therefore, a developing core mechanism supported by the earlier cortical maturation for social-cognitive processes helps infants at a very early stage of development to reason about other people’s thoughts and infer what is on their mind; a central developmental pattern that serves to enhance social affiliations in early life and later in adulthood.

Beside the correlational models and evidence, social neuroscience also needs to proceed with causal experimental designs that are supported by highly controlled manipulations and multivariate analyses with sufficient statistical power. This level of design optimization can open a broader window of explanations into the brain-social causal relations. Therefore, social neuroscience should ask, for instance, to what extent are cortical developmental dynamics casually related to changes in “other/self” concepts or to the perception of social interactions (180) in early life. How do early neural developmental patterns predict certain types of developmental trajectories or information processing (e.g., distinguishing helping and hindering) that are linked to sociality in later life? Furthermore, how can lifelong plasticity in social brain networks and the regional specialization by which cortical regions selectively respond to social interactions (180, 188) operate together to help humans navigate a social world and understand social demands? Does the lack of sufficient social stimuli, particularly in terms of the quality of social interactions change the pattern observed in cortical regional sensitivity? Is there an opening-and-closing critical window for regional selectivity in early life when a socially relevant specific developmental process begins and may be triggered by social inputs? Such questions may drive future research to further elucidate how developmental changes in cortical networks causally impact social networks and vice versa.

Sex differences in the cortical determinants of the ToM development are also important. For instance, it is now known when ToM develops in girls (187), however, whether the same developmental pattern could be followed in boys or if SMG- or dorsal PC-related processes equally drive ToM-dependent behaviours in both sexes still are open questions.

Many behaviours in humans are learned through and influenced by social context (137). However, the impact of social context is based on the brain’s capability to discriminate between social and non-social contents of information. Further, the human brain shows a high sensitivity to the mere presence of social information (183), presumably reflecting the preferential processing of social versus non-social information in the brain (194). This implies that, when required to respond in social versus non-social conditions, a typical brain is predominantly driven by a social effect. The social effect mainly seems credible in cortical regions such as the dmPFC, dorsoventral PFC (dvPFC), posterior cingulate cortex (PCC), PC, occipitotemporal junction (OTJ), right fusiform gyrus, temporal pole, and right inferior frontal gyrus (183) that accompanied with other regions (e.g., amygdala) robustly and preferentially react to social stimuli.

To what extend may this level of specificity in cortical social processing be applied to the interregional processing collaboration in the brain? The ACC and its subregions, for example, can be the key candidates here that are shown to be a socially specific processing system in humans (195, 196), monkeys (197, 198) and rodents (199, 200). Also, the ACC responds to social experience by morphological plasticity such as increased thickness, and such socially driven structural alterations relate to improvements in targeted behavioural capacities (201). However, it seems that the ACC function relies upon a non-social information-processing network such as NAc which contributes to the valance of information (e.g., pain) and do not individually reflect pure social content (202). Interestingly, the ACC generates socially appropriate behavioural responses (e.g., empathy) through distinct downstream targets that share pain-related contents of social information with the NAc, while fear-related valence of information will be processed in conjunction with the basolateral amygdala (BLA). Moreover, in a series of fMRI examinations, McCormick and others have assessed the functional architecture of the social brain using a multimethod approach to circumvent limitations underlying the traditional univariate methodologies. Results showed strong functional relationships within the social brain, and between the social brain networks and non-social regions (203). Thus, despite the fact that all streams involved in social information processing depend upon distinct social neural networks, social and non-social modules seem exchange signals and inputs to generate appropriate and more specific responses in social encounters.

This aspect of interregional functional connection in the brain is particularly critical in children with ASD whose brain abnormalities are related to both social and non-social processing (204). An aberrant cortico-subcortical connectivity, such as underconnectivity between the pSTS-to-ventral tegmental area (VTA) and NAc, is associated with the severity of social skills and language deficits. Conversely, the strength of functional connectivity between these regions predicts standardized scores of communication abilities in ASD (205). Also, preferential responses to social versus non-social reinforcers seem also reversed in children with ASD compared to normally developing children, and this affinity for non-social stimuli was also shown when ASD children were exposed to non-social cues alone (191). The distinction between social and non-social systems and processing, therefore, may have important implications for investigation of the neural mechanisms underlying atypical developmental dynamics and functional specialization in the brain. For instance, dendritic spine loss and impaired glutamatergic synaptic transmission and plasticity in pyramidal neurons of ACC induced social deficits in a mouse model of ASD (200). However, it is important to note that cortical responses (e.g., increase in glutamatergic/GABAergic synapse numbers) to social requirements developmentally follow a timeframe of synaptogenesis that arguably facilitates normal functional specialization in early life, thus affecting altricial social behaviours in favour of survival, experience-dependent development and social interactions (206). It is possible that a disruption of timing for cortical synaptogenesis in children with ASD have dramatic impacts on sociability in early development and later in life.

