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The target article “Thinking Through Other Minds” (TTOM) offered an account of the distinctively human capacity to acquire cultural knowledge, norms, and practices. To this end, we leveraged recent ideas from theoretical neurobiology to understand the human mind in social and cultural contexts. Our aim was both synthetic – building an integrative model adequate to account for key features of cultural learning and adaptation; and prescriptive – showing how the tools developed to explain brain dynamics can be applied to the emergence of social and cultural ecologies of mind. In this reply to commentators, we address key issues, including: (1) refining the concept of culture to show how TTOM and the free-energy principle (FEP) can capture essential elements of human adaptation and functioning; (2) addressing cognition as an embodied, enactive, affective process involving cultural affordances; (3) clarifying the significance of the FEP formalism related to entropy minimization, Bayesian inference, Markov blankets, and enactivist views; (4) developing empirical tests and applications of the TTOM model; (5) incorporating cultural diversity and context at the level of intra-cultural variation, individual differences, and the transition to digital niches; and (6) considering some implications for psychiatry. The commentators’ critiques and suggestions point to useful refinements and applications of the model. In ongoing collaborations, we are exploring how to augment the theory with affective valence, take into account individual differences and historicity, and apply the model to specific domains including epistemic bias.
The processes underwriting the acquisition of culture remain unclear. How are shared habits, norms, and expectations learned and maintained with precision and reliability across large-scale sociocultural ensembles? Is there a unifying account of the mechanisms involved in the acquisition of culture? Notions such as “shared expectations,” the “selective patterning of attention and behaviour,” “cultural evolution,” “cultural inheritance,” and “implicit learning” are the main candidates to underpin a unifying account of cognition and the acquisition of culture; however, their interactions require greater specification and clarification. In this article, we integrate these candidates using the variational (free-energy) approach to human cognition and culture in theoretical neuroscience. We describe the construction by humans of social niches that afford epistemic resources called cultural affordances. We argue that human agents learn the shared habits, norms, and expectations of their culture through immersive participation in patterned cultural practices that selectively pattern attention and behaviour. We call this process “thinking through other minds” (TTOM) – in effect, the process of inferring other agents’ expectations about the world and how to behave in social context. We argue that for humans, information from and about other people's expectations constitutes the primary domain of statistical regularities that humans leverage to predict and organize behaviour. The integrative model we offer has implications that can advance theories of cognition, enculturation, adaptation, and psychopathology. Crucially, this formal (variational) treatment seeks to resolve key debates in current cognitive science, such as the distinction between internalist and externalist accounts of theory of mind abilities and the more fundamental distinction between dynamical and representational accounts of enactivism.
We discuss how uncertainty underwrites exploration and epistemic foraging from the perspective of active inference: a generic scheme that places pragmatic (utility maximization) and epistemic (uncertainty minimization) imperatives on an equal footing – as primary determinants of proximal behavior. This formulation contextualizes the complementary motivational incentives for reward-related stimuli and environmental uncertainty, offering a normative treatment of their trade-off.
The neurobiological understanding of mood, and by extension mood disorders, remains elusive despite decades of research implicating several neuromodulator systems. This review considers a new approach based on existing theories of functional brain organisation. The free energy principle (a.k.a. active inference), and its instantiation in the Bayesian brain, offers a complete and simple formulation of mood. It has been proposed that emotions reflect the precision of – or certainty about – the predicted sensorimotor/interoceptive consequences of action. By extending this reasoning, in a hierarchical setting, we suggest mood states act as (hyper) priors over uncertainty (i.e. emotions). Here, we consider the same computational pathology in the proprioceptive and interoceptive (behavioural and autonomic) domain in order to furnish an explanation for mood disorders. This formulation reconciles several strands of research at multiple levels of enquiry.
The main question that Firestone & Scholl (F&S) pose is whether “what and how we see is functionally independent from what and how we think, know, desire, act, and so forth” (sect. 2, para. 1). We synthesize a collection of concerns from an interdisciplinary set of coauthors regarding F&S's assumptions and appeals to intuition, resulting in their treatment of visual perception as context-free.
All organisms must integrate cognition, emotion, and motivation to guide action toward valuable (goal) states, as described by active inference. Within this framework, cognition, emotion, and motivation interact through the (Bayesian) fusion of exteroceptive, proprioceptive, and interoceptive signals, the precision-weighting of prediction errors, and the “affective tuning” of neuronal representations. Crucially, misregulation of these processes may have profound psychopathological consequences.
Ever since their discovery, mirror neurons have generated much interest and debate. A commonly held view of mirror neuron function is that they transform “visual information into knowledge,” thus enabling action understanding and non-verbal social communication between con-specifics (Rizzolatti & Craighero 2004). This functionality is thought to be so important that it has been argued that mirror neurons must be a result of selective pressure.
This commentary takes a closer look at how “constructive models of subjective perception,” referred to by Collerton et al. (sect. 2), might contribute to the Perception and Attention Deficit (PAD) model. It focuses on the neuronal mechanisms that could mediate hallucinations, or false inference – in particular, the role of cholinergic systems in encoding uncertainty in the context of hierarchical Bayesian models of perceptual inference (Friston 2002b; Yu & Dayan 2002).
PET studies of verbal fluency in schizophrenia report a failure of ‘deactivation’ of left superior temporal gyrus (STG) in the presence of activation of left dorsolateral prefrontal cortex (DLPFC), which deficit has been attributed to underlying ‘functional disconnectivity’.
To test whether these findings provide trait-markers for schizophrenia.
We used H215O PET to examine verbal fluency in 10 obligate carriers of the predisposition to schizophrenia, 10 stable patients and 10 normal controls.
We found no evidence of a failure of left STG deactivation in carriers or patients. Instead, patients failed to deactivate the precuneus relative to other groups. We found no differences in functional connectivity between left DLPFC and left STG but patients exhibited significant disconnectivity between left DLPFC and anterior cingulate cortex.
Failure of left STG ‘deactivation’ and left fronto-temporal disconnectivity are not consistent findings in schizophrenia; neither are they trait-markers for genetic risk. Prefrontal functional disconnectivity here may characterise the schizophrenic phenotype.
This commentary considers how far one can go in making
inferences about functional modularity or segregation, based on the
sorts of analyses used by Caplan & Waters in relation to the
underlying neuronal infrastructure. Specifically, an attempt is made
to relate the “functionalist” approach adopted in the
target article to “neuroreductionist” perspectives on
the same issue.
Using positron emission tomography (PET) and 15Oxygen, regional cerebral blood flow (rCBF) was measured in 33 patients with primary depression, 10 of whom had an associated severe cognitive impairment, and 23 age-matched controls. PET scans from these groups were analysed on a pixel-by-pixel basis and significant differences between the groups were identified on Statistical Parametric Maps (SPMs). In the depressed group as a whole rCBF was decreased in the left anterior cingulate and the left dorsolateral prefrontal cortex (P < 0·05 Bonferroni-corrected for multiple comparisons). Comparing patients with and without depression-related cognitive impairment, in the impaired group there were significant decreases in rCBF in the left medial frontal gyrus and increased rCBF in the cerebellar vermis (P < 0·05 Bonferroni-corrected). Therefore an anatomical dissociation has been described between the rCBF profiles associated with depressed mood and depression-related cognitive impairment. The pre-frontal and limbic areas identified in this study constitute a distributed anatomical network that may be functionally abnormal in major depressive disorder.
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