Atran & Norenzayan's (A&N's) analysis fits with other perspectives on evoked culture: Cultural beliefs might emerge simply from the fact that people share a common cognitive architecture. But no perspective on culture can be complete without incorporating the unstoppable role of communication. The evolutionary landscape of culture will be most completely mapped by theories that describe specifically how communication translates evolved cognitive canals into cultural beliefs.

We argue that religious ritual's ability to facilitate communication and the pervasiveness of its basic characteristics across societies, as well as its precedence in other social species, suggests that religious behavior is more than a mere by-product. Religious constructs constitute associationally conditioned mnemonics that trigger neuroendocrine responses which motivate religious behaviors. The adaptive value of these constructs resides in their utility as memorable and emotionally evocative primes.

Atran & Norenzayan (A&N) ask: “Why do agent concepts predominate in religion?” This question presupposes that we have a notion of religion that is (1) well enough defined, and (2) characterized independently of that of supernatural agents. I question these two presuppositions. I argue that “religion” is a family resemblance notion built around the idea of supernatural agency.

The target article proposes an error theory for religious belief. In contrast, moral beliefs are typically not counterintuitive, and some moral cognition and motivation is functional. Error theories for moral belief try to reduce morality to nonmoral psychological capacities because objective moral beliefs seem too fragile in a competitive environment. An error theory for religious belief makes this unnecessary.

Atran & Norenzayan (A&N) survey a substantial body of theory and evidence on which there is broad agreement in the cognitive science of religion. Some parts of their argument (for instance, concerning the causes of costly commitment to religious beliefs) are more speculative and remain a focus of lively debate and further research.

The authors are working with a limited notion of religion. They have confined themselves to a view of it as superstition, “counterintuitive,” as they put it. What they have not seen is that faith does in a real sense involve a paradox in that it projects an impossibility as a methodological device, a fictive ploy, which in the best interpretation necessarily involves a commitment to the likelihood of self-sacrifice.

The evolutionary landscape that canalizes human thought and behavior into religious beliefs and practices includes naturally selected emotions, cognitive modules, and constraints on social interactions. Evolutionary by-products, including metacognitive awareness of death and possibilities for deception, further channel people into religious paths. Religion represents a community's costly commitment to a counterintuitive world of supernatural agents who manage people's existential anxieties. Religious devotion, though not an adaptation, informs all cultures and most people.

Based on recent insight into the thalamocortical system and its role in perception and conscious experience, a unified pathophysiological framework for hallucinations in neurological and psychiatric conditions is proposed, which integrates previously unrelated neurobiological and psychological findings. Gamma-frequency rhythms of discharge activity from thalamic and cortical neurons are facilitated by cholinergic arousal and resonate in networks of thalamocortical circuits, thereby transiently forming assemblies of coherent gamma oscillations under constraints of afferent sensory input and prefrontal attentional mechanisms. If perception is based on synchronisation of intrinsic gamma activity in the thalamocortical system, then sensory input to specific thalamic nuclei may merely play a constraining role. Hallucinations can be regarded as underconstrained perceptions that arise when the impact of sensory input on activation of thalamocortical circuits and synchronisation of thalamocortical gamma activity is reduced. In conditions that are accompanied by hallucinations, factors such as cortical hyperexcitability, cortical attentional mechanisms, hyperarousal, increased noise in specific thalamic nuclei, and random sensory input to specific thalamic nuclei may, to a varying degree, contribute to underconstrained activation of thalamocortical circuits. The reticular thalamic nucleus plays an important role in suppressing random activity of relay cells in specific thalamic nuclei, and its dysfunction may be implicated in the biological vulnerability to hallucinations in schizophrenia. Combined with general activation during cholinergic arousal, this leads to excessive disinhibition in specific thalamic nuclei, which may allow cortical attentional mechanisms to recruit thalamic relay cells into resonant assemblies of gamma oscillations, regardless of their actual sensory input, thereby producing an underconstrained perceptual experience.

Although the evidence remains tentative at best, the conception of hallucinations in schizophrenia as being underconstrained perception resulting from intrinsic thalamocortical resonance in sensory areas might complement current models of hallucination. However, in itself, the approach falls short of comprehensively explaining the neurogenesis of hallucinations in schizophrenia, as it neglects the role of external attributional biases, mental imagery, and a disconnection between frontal and temporal areas.