Although, the social brain has an independent processing identity formed by ecological and organismic effects (see assumption IV), it is not an isolated module. Therefore, the duality of social/non-social brain networks in assumption III may implicitly challenge results and conclusions through procedural issues (191) when either neural or behavioural responses to social versus non-social stimuli are investigated. For example, because social and non-social stimuli typically represent cultural values, and responses to these stimuli may be also influenced by the cultural atmosphere, links of anatomical differences to observed preferences between different stimuli in ASD should be carefully interpreted unless these methodological concerns are appropriately addressed. This also implies that not only extrinsic, but intrinsic factors such as sex and/or gender can also contaminate final conclusions if not carefully controlled. Given the male-bias in the prevalence of ASD (207) and the critical role of androgens in prenatal development of the brain social circuitry (208), research in this context is required to include both sexes in order to avoid sex/gender hegemony. Further, a developmental trajectory that simultaneously profiles changes in social/non-social brain systems along with the corresponding behavioural symptoms in ASD seems an absolute necessity. Thus, longitudinal studies focused on the early social developmental predictors of ASD, such as diminished eye fixation in the first months of life (209), would also be a fruitful asset to identify the neurobiological mechanisms underlying increased preference for non-social stimuli in ASD. Interventions aimed to affect atypical social behaviours in ASD can also benefit from the distinguished social and non-social networks. Because oxytocin increases the salience of social stimuli [(188), see also (210) for more discussion], it appears reasonable to apply oxytocin for boosting the social brain to mitigate social impairments of ASD (211). Therapeutic policies also need to revisit the one-size-fits-all approach to develop sex-specific treatments of disorders like ASD and schizophrenia, which represent social and non-social information processing impairments in a sexually dimorphic manner.

How do brain dynamics relate to different social network properties? An idea originally grown up in the lap of network neuroscience (15, 16) suggests that the brain and social network dynamics must be studied in parallel (212). Inspired by a number of studies (15, 217), one might then expect that brain structural and connectional measures can predict how people think and behave, and vice versa. In the context of social relationships and cortical correlates of social behaviours, interpersonal closeness in the social network anticipates brain functional connectomes. For example, friends or individuals who are close together in their real-world social network in a village share similar resting-state functional connectomes reflected by the task-based fMRI (213). Such findings suggest that geographic-physical proximity in the extrinsic world determines similarity in the brain resting-state activity as an index for interbrain functional coupling. While a top-down (brain-to-behaviour) approach leads to the conclusion that brain connectomes form social cognition and behaviour, it can also be presumed that a bottom-up (behaviour-to-brain) process influenced by social network dynamics also shapes the brain functional networks (1). It appears that these two axes of influence together represent key contributors to human social experience and must be seen as bidirectional processes.

It is beyond the scope of the present review to explain how the conjoined processes of the brain-social networks offered by network neuroscience act together to surpass theoretical limitations in the traditional models of brain and social dynamics [see (212) for discussion]. Instead, we argue that the more fundamental psychological outcomes of brain function such as self-awareness or the brain’s theory about itself can be easier to understand within the multiscale network framework in which brain and social network dynamics are unified.

Recent efforts show that self-awareness is an abstract representation of ourselves (e.g., cortical network dynamics) and the external world (e.g., competitive and cooperative social encounters) (218) enriched by learning and plasticity (219). Self-awareness is thus underpinned by interaction with itself and others. This being said, the long-term ongoing self-knowledge [radical plasticity (219)] follows an information processing influenced by a pattern of connectivity not only between intrinsic and extrinsic modules, but also within units of each module such as neural network. A within-module approach that attempts to identify neurobiological substrates of self shows that cortical paralimbic networks such as temporal pole, frontal lobe (e.g., medial frontal pole), retrosplenial cortex and more specifically parietal/posterior cingulate cortex (PPCC) play a crucial role in processing declarative information about the self (220–223), although an elemental part of this information is through interaction with others. To address the molecular organization of self-awareness also it was recently shown that self-awareness is controlled by dopaminergic-GABA interaction in the paralimbic network (default mode network for self-awareness). Paralimbic dopaminergic agents appear to casually stimulate conscious experience through GABA receptors (214). Notably, such findings provide further insights into mechanisms underlying the faltered self-awareness and consciousness in clinical conditions such as schizophrenia, addiction and developmental disorders as well as in people with disorders of consciousness (DoC) (224), all characterised by a profile of impaired social relationships.

