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Bruxism is a complex orofacial behavior that can occur during sleep or wakefulness, characterized by the involuntary grinding or clenching of teeth, involving repetitive activity of the jaw muscles. Its etiology is multifactorial, influenced by genetic, psychological, physiological, and lifestyle factors. While the mild bruxism may not necessitate treatment, severe bruxism can lead to significant consequences, including tooth damage, jaw pain, fatigue, and headaches. The bruxism has been associated with medical conditions, such as stress, anxiety, sleep disorders, and various neurological disorders; however, the exact pathophysiology remains elusive. Although the central nervous system is strongly implicated in the development of bruxism, specific neural substrates have not yet been conclusively established. Furthermore, there is evidence to suggest that individuals with bruxism may exhibit neural plasticity, resulting in the establishment of distinct neural circuitry that control the jaw movements. The application of various neurophysiological techniques in both clinical and pre-clinical studies provides valuable insights into the neural mechanisms underlying bruxism. This review aims to comprehensively examine the current literature on the neural pathways involved in bruxism, with the goal of improving the clinical approach and therapeutics for this condition. A deeper understanding of the neural circuitry controlling bruxism holds the potential to advance future treatment approaches and improve the management of patients with bruxism. [ABSTRACT FROM AUTHOR]

Bruxism is a complex orofacial behavior that can occur during sleep or wakefulness, characterized by the involuntary grinding or clenching of teeth, involving repetitive activity of the jaw muscles. Its etiology is multifactorial, influenced by genetic, psychological, physiological, and lifestyle factors. While the mild bruxism may not necessitate treatment, severe bruxism can lead to significant consequences, including tooth damage, jaw pain, fatigue, and headaches. The bruxism has been associated with medical conditions, such as stress, anxiety, sleep disorders, and various neurological disorders; however, the exact pathophysiology remains elusive. Although the central nervous system is strongly implicated in the development of bruxism, specific neural substrates have not yet been conclusively established. Furthermore, there is evidence to suggest that individuals with bruxism may exhibit neural plasticity, resulting in the establishment of distinct neural circuitry that control the jaw movements. The application of various neurophysiological techniques in both clinical and pre-clinical studies provides valuable insights into the neural mechanisms underlying bruxism. This review aims to comprehensively examine the current literature on the neural pathways involved in bruxism, with the goal of improving the clinical approach and therapeutics for this condition. A deeper understanding of the neural circuitry controlling bruxism holds the potential to advance future treatment approaches and improve the management of patients with bruxism. [ABSTRACT FROM AUTHOR]

Bruxism is a complex orofacial behavior that can occur during sleep or wakefulness, characterized by the involuntary grinding or clenching of teeth, involving repetitive activity of the jaw muscles. Its etiology is multifactorial, influenced by genetic, psychological, physiological, and lifestyle factors. While the mild bruxism may not necessitate treatment, severe bruxism can lead to significant consequences, including tooth damage, jaw pain, fatigue, and headaches. The bruxism has been associated with medical conditions, such as stress, anxiety, sleep disorders, and various neurological disorders; however, the exact pathophysiology remains elusive. Although the central nervous system is strongly implicated in the development of bruxism, specific neural substrates have not yet been conclusively established. Furthermore, there is evidence to suggest that individuals with bruxism may exhibit neural plasticity, resulting in the establishment of distinct neural circuitry that control the jaw movements. The application of various neurophysiological techniques in both clinical and pre-clinical studies provides valuable insights into the neural mechanisms underlying bruxism. This review aims to comprehensively examine the current literature on the neural pathways involved in bruxism, with the goal of improving the clinical approach and therapeutics for this condition. A deeper understanding of the neural circuitry controlling bruxism holds the potential to advance future treatment approaches and improve the management of patients with bruxism.

