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The first two chapters of this book offer a modern, self-contained exposition of the elementary theory of triangulated categories and their quotients. The simple, elegant presentation of these known results makes these chapters eminently suitable as a text for graduate students. The remainder of the book is devoted to new research, providing, among other material, some remarkable improvements on Brown's classical representability theorem. In addition, the author introduces a class of triangulated categories\"--the \"well generated triangulated categories\"--and studies their properties. This exercise is particularly worthwhile in that many examples of triangulated categories are well generated, and the book proves several powerful theorems for this broad class. These chapters will interest researchers in the fields of algebra, algebraic geometry, homotopy theory, and mathematical physics.

Discussions of the function of early nervous systems usually focus on a causal flow from sensors to effectors, by which an animal coordinates its actions with exogenous changes in its environment. We propose, instead, that much early sensing was reafferent; it was responsive to the consequences of the animal's own actions. We distinguish two general categories of reafference—translocational and deformational—and use these to survey the distribution of several often-neglected forms of sensing, including gravity sensing, flow sensing and proprioception. We discuss sensing of these kinds in sponges, ctenophores, placozoans, cnidarians and bilaterians. Reafference is ubiquitous, as ongoing action, especially whole-body motility, will almost inevitably influence the senses. Corollary discharge—a pathway or circuit by which an animal tracks its own actions and their reafferent consequences—is not a necessary feature of reafferent sensing but a later-evolving mechanism. We also argue for the importance of reafferent sensing to the evolution of the body-self, a form of organization that enables an animal to sense and act as a single unit. This article is part of the theme issue ‘Basal cognition: multicellularity, neurons and the cognitive lens’.

During vocalization, efference copy/corollary discharge mechanisms suppress the auditory cortical response to self-generated sounds. Previously, we found attenuated vocalization-related auditory cortical suppression in psychosis and a similar trend in the psychosis risk syndrome. Here, we report data from the final sample of early illness schizophrenia patients (ESZ), individuals at clinical high risk for psychosis (CHR), and healthy controls (HC). Event-related potentials (ERP) were recorded from ESZ (n = 84), CHR (n = 71), and HC (n = 103) participants during a vocalization paradigm. The N1 ERP component was elicited during production (Talk) and playback (Listen) of vocalization. Age effects on N1 suppression (Talk-Listen), Talk N1, and Listen N1 were compared across groups. N1 measures were adjusted for normal aging before testing for group differences. Both ESZ and CHR groups showed reduced Talk-Listen N1 suppression relative to HC, but did not differ from each other. Listen N1 was reduced in ESZ, but not in CHR, relative to HC. Deficient Talk-Listen N1 suppression was associated with greater unusual thought content in CHR individuals. N1 suppression increased with age in HC (12-36 years), and while CHR individuals showed a similar age-related increase, no such relationship was evident in ESZ. Putative efference copy/corollary discharge-mediated auditory cortical suppression during vocalization is deficient in ESZ and precedes psychosis onset, particularly in CHR individuals with greater unusual thought content. Furthermore, this suppression increases from adolescence through early adulthood, likely reflecting the effects of normal brain maturation. This maturation effect is disrupted in ESZ, presumably due to countervailing illness effects.

•Activation likelihood estimation meta-analysis of neuroimaging inner speech studies.•Distinct neural activation observed when stratifying inner speech by phenomenology.•Activation of speech production regions not observed in all inner speech subtypes. The neural mechanisms of inner speech remain unclear despite its importance in a variety of cognitive processes and its implication in aberrant perceptions such as auditory verbal hallucinations. Previous research has proposed a corollary discharge model in which inner speech is a truncated form of overt speech, relying on speech production-related regions (e.g. left inferior frontal gyrus). This model does not fully capture the diverse phenomenology of inner speech and recent research suggesting alternative perception-related mechanisms of generation. Therefore, we present and test a framework in which inner speech can be generated by two separate mechanisms, depending on its phenomenological qualities: a corollary discharge mechanism relying on speech production regions and a perceptual simulation mechanism within speech perceptual regions. The results of the activation likelihood estimation meta-analysis examining inner speech studies support the idea that varieties of inner speech recruit different neural mechanisms.

Moving through our environment generates multiple changes in my sensations. But I do not experience the environment as changing. My conscious perceptual experience is of a stable environment through which I move. This perception is created by intricate neural computations that automatically take account of my movements. The stable environment that I experience is independent of my actions. As a result, I experience it as objective: a set of facts about the world that constrain my movements. Because it is objective I expect that it will also constrain the movements of others in the same way, whether these are rocks rolling down a hill or animals foraging for food. This experience of objectivity creates a shared understanding of the world that enhances our interactions with others. Our perceptual experiences, while personal, are shaped by our model of the world, and since others are modelling the same world, their models will be very similar. Interactions with others will further increase this similarity. The models create a form of common knowledge. This common knowledge is an inherent feature of our basic conscious perception, even when we’re not actively reflecting on or deliberately sharing our experiences. The common knowledge created by our conscious perception of the world enables the coordination of behaviour which is a critical precursor for the evolution of cooperative behaviour.