Despite the critical role of social determinants in self-awareness (2, 216), it is unknown whether an optimized self-awareness represents an enriched social network. Further, does an optimized self-awareness predict an optimized central social information processing, too? To what extent do social network properties (quantity, quality, dynamics, social ranks and dominance, etc.) drive changes in the corresponding neural network and the self-awareness or self-regulation development? Do these effects follow a developmental trajectory during a sensitive period? If self-awareness develops in a social background and through an active spontaneous social cognition, then it would seem reasonable to teach self-awareness considering the evolutionarily conserved plasticity in neural networks (225). More importantly, because males and females respond differently to the social interactions (226), future studies might also investigate such questions in the context of sex differences. For example, are males and females influenced by the same social signals (inputs and feedback) and dynamics to develop self-awareness? Then how would the neural networks that are persistently sensitive to social context determine sex-specific responses to socially significant stimuli for establishing a conscious knowledge of the self (identity) and the world?

Social affiliation, in fact, represents an innate allostatic need. That is, sociality serves as a surviving strategy evolutionarily designed to buffer against life-threatening challenges of aloneness. Many animals require social affiliation for survival as well as for their physiological needs (allostatic demands), for growing and reproduction (190, 228). Newborns among all mammals require at least one dedicated caregiver, typically the mother, who provides the young with maximum protection during early development via a persistent closeness. It appears that when mothers express their prototypical behaviours, such as feeding, vocalization or touching, during early social communication with children infer a profound effect on infant sociality through allostatic support for later homeodynamic resilience. Interestingly, in an innovative fMRI study, Shimon-Raz and colleagues recently showed (229) moments of social synchrony between mother and child, and these brief moments of mother–child social alignment and attachment likely regulate the ongoing adjustment of the child’s internal milieu for survival and growth. Given that the neural substrates required for social connectedness are not clearly evident in newborns and develop during childhood (230), it seems justified to consider allostasis as a domain-general process which plays a key role in social affiliation in early life. The experience of social synchrony in the maternal-newborn contact is shown necessary for tuning the social brain in later life, specially in cortical regions such as insular cortex, temporal pole and vmPFC (153). Notably, it has been shown that a distinct pattern of mPFC sensitivity to early social stimulations can be transmitted transgenerationally via the female lineage (mother-to-daughter) to the next generation who never experienced social life (173). Therefore, not only allostatic demands for growth, protection and reproduction potentiate the brain susceptibility to the early social inputs, but also there is a lineage-dependent mechanism that tends to transmit the so-called allostasis dependence through the social ancestors to their non-social descendants.

Social network also encompasses multiple forms of interactions. On the one hand, it may result in full engagement in social communication, thus providing reciprocal support and acceptance (231). On the other hand, it may be associated with impoverished interaction or even with “sociotoxicity,” typically contaminated with rejection, isolation and loneliness (232). The potential mechanisms that might link each form of interaction to cortical structure and function have been extensively investigated (145, 226, 227, 233). For instance, a recent study showed that early sensorimotor stimulation and social enrichment synergistically induce a region-specific response in the mPFC through an axis linking oxytocin to brain-derived neurotrophic factor (BDNF) expression, showing that oxytocin is essential to brain maturation and neurodevelopment (188).

If early social interactions are crucial for survival, then how does the absence of sufficient interpersonal relationships act on neurobiological integrity? The key answer underlines social isolation (being alone) and loneliness (feeling alone); the negative social determinants of cortical structural remodeling. Loneliness in approximately 40,000 United Kingdom Biobank adult participants was associated with a unique neural signature in grey matter volume, intrinsic functional connectivity as well as in white matter tract integrity characterising distinctive structural and functional features of the “lonely brain” (227). Interestingly, grey matter volume shows more consistent correlation with loneliness than other cortical brain networks. In parallel with human studies, animal research also indicate a robust sensitivity of cortical neural circuits to the social void (234). One example of how early-development social isolation might have an impact on brain morphology and function is a recent study (235) in which social isolation reduced hippocampal volume and BDNF expression. In line with these findings, care-deprived mice in early life displayed dendritic atrophy of pyramidal neurons in layers II/III and enhanced inhibitory synaptic inputs in the mPFC neurons (236). Thus, maternal separation in children can form a neuronal morphological phenotype that are, at least in part, related to the early life impaired allostatic adjustment such as the hypothalamic–pituitary–adrenal (HPA) axis dysregulation (235).