The cortex contains multiple motor areas, including the primary motor cortex (M1) and supplementary motor area (SMA). Many muscles are represented in both the M1 and SMA, but the reason for this dual representation remains unclear. Previous work has shown that the M1 and SMA representations of a specific human muscle can be differentiated according to their functional connectivity with different brain areas located outside of the motor cortex. It is our perspective that this differential functional connectivity may be the neural substrate that allows an individual muscle to be accessed by distinct neural processes, such as those implementing volitional vs. postural task control. Here, we review existing human and animal literature suggesting how muscles are represented in the M1 and SMA and how these brain regions have distinct functions. We also discuss potential studies to further elucidate the distinct roles of the SMA and M1 in normal and dysfunctional motor control. [ABSTRACT FROM AUTHOR]

This integrative review rearticulates the notion of human aesthetics by critically appraising the conventional definitions, offerring a new, more comprehensive definition, and identifying the fundamental components associated with it. It intends to advance holistic understanding of the notion by differentiating aesthetic perception from basic perceptual recognition, and by characterizing these concepts from the perspective of information processing in both visual and nonvisual modalities. To this end, we analyze the dissociative nature of information processing in the brain, introducing a novel local-global integrative model that differentiates aesthetic processing from basic perceptual processing. This model builds on the current state of the art in visual aesthetics as well as newer propositions about nonvisual aesthetics. This model comprises two analytic channels: aesthetics-only channel and perception-to-aesthetics channel. The aesthetics-only channel primarily involves restricted local processing for quality or richness (e.g., attractiveness, beauty/prettiness, elegance, sublimeness, catchiness, hedonic value) analysis, whereas the perception-to-aesthetics channel involves global/extended local processing for basic feature analysis, followed by restricted local processing for quality or richness analysis. We contend that aesthetic processing operates independently of basic perceptual processing, but not independently of cognitive processing. We further conjecture that there might be a common faculty, labeled as aesthetic cognition faculty, in the human brain for all sensory aesthetics albeit other parts of the brain can also be activated because of basic sensory processing prior to aesthetic processing, particularly during the operation of the second channel. This generalized model can account not only for simple and pure aesthetic experiences but for partial and complex aesthetic experiences as well. [ABSTRACT FROM AUTHOR]

Assigning behavioral functions to neural structures has long been a central goal in neuroscience and is a necessary first step toward a circuit-level understanding of how the brain generates behavior. Here, we map the neural substrates of locomotion and social behaviors for Drosophila melanogaster using automated machine-vision and machine-learning techniques. From videos of 400,000 flies, we quantified the behavioral effects of activating 2,204 genetically targeted populations of neurons. We combined a novel quantification of anatomy with our behavioral analysis to create brain-behavior correlation maps, which are shared as browsable web pages and interactive software. Based on these maps, we generated hypotheses of regions of the brain causally related to sensory processing, locomotor control, courtship, aggression, and sleep. Our maps directly specify genetic tools to target these regions, which we used to identify a small population of neurons with a role in the control of walking.

Resilience to stressful life events has received considerable attention in both clinical and preclinical studies. A number of neural substrates have been identified as putatively mediating resilience to stress. However, there remains considerable diversity in how resilience is defined and studied. This article aims to examine how resilience is defined and conceptualized in social psychology, public health, and related fields, to better inform the understanding of stress resilience in the neurobiological context, and to differentiate resilience from other patterns of response to stressful experiences. An understanding of resilience through the lens of clinical and applied sciences is likely to lead to the identification of more robust and reproducible neural substrates, though many challenges remain. Resilience to stress is characterized by an initial response to a stressful stimulus but a relative recovery towards baseline. It is, therefore, both a process that occurs over time and an outcome. It is important to differentiate resilience from resistance or from other response patterns because different neural substrates are likely to mediate these different response patterns. A focus on the trajectory of an individual's response to stress is required to identify neural substrates that can be engaged to promote resilience. Numerous putative neural substrates underlying resilience to stress have been identified, reflecting the complexity of the mammalian lifespan and environment. To translate preclinical findings into meaningful clinical advances, efforts should focus on how divergent neural substrates of resilience work together to drive a trajectory of resilience. [ABSTRACT FROM AUTHOR]

This paper aims to discuss old and contemporary perspectives in understanding language acquisition taking into account the neural theory of language. Discussing a recent theory by Kuhl (2010), neural substrates of first language learning will be put forward (Berwick et al., 2013). Neural substrates of phonetic learning, word learning, sentence processing, and syntax development are separately discussed. As a novel window to look into language learning in a greater detail, second language learning in relation to the theories of language acquisition is further discussed. Second language learning and dual vs. single coding structure relating to language acquisition are discussed in relation to the theories that have previously been explained. Finally, a discussion of contemporary issues in understanding both first and second language acquisition in relation to bilingualism is presented. In sum, investigating language acquisition requires a multi-disciplinary approach taking psychology, linguistics, and cognitive neuroscience of language into account is necessary. [ABSTRACT FROM AUTHOR]