When divergent populations interbreed, their alleles are brought together in hybrids. In the initial F1 cross, most divergent loci are heterozygous. Therefore, F1 fitness can be influenced by dominance effects that could not have been selected to function well together. We present a systematic study of these F1 dominance effects by introducing variable phenotypic dominance into Fisher’s geometric model. We show that dominance often reduces hybrid fitness, which can generate optimal outbreeding followed by a steady decline in F1 fitness, as is often observed. We also show that “lucky” beneficial effects sometimes arise by chance, which might be important when hybrids can access novel environments. We then show that dominance can lead to violations of Haldane’s Rule (reduced fitness of the heterogametic F1) but strengthens Darwin’s Corollary (F1 fitness differences between cross directions). Taken together, results show that the effects of dominance on hybrid fitness can be surprisingly difficult to isolate, because they often resemble the effects of uniparental inheritance or expression. Nevertheless, we identify a pattern of environment-dependent heterosis that only dominance can explain, and for which there is some suggestive evidence. Our results also show how existing data set upper bounds on the size of dominance effects. These bounds could explain why additive models often provide good predictions for later-generation recombinant hybrids, even when dominance qualitatively changes outcomes for the F1.

Self-generated speech produces a smaller N1 amplitude in the auditory-evoked potential than externally generated speech; this phenomenon is known as N1-suppression. Schizophrenia patients show less N1-suppression than healthy controls. This failure to self-suppress may underlie patients' characteristic tendency to misattribute self-generated thoughts and actions to external sources. While the cause of N1-suppression deficits to speech in schizophrenia remains unclear, structural damage to the arcuate fasciculus is a candidate, due to its ostensible role in transmitting the efference copy of the motor plan to speak. Fifty-one patients with early illness schizophrenia (ESZ), 40 individuals at clinical high-risk for psychosis (CHR), and 59 healthy control (HC) participants underwent an electroencephalogram while they spoke and then listened to a recording of their speech. N1-suppression to the spoken sounds was calculated. Participants also underwent a diffusion-tensor imaging (DTI) scan, from which the arcuate fasciculus and pyramidal tract were extracted with deterministic tractography. ESZ patients exhibited significantly less N1-suppression to self-generated speech than HC participants, with CHR participants exhibiting intermediate levels. ESZ patients also exhibited structural abnormalities in the arcuate fasciculus-specifically, reduced fractional anisotropy and increased radial diffusivity-relative to both HC and CHR. There were no between-group differences in the structural integrity of the pyramidal tract. Finally, level of N1-suppression was linearly related to the structural integrity of the arcuate fasciculus, but not the pyramidal tract, across groups. These results suggest that the self-suppression deficits to willed speech consistently observed in schizophrenia patients may be caused, at least in part, by structural damage to the arcuate fasciculus.

Efference copies refer to internal duplicates of movement-producing neural signals. Their primary function is to predict, and often suppress, the sensory consequences of willed movements. Efference copies have been almost exclusively investigated in the context of overt movements. The current electrophysiological study employed a novel design to show that inner speech – the silent production of words in one’s mind – is also associated with an efference copy. Participants produced an inner phoneme at a precisely specified time, at which an audible phoneme was concurrently presented. The production of the inner phoneme resulted in electrophysiological suppression, but only if the content of the inner phoneme matched the content of the audible phoneme. These results demonstrate that inner speech – a purely mental action – is associated with an efference copy with detailed auditory properties. These findings suggest that inner speech may ultimately reflect a special type of overt speech. As you read this text, the chances are you can hear your own inner voice narrating the words. You may hear your inner voice again when silently considering what to have for lunch, or imagining how a phone conversation this afternoon will play out. Estimates suggest that we spend at least a quarter of our lives listening to our own inner speech. But to what extent does the brain distinguish between inner speech and the sounds we produce when we speak out loud? Listening to a recording of your own voice activates the brain more than hearing yourself speak out loud. This is because when the brain sends instructions to the lips, tongue, and vocal cords telling them to move, it also makes a copy of these instructions. This is known as an efference copy, and it enables regions of the brain that process sounds to predict what they are about to hear. When the actual sounds match those predicted – as when you hear yourself speak out loud – the brain’s sound-processing regions dampen down their responses. But does the inner speech in our heads also generate an efference copy? To find out, Whitford et al. tracked the brain activity of healthy volunteers as they listened to speech sounds through headphones. While listening to the sounds, the volunteers had to produce either the same speech sound or a different speech sound inside their heads. A specific type of brain activity decreased whenever the inner speech sound matched the external speech sound. This decrease did not occur when the two sounds were different. This suggests that the brain produces an efference copy for inner speech similar to that for external speech. These findings could ultimately benefit people who suffer from psychotic symptoms, for example as part of schizophrenia. Symptoms such as hearing voices are thought to reflect problems with producing and interpreting inner speech. The technique that Whitford et al. have developed will enable us to test this long-held but hitherto untestable idea. The results should increase our understanding of these symptoms and may eventually lead to new treatments.

Abstract The motor system in its manifold articulations is receiving increasing clinical and research attention. This is because motor impairments constitute a central, expressive component of the mental state examination and a key transdiagnostic feature indexing disease severity. Furthermore, within the schizophrenia spectrum, the integration of neurophysiological, developmental, and phenomenological perspectives suggests that motor impairment is not simply a generic, extrinsic proxy of an altered neurodevelopment, but might be more intimately related to psychotic risk. Therefore, an increased understanding, conceptualization, and knowledge of such motor system and its anomalies could empower contemporary risk prediction and diagnostic procedures.

It is essential to keep track of the movements we make, and one way to do that is to monitor correlates, or corollary discharges, of neuronal movement commands. We hypothesized that a previously identified pathway from brainstem to frontal cortex might carry corollary discharge signals. We found that neuronal activity in this pathway encodes upcoming eye movements and that inactivating the pathway impairs sequential eye movements consistent with loss of corollary discharge without affecting single eye movements. These results identify a pathway in the brain of the primate Macaca mulatta that conveys corollary discharge signals.