Notably, the structure of self-other representation in the mPFC follows an intrinsic social categorisation which directly reflects social connection and connectedness (see assumption IV) (234). Therefore, individuals who are less socially connected or feel lonelier, show altered self-other mapping in social brain regions including the mPFC. Consequently, when neural responses to self and others were examined during an fMRI scan, loneliness was shown to be associated with reduced representational similarities between the self and others (Courtney & Meyer, 2020). It appears that chronic social isolation during which people feel socially disconnected can be reflected in a lonelier neural self-representation (234). These morphological changes and dynamics in turn influence emotion processing and preferences during navigation within the social world and contribute to the shape of friendship networks (137).

Much of variability in behavioural responses of primates including humans can be explained by sex/gender, and attributed to the sex-based differentiation in brain anatomy (7). The need for physiological regulations, at least in part, may have natural characteristics to cover most differences between sexes during social affiliation, however next steps may delineate patterns of sex-dependent dissimilarities in allostasis regulation in early development. Accordingly, an empirical systematic approach to sex differences in the light of the “allostatic support” assumption may provide further insights to the critical influence of early social relationships on physiology and neural network. For instance, the activity of the hypothalamic–pituitary–adrenal (HPA) axis, a neurohormonal hallmark of emotionality, is characterized by prominent sex differences (237) that are evident already early in life (238). How and to which extent early social interactions involve in the neurohormonal differentiation remain key questions for future research. Importantly, the HPA-axis activity in turn modulates the normal biobehavioural reactions such as oxytocinergic responses to social signals in a sexually dimorphic manner (226). What is the actual basis of such very early sex disparities prior to receiving sufficient allostatic support if the brain is not fully predetermined to respond to social signals? To what extent do these differences determine the cortical specialization for social inputs in both sexes before their exposure to allostatic feedback? In other words, do the biological sex differences drive a sex-specific allostatic regulation? This also leads to the central question if male or female social brains (7, 239) shape in the absence of the early allostatic supports provided by close others.

It can be expected that a negative social interaction, which may involve rejection or the perception of social isolation, results in dysregulation of HPA axis activity and consequently reduced OT-mediated signals. How do such allostatic disturbances [i.e., the inhibitory effect of the glucocorticoid action on the OT function (240)] during early interpersonal crises and perturbations, especially if they occur chronically, impact functional connectivity in male and female infants? In other words, do males and females follow similar patterns in brain vulnerability to negative interactions in early life? Such questions seem more critical when one is investigating the sex-specific strategies in social regulation of human survival and their effects on neural capacities for social functioning (7). Interestingly, neocortex size was shown to be differently correlated with group size in males and females (239). Because the neocortex’s size is related to the degree of social complexity (241) to enable the higher cognitive demands in larger groups and more complex social exchanges, it is justified to investigate how sex and sex-specific roles determine the relationship between neocortex size and sociality. Also, if relative neocortex size is positively correlated with group size in females and negatively correlated in males, then sex-specific responses to sociotoxicity in social relationships (e.g., rejection or loneliness) can be better understood by different neurocognitive changes induced by the quantitative and qualitative aspects of social interactions in both sexes. Furthermore, because social rejection and physical pain share a common somatosensory representation in the secondary somatosensory cortex and dorsal posterior insula (242), this may help to identify, for example, if there would be a sex-specific cortical response to social rejection which is engrained as a physically “painful” stimulation.

In the context of sex-dependent differences, future work also needs to explore the fundamental mechanisms by which male and female brains differentially reconfigure to create meaning needed to properly respond during social exchanges. Are these inter-individual differences in humans actually dictated by cultural pressures to elicit context-appropriate responses (135) or developmentally by biological determinants (243)? The way via which we answer these questions, especially by causal-empirical conceptualizations and models, can ultimately help redefine the social brain concept in the context of current and topical frameworks.