Selective attention, the ability to filter relevant from a sea of sensory information, relies on the prioritization of goal-relevant information (target facilitation) and the suppression of goal-irrelevant information (distractor suppression). Although several lines of evidence have shown that target facilitation and distractor suppression were mediated by distinct mechanisms, the underlying neural substrates remain unclear. To address this question, we acquired structural and resting-state magnetic resonance imaging scans, as well as behavioral data from a modified Posner cueing task. Specifically, the location of a target (Target Cue, TC) and a distractor (Distractor Cue, DC) was either cued in advance to separately trigger target facilitation and distractor suppression, or no predictive information was provided, serving as a baseline. We combined voxel-based morphometry (VBM) and resting-state functional connectivity (rsFC) analyses to explore the neural correlates of behavioral benefits, yielding the following results. First, behavioral data showed faster responses to TC and DC conditions compared to baseline, the benefits of which were named TC-benefit and DC-benefit. Second, the VBM analysis revealed that the gray matter volume (GMV) in the superior frontal (SFG) and postcentral gyrus inversely correlated with individual TC-benefit, while the GMV in the superior parietal lobe, middle frontal gyrus, and angular gyrus inversely correlated with individual DC-benefit, indicating that target facilitation and distractor suppression was associated with the GMV of distinct and distributed regions in the frontoparietal cortex. Third, the rsFC analysis with the SFG as a seed region further found distinct patterns of rsFC for target facilitation and distractor suppression. Specifically, individual TC-benefit were positively correlated with distributed connections between the SFG and brain regions, mainly within the ventral attention and somato-motor network; but individual DC-benefit were positively correlated with centralized connections between the SFG and brain regions, mainly within the frontoparietal, dorsal attention and ventral attention network. Finally, a multiple linear regression analysis showed that the GMV and rsFC could jointly explain individual differences in TC- and DC-benefit. Taken together, these results provided neural evidence for different structural and functional substrates underlying target facilitation and distractor suppression.

Background: Wilson’s disease manifests as neuro-psychological or psychiatric symptoms along with neurological and liver disease. The present study aimed to probe into the declarative and non-declarative memory profile of Wilson’s disease patients from a neurocognitive perspective. Methods: The study involved a sample of 12 Wilson’s disease patients and 12 matched non-patient individuals who were assessed on Global Assessment Scale for Wilson’s disease, the Edinburgh handedness inventory, memory scales from PGI Battery of Brain Dysfunction, Rey Auditory Verbal Learning Test, and mirror tracing task. Results: The overall result indicated that the Wilson’s disease patient group differed with their non-patient counterparts with respect to immediate memory, recall, recognition, semantic memory, and procedural learning. Conclusion: The neural substrates related to the neuro-psychological symptoms of Wilson’s disease patients are found to be a neural network involving basal ganglia, fronto-striatal circuits, and cerebellar region.

Mirror-induced visual illusion obtained through mirror therapy is widely used to facilitate motor recovery after stroke. Activation of primary motor cortex (M1) ipsilateral to the moving limb has been reported during mirror-induced visual illusion. However, the mechanism through which the mirror illusion elicits motor execution processes without movements observed in the mirrored limb remains unclear. This study aims to review evidence based on brain imaging studies for testing the hypothesis that neural processes associated with kinaesthetic motor imagery are attributed to ipsilateral M1 activation. Four electronic databases were searched. Studies on functional brain imaging, investigating the instant effects of mirror-induced visual illusion among stroke survivors and healthy participants were included. Thirty-five studies engaging 78 stroke survivors and 396 healthy participants were reviewed. Results of functional brain scans (n = 20) indicated that half of the studies (n = 10, 50%) reported significant changes in the activation of ipsilateral M1, which mediates motor preparation and execution. Other common neural substrates included primary somatosensory cortex (45%, kinaesthesia), precuneus (40%, image generation and self-processing operations) and cerebellum (20%, motor control). Similar patterns of ipsilateral M1 activations were observed in the two groups. These neural substrates mediated the generation, maintenance, and manipulation of motor-related images, which were the key processes in kinaesthetic motor imagery. Relationships in terms of shared neural substrates and mental processes between mirror-induced visual illusion and kinaesthetic motor imagery generate new evidence on the role of the latter in mirror therapy. Future studies should investigate the imagery processes in illusion training for post-stroke patients. [ABSTRACT FROM AUTHOR]

