The subcortex as a trainer for cortical automaticity

ElsevierVolume 57, June 2024, 101371Current Opinion in Behavioral SciencesAuthor links open overlay panel, Highlights•

The exact relationship between cortical and subcortical regions remains elusive.

Accumulated evidence challenges the exclusive role of the cortex in social behavior.

SPEED model: The Subcortex facilitates automatic processes by transferring control to the cortex.

The subcortex may serve as a trainer to the cortex, also in social behaviors.

Insights into face perception, prosociality, and social disorders are discussed

The need to cope in a complex social environment has been suggested as the reason for the evolutionary development of our large brains. In contrast to this claim, growing evidence suggests that having a cortex is not a necessary condition for demonstrating prosocial behavior. Here, we suggest examining this issue through theoretical perspectives considering the relations between subcortical and cortical mechanisms. According to Ashby et al., (2007)'s SPEED (Subcortical Pathways Enable Expertise Development) model, the development of automaticity is characterized by a transfer of control from subcortical regions to faster cortical–cortical projections. Thus, subcortical regions may be perceived as trainers for the cortex. We apply this model to the social domain, suggesting that the automaticity associated with social processes begins in subcortical regions that direct attention to relevant events, allowing cortical regions to take control. We discuss this perspective in the context of face perception, prosociality, and social deficit disorders.

Section snippetsThe subcortical–cortical relations in human cognition

Saban et al. (2023) [19] have suggested that neuroscientific literature explicitly or implicitly portrays several models to describe the relationship between cortical and subcortical regions. The first, more traditional view, the ‘solitary cortex’ account, states that subcortical regions have no role in higher cognition. According to this view, prosocial behavior requires the development of the cortex, and should not be manifested in species lacking cortical tissue. This claim is in contrast to

The subcortex as a trainer of the cortex

One form of the ‘Dynamic Network model,’ which, as indicated earlier, suggests a tight collaboration between cortical and subcortical mechanisms, might be the theoretical model proposed by Ashby et al. (2007) [30], termed the 'SPEED' (Subcortical Pathways Enable Expertise Development) model. Although this model was developed to account for categorization and associated behaviors, it might also be relevant for higher and more complex cognitive abilities. According to the SPEED model, at early

The subcortical trainer model in the social domain

The term ‘social brain’ refers to a complex network of brain areas enabling the recognition, assessment, and prediction of others' mental states, feelings, and actions [34]. Key brain regions involved in social cognition encompass the medial prefrontal cortex (mPFC), anterior cingulate cortex, inferior frontal gyrus, superior temporal sulcus, amygdala, and anterior insula 34••, 35. Research over the past two decades has revealed how the brain facilitates various functions such as face and

‘The subcortex as a trainer’ account in social deficit disorders

The theoretical perspective of the subcortex as a trainer might also be relevant when examining the neural underpinning of different social deficit disorders. A social deficit may be related to abnormal subcortical functioning (the trainer), to abnormal cortical functioning (the trainee), or to the relationship between the two (the training process). Distinguishing the associated mechanism involved in each social disorder may lead to new insights and interventions. For instance, autism spectrum

CRediT authorship contribution statement

Both authors contributed equally to the conceptualization and the writing of the article. All authors have seen and approved the final version.

Declaration of Competing Interest

None.

Acknowledgements

S.G. was supported by the Israel Science Foundation (574/22).

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