Hallucination lies at an intriguing border between psychiatry and philosophy. Although Behrendt & Young (B&Y) tie their proposal to Kantian transcendental idealism, other philosophical positions are equally consistent. Cognition is underconstrained by reality not only in hallucination but also in autism and dreaming. Sensory underconstraint is insufficient to encompass schizophrenia. There is also a breakdown in integrative capacity on the cognitive side. From a wider clinical perspective than schizophrenia, there can be underconstraint or overconstraint in sensory and cognitive functionalities.

Applying Behrendt & Young's (B&Y's) model of thalamocortical synchrony to complex visual hallucinations in neurodegenerative disorders, such as dementia with Lewy bodies and progressive supranuclear palsy, leads us to propose that the primary pathology may be cortical rather than thalamic. Additionally, the extinction of active hallucinations by eye closure challenges their conception of the role of reduced sensory input.

The cholinergic system is a good candidate for the role of determining the relative weight given in cortical information processing to new sensory information versus prior knowledge. We discuss the physiological data supporting this, and suggest that this Bayesian perspective can easily be reconciled with the dynamical framework proposed by Behrendt & Young (B&Y).

Behrendt's & Young's (B&Y's) persuasive scientific theory explains hallucinations, and is supported by a wide variety of psychological evidence, both normal and abnormal – unlike their philosophical thesis, Kantian idealism. I argue that the evidence cited by the authors in support of idealism actually favors realism. Fortunately, their scientific theory is separable from their philosophy, and is methodologically consistent with realism.

In agreement with Behrendt & Young (B&Y), we considered the role of perception disturbances in schizophrenia in our first clinical approaches, using the Bender test with schizophrenic patients. Following this, we reproduced nuclear symptoms of schizophrenia in animal models, showing that perceptual disturbances, acquisition disturbances, and decrease in affective levels can be induced by glutamatergic blockade within the nucleus accumbens septi. Our results link the proposed corticostriatal dysfunction with the thalamocortical disturbances underlying perceptual problems reviewed by B&Y.

The target article, in stressing the balance between neurobiological and psychological factors, makes a compelling argument in support of a continuum of perceptual and hallucinatory experience. Nevertheless, two points need to be addressed. First, the authors are probably underestimating the incidence of hallucinations in the normal population. Second, one should consider the role of absorption as a predisposing factor for hallucinations.

During the paradoxical dreaming sleep stage, characterized by hallucinations and delusions, as in schizophrenia, the increased subcortical release of dopamine, the presynaptic inhibition of thalamic relay nuclei, and serotonergic disinhibition are in accordance with the model for the mechanism of hallucination-induction.

Behrendt & Young's (B&Y's) novel “unifying model” of hallucinations, although comprehensive, fails to incorporate research into the possible role of 5-HT2A receptors in the mode of action of novel “atypical” antipsychotic drugs (which treat hallucinations effectively), and into the role of such receptors, which are located in thalamocortical circuits, in mediating drug-induced hallucinations.

Behrendt & Young (B&Y) suggest that hallucinations occur as a result of decoupling of neuronal populations from sensory control. I propose that such a decoupling is in fact a constant feature of brain activity, even under nonpathological conditions. This position is justified by evidence from recent neurophysiological recording studies. I suggest that hallucinations arise because of a breakdown in segregation of internally and externally generated activity in a neuronal population.

Transcranial magnetic stimulation, EEG, and behavioral studies by our group implicate spurious activation of speech perception neurocircuitry in the genesis of auditory hallucinations in schizophrenia. The neurobiological basis of these abnormalities remains uncertain, however. We review our ongoing studies, which suggest that altered cortical coupling underlies speech processing in schizophrenia and is expressed via disrupted gamma resonances and impaired corollary discharge function of self-generated verbal thought.

Behrendt & Young (B&Y) propose a useful theoretical framework for the study of processes underlying perception and hallucinations. It focuses on gamma oscillations in thalamocortical networks and the role of the reticular thalamic nucleus in modulating these oscillations. I suggest that their theoretical model might also be applied to the investigation of temporal encoding deficits in disorders such as dyslexia. I further suggest, however, that a role for slower rhythms, such as theta, might also be considered when investigating perceptual experience.