During the past two decades, the number of animal models of psychiatric disorders has grown exponentially. Of these, genetic animal models that are modeled after rare but highly penetrant mutations hold great promise for deciphering critical molecular, synaptic, and neurocircuitry deficits of major psychiatric disorders, such as schizophrenia. Animal models should aim to focus on core aspects rather than capture the entire human disease. In this context, animal models with strong etiological validity, where behavioral and neurophysiological phenotypes and the features of the disease being modeled are in unambiguous homology, are being used to dissect both elementary and complex cognitive and perceptual processing deficits present in psychiatric disorders at the level of neurocircuitry, shedding new light on critical disease mechanisms. Recent progress in neuroscience along with large-scale initiatives that propose a consistent approach in characterizing these deficits across different laboratories will further enhance the efficacy of these studies that will ultimately lead to identifying new biological targets for drug development. [ABSTRACT FROM AUTHOR]

The effects of epilepsy and its treatments have contributed significantly to language models. The setting of epilepsy surgery, which allows for careful pre- and postsurgical evaluation of patients with cognitive testing and neuroimaging, has produced a wealth of language findings. Moreover, a new wave of surgical interventions, including stereotactic laser ablation and radio frequency ablation, have contributed new insights and corrections to language models as they can make extremely precise, focal lesions. This review covers the common language deficits observed in focal dyscognitive seizure syndromes. It also addresses the effects of surgical interventions on language, and highlights insights gained from unique epilepsy assessment methods (e.g., cortical stimulation mapping, Wada evaluation). Emergent findings are covered including a lack of involvement of the hippocampus in confrontation word retrieval, possible roles for key white matter tracts in language, and the often-overlooked basal temporal language area. The relationship between language and semantic memory networks is also explored, with brief consideration given to the prevailing models of semantic processing, including the amodal Hub and distributed, multi-modal processing models. [ABSTRACT FROM AUTHOR]

Inhibition of action is involved in stopping a movement, as well as terminating unnecessary movement during performance of a behavior. The inhibition of single actions, known as response inhibition (Inhibition of the urge to respond before or after actions) has been widely investigated using the go/no-go task and stop signal task. However, few studies focused on phase and volition-related inhibition after an action has been initiated. Here, we used functional magnetic resonance imaging (fMRI) to investigate the neural correlates of planning and execution underlying the voluntary inhibition of ongoing action. We collected fMRI data while participants performed a continuous finger-tapping task involving voluntary and involuntary (externally directed) inhibition, and during the initiation of movement. The results revealed areas of significantly greater activation during the preparation of inhibition of an ongoing action during voluntary inhibition, compared with involuntary inhibition, in the supplementary (SMA) and pre-supplementary motor areas, dorsolateral prefrontal cortex, inferior frontal gyrus (IFG), inferior parietal lobe, bilateral globus pallidus/putamen, bilateral insula and premotor cortex. Focusing on the period of execution of inhibition of ongoing actions, an event-related fMRI analysis revealed significant activation in the SMA, middle cingulate cortex, bilateral insula, right IFG and inferior parietal cortex. Additional comparative analyses suggested that brain activation while participants were planning to inhibit an ongoing action was similar to that during planning to start an action, indicating that the same neural substrates of motor planning may be recruited even when an action is ongoing. The present finding that brain activation associated with inhibiting ongoing actions was compatible with that seen in response inhibition (urge to stop before/after actions) suggests that common inhibitory mechanisms for motor movement are involved in both actual and planned motor action, which makes our behavior keep going seamlessly.

Apathy is a common non-motor symptom in Parkinson’s disease (PD). We aimed to explore its associated neural substrates changes via amplitude of low-frequency fluctuations (ALFF) and granger causality analysis (GCA). Resting-state functional magnetic resonance imaging (rs-fMRI) scans were performed in 20 PD patients with apathy (PD-A), 22 PD patients without apathy (PD-NA) and 19 healthy volunteers. GCA, a new method exploring direction from one brain region to another, was based on brain regions showing alterations of neural activity as seeds, which were examined utilizing ALFF approach. The relationships between ALFF or GCA and apathetic symptoms were also assessed. Relative to PD-NA group, PD-A group indicated decreased ALFF in left orbital middle frontal gyrus and bilateral superior frontal gyrus (SFG). Only ALFF values in right SFG were negatively correlated with Apathy Scale (AS) scores. Then GCA with the seed of right SFG showed a positive feedback from right thalamus to ipsilateral SFG, which was positively correlated with AS scores. In conclusion, dysfunction in SFG and a positive feedback from thalamus to ipsilateral SFG contributed to presence of PD-related apathy, providing a new perspective for future studies on apathy in PD. [ABSTRACT FROM AUTHOR]

Procrastination is a pervasive phenomenon across different cultures and brings about lots of serious consequences, including performance, subjective well-being, and even public policy. However, little is known about the neural substrates of procrastination. In order to shed light upon this question, we investigated the neuroanatomical substrates of procrastination across two independent samples using voxel-based morphometry (VBM) method. The whole-brain analysis showed procrastination was positively correlated with the graymatter (GM) volume of clusters in the parahippocampal gyrus (PHG) and the orbital frontal cortex (OFC), while negatively correlated with the GM volume of clusters in the inferior frontal gyrus (IFG) and the middle frontal gyrus (MFG) in sample one (151 participants). We further conducted a verification procedure on another sample (108 participants) using region-of-interest analysis to examine the reliability of these results. Results showed procrastination can be predicted by the GM volume of the OFC and the MFG. The present findings suggest that the MFG and OFC, which are the key regions of self-control and emotion regulation, may play an important role in procrastination. [ABSTRACT FROM AUTHOR]

Post-stroke depression affects about 30% of stroke patients and often hampers functional recovery. The diagnosis of depression encompasses heterogeneous symptoms at emotional, motivational, cognitive, behavioural or somatic levels. Evidence indicates that depression is caused by disruption of bio-aminergic fibre tracts between prefrontal and limbic or striatal brain regions comprising different functional networks. Voxel-based lesion-symptom mapping studies reported discrepant findings regarding the association between infarct locations and depression. Inconsistencies may be due to the usage of sum scores, thereby mixing different symptoms of depression. In this cross-sectional study, we used multivariate support vector regression for lesion-symptom mapping to identify regions significantly involved in distinct depressive symptom domains and global depression. MRI lesion data were included from 200 patients with acute first-ever ischaemic stroke (mean 0.9 ± 1.5 days of post-stroke). The Montgomery-Åsberg Depression Rating interview assessed depression severity in five symptom domains encompassing motivational, emotional and cognitive symptoms deficits, anxiety and somatic symptoms and was examined 8.4 days of post-stroke (±4.3). We found that global depression severity, irrespective of individual symptom domains, was primarily linked to right hemispheric lesions in the dorsolateral prefrontal cortex and inferior frontal gyrus. In contrast, when considering distinct symptom domains individually, the analyses yielded much more sensitive results in regions where the correlations with the global depression score yielded no effects. Accordingly, motivational deficits were associated with lesions in orbitofrontal cortex, dorsolateral prefrontal cortex, pre- and post-central gyri and basal ganglia, including putamen and pallidum. Lesions affecting the dorsal thalamus, anterior insula and somatosensory cortex were significantly associated with emotional symptoms such as sadness. Damage to the dorsolateral prefrontal cortex was associated with concentration deficits, cognitive symptoms of guilt and self-reproach. Furthermore, somatic symptoms, including loss of appetite and sleep disturbances, were linked to the insula, parietal operculum and amygdala lesions. Likewise, anxiety was associated with lesions impacting the central operculum, insula and inferior frontal gyrus. Interestingly, symptoms of anxiety were exclusively left hemispheric, whereas the lesion-symptom associations of the other domains were lateralized to the right hemisphere. In conclusion, this large-scale study shows that in acute stroke patients, differential post-stroke depression symptom domains are associated with specific structural correlates. Our findings extend existing concepts on the neural underpinnings of depressive symptoms, indicating that differential lesion patterns lead to distinct depressive symptoms in the first weeks of post-stroke. These findings may facilitate the development of personalized treatments to improve post-stroke rehabilitation., Competing Interests: The authors report no competing interests., (© The Author(s) 2023. Published by Oxford University Press on behalf of the Guarantors of Brain.)

Introduction: In this systematic review, we aimed to evaluate the role of alexithymia in Parkinson's disease (PD) and its relationship to neurological, neuropsychiatric, cognitive, and neuroimaging correlates.Methods: The database was selected using PubMed Services, Cochrane, PsycNET and Scopus and a number of key words. Further studies were sought by manually searching for secondary sources, including relevant journals and references in primary articles. The search was restricted to articles written in English between January 1980 and August 2015.Results: Ten studies reported that alexithymia prevalence was about double in PD patients compared to control subjects and that specific dimensions of alexithymia might be related to depression, anxiety, apathy and impulsivity. Some studies investigated the relationship between alexithymia and neuropsychological symptoms and found correlations with frontal and parietal lobe functions. Two studies on neurological features reported a link between alexithymia and disease stage or a specific motor subtype of PD; the remaining studies found that alexithymia was independent from neurological symptoms, dopaminergic therapy and laterality of motor symptom onset. Data on neuroimaging correlates and therapeutic intervention on alexithymia in PD patients are still lacking.Conclusion: Although results suggest that alexithymia is a primary characteristics of PD, further studies with larger patient samples are needed to definitively clarify the impact of alexithymia on the clinical features of PD patients. [ABSTRACT FROM AUTHOR]

In this commentary, I critically assess Rex Welshon’s position on the neural substrates of ownership unity. First, I comment on Welshon’s definition of ownership unity and underline some of the problems stemming from his phenomenological analysis. Second, I analyze Welshon’s proposal to establish a mechanistic relation between neural substrates and ownership unity. I show that it is insufficient and defend my own position on how neural mechanisms may give rise to whole subjects of experience, which I call the neuro-integrative account of consciousness. Lastly, I comment on Welshon’s (2013) philosophical contribution and claim that it leaves the reader theoretically stranded. [ABSTRACT FROM AUTHOR]

Infants born prematurely are at risk for cardiovascular events causing hypoxia-ischemia (HI; reduced blood and oxygen to the brain). HI in turn can cause neuropathology, though patterns of damage are sometimes diffuse and often highly variable (with clinical heterogeneity further magnified by rapid development). As a result, though HI injury is associated with long-term behavioral and cognitive impairments in general, pathology indices for specific infants can provide only limited insight into individual prognosis. The current paper addresses this important clinical issue using a rat model that simulates unilateral HI in a late preterm infant coupled with long-term behavioral evaluation in two processing domains - auditory discrimination and spatial learning/memory. We examined the following: (1) whether deficits on one task would predict deficits on the other (suggesting that subjects with more severe injury perform worse across all cognitive domains) or (2) whether domain-specific outcomes among HI-injured subjects would be uncorrelated (suggesting differential damage to orthogonal neural systems). All animals (sham and HI) received initial auditory testing and were assigned to additional auditory testing (group A) or spatial maze testing (group B). This allowed within-task (group A) and between-task (group B) correlation. Anatomic measures of cortical, hippocampal and ventricular volume (indexing HI damage) were also obtained and correlated against behavioral measures. Results showed that auditory discrimination in the juvenile period was not correlated with spatial working memory in adulthood (group B) in either sham or HI rats. Conversely, early auditory processing performance for group A HI animals significantly predicted auditory deficits in adulthood (p = 0.05; no correlation in shams). Anatomic data also revealed significant relationships between the volumes of different brain areas within both HI and shams, but anatomic measures did not correlate with any behavioral measure in the HI group (though we saw a hippocampal/spatial correlation in shams, in the expected direction). Overall, current data provide an impetus to enhance tools for characterizing individual HI-related pathology in neonates, which could provide more accurate individual prognoses within specific cognitive/behavioral domains and thus improved patient-specific early interventions. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The duration and quality of human performance depend on both intrinsic motivation and external incentives. However, little is known about the neuroscientific basis of this interplay between internal and external motivators. Here, we used functional magnetic resonance imaging to examine the neural substrates of intrinsic motivation, operationalized as the free-choice time spent on a task when this was not required, and tested the neural and behavioral effects of external reward on intrinsic motivation. We found that increased duration of free-choice time was predicted by generally diminished neural responses in regions associated with cognitive and affective regulation. By comparison, the possibility of additional reward improved task accuracy, and specifically increased neural and behavioral responses following errors. Those individuals with the smallest neural responses associated with intrinsic motivation exhibited the greatest error-related neural enhancement under the external contingency of possible reward. Together, these data suggest that human performance is guided by a 'tonic' and 'phasic' relationship between the neural substrates of intrinsic motivation (tonic) and the impact of external incentives (phasic). [ABSTRACT FROM AUTHOR]

The Coronavirus disease of 2019 (COVID-19) and measures to curb it created population-level changes in male-dominant impulsive and risky behaviors such as violent crimes and gambling. One possible explanation for this is that the pandemic has been stressful, and males, more so than females, tend to respond to stress by altering their focus on immediate versus delayed rewards, as reflected in their delay discounting rates. Delay discounting rates from healthy undergraduate students were collected twice during the pandemic. Discounting rates of males (n=190) but not of females (n=493) increased during the pandemic. Using machine learning, we show that prepandemic functional connectome predict increased discounting rates in males (n=88). Moreover, considering that delay discounting is associated with multiple psychiatric disorders, we found the same neural pattern that predicted increased discounting rates in this study, in secondary datasets of patients with major depression and schizophrenia. The findings point to sex-based differences in maladaptive delay discounting under real-world stress events, and to connectome-based neuromarkers of such effects. They can explain why there was a population-level increase in several impulsive and risky behaviors during the pandemic and point to intriguing questions about the shared underlying mechanisms of stress responses, psychiatric disorders and delay discounting., (© The Author(s) 2022. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Female mate choice is a dynamic process that allows individuals to selectively mate with those of the opposite sex that display a preferred set of traits. Because in many species males compete with each other for fertilization opportunities, female mate choice can be a powerful agent of sexual selection, often resulting in highly conspicuous traits in males. Although the evolutionary causes and consequences of the ornamentation and behaviors displayed by males to attract mates have been well studied, embarrassingly little is known about the proximate neural mechanisms through which female choice occurs. In vertebrates, female mate choice is inherently a social behavior, and although much remains to be discovered about this process, recent evidence suggests the neural substrates and circuits underlying other fundamental social behaviors (such as pair bonding, aggression and parental care) are likely similarly recruited during mate choice. Notably, female mate choice is not static, as social and ecological environments can shape the brain and, consequently, behavior in specific ways. In this Review, we discuss how social and/or ecological influences mediate female choice and how this occurs within the brain. We then discuss our current understanding of the neural substrates underlying female mate choice, with a specific focus on those that also play a role in regulating other social behaviors. Finally, we propose several promising avenues for future research by highlighting novel model systems and new methodological approaches, which together will transform our understanding of the causes and consequences of female mate choice., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2020. Published by The Company of Biologists Ltd.)

• The Cg1, IL, PrL, BLA, NAc, and DG probably mediated the paradoxical effect—reward and aversion. • Rewarding and aversive neural substrates involve in methamphetamine's conditioned suppression. • Our data conflict the reward comparison but support the paradoxical effect hypothesis of abused drugs. • The findings provide some clinical insights for drug addiction. Clinical studies of drug addiction focus on the reward impact of abused drugs that produces compulsive drug-seeking behavior and drug dependence. However, a small amount of research has examined the opposite effect of aversion to abused drugs to balance the reward effect for drug taking. An aversive behavioral model of abused drugs in terms of conditioned taste aversion (CTA) was challenged by the reward comparison hypothesis (Grigson, 1997). To test the reward comparison hypothesis, the present study examined the rewarding or aversive neural substrates involved in methamphetamine-induced conditioned suppression. The behavioral data showed that methamphetamine induced conditioned suppression on conditioning and reacquisition but extinguished it on extinction. A higher level of stressful aversive corticosterone occurred on conditioning and reacquisition but not extinction. The c-Fos or p-ERK immunohistochemical activity showed that the cingulated cortex area 1 (Cg1), infralimbic cortex (IL), prelimbic cortex (PrL), basolateral amygdala (BLA), nucleus accumbens (NAc), and dentate gyrus (DG) of the hippocampus were overexpressed in aversive CTA induced by methamphetamine. These data may indicate that the Cg1, IL, PrL, BLA, NAc, and DG probably mediated the paradoxical effect—reward and aversion. Altogether, our data conflicted with the reward comparison hypothesis, and methamphetamine may simultaneously induce the paradoxical effect of reward and aversion in the brain to support the paradoxical effect hypothesis of abused drugs. The present data implicate some insights for drug addiction in clinical aspects. [ABSTRACT FROM AUTHOR]

Summary Animals use sensory information to move toward more favorable conditions. Drosophila larvae can move up or down gradients of odors (chemotax), light (phototax), and temperature (thermotax) by modulating the probability, direction, and size of turns based on sensory input. Whether larvae can anemotax in gradients of mechanosensory cues is unknown. Further, although many of the sensory neurons that mediate taxis have been described, the central circuits are not well understood. Here, we used high-throughput, quantitative behavioral assays to demonstrate Drosophila larvae anemotax in gradients of wind speeds and to characterize the behavioral strategies involved. We found that larvae modulate the probability, direction, and size of turns to move away from higher wind speeds. This suggests that similar central decision-making mechanisms underlie taxis in somatosensory and other sensory modalities. By silencing the activity of single or very few neuron types in a behavioral screen, we found two sensory (chordotonal and multidendritic class III) and six nerve cord neuron types involved in anemotaxis. We reconstructed the identified neurons in an electron microscopy volume that spans the entire larval nervous system and found they received direct input from the mechanosensory neurons or from each other. In this way, we identified local interneurons and first- and second-order subesophageal zone (SEZ) and brain projection neurons. Finally, silencing a dopaminergic brain neuron type impairs anemotaxis. These findings suggest that anemotaxis involves both nerve cord and brain circuits. The candidate neurons and circuitry identified in our study provide a basis for future detailed mechanistic understanding of the circuit principles of anemotaxis. Graphical Abstract Highlights • Drosophila larvae perform negative anemotaxis • To anemotax, larvae modulate the turn rate, size, and direction as in other taxis • Chordotonal and multidendritic class III sensory neurons together mediate anemotaxis • The anemotactic circuitry involves both the nerve cord and the brain Jovanic et al. use high-throughput quantitative behavioral analysis, manipulation of neuronal activity, and EM reconstruction of neuronal connectivity to characterize Drosophila larva anemotactic behavior and identify two types of sensory neurons, six nerve cord neurons, and a brain dopaminergic neuron cluster all implicated in anemotaxis. [ABSTRACT FROM AUTHOR]

Summary Sparse manipulation of neuron excitability during free behavior is critical for identifying neural substrates of behavior. Genetic tools for precise neuronal manipulation exist in the fruit fly, Drosophila melanogaster , but behavioral tools are still lacking to identify potentially subtle phenotypes only detectible using high-throughput and high spatiotemporal resolution. We developed three assay components that can be used modularly to study natural and optogenetically induced behaviors. FlyGate automatically releases flies one at a time into an assay. FlyDetect tracks flies in real time, is robust to severe occlusions, and can be used to track appendages, such as the head. GlobeDisplay is a spherical projection system covering the fly's visual receptive field with a single projector. We demonstrate the utility of these components in an integrated system, FlyPEZ, by comprehensively modeling the input-output function for directional looming-evoked escape takeoffs and describing a millisecond-timescale phenotype from genetic silencing of a single visual projection neuron type. Graphical Abstract Highlights • FlyGate automatically releases flies one at a time into an assay • FlyDetect tracks flies in real time and is robust to severe occlusions • GlobeDisplay is a panoramic spherical projection system that uses a single projector • FlyPEZ uses these tools to quantify natural and optogenetically induced behavior Williamson et al. developed a high-throughput device to automatically isolate individual flies and record their behavior with high-speed video. They demonstrate the system's utility for studying the Drosophila brain using modern genetic tools by discovering behavioral phenotypes that result from manipulation of small groups of neurons. [ABSTRACT FROM AUTHOR]

Scope: Caffeine is one of the most frequently used psychoactive substances ingested mainly via beverage or food products. Major depressive disorder is a serious and devastating psychiatric disorder. Emerging evidence indicates that caffeine enhances the antidepressant-like activity of common antidepressant drugs in rodents. However, whether joint administration of low dose of caffeine enhances the antidepressant actions in depressed patients remains unclear., Methods and Results: A total of 95 male inpatients were assigned to three groups and were asked to take either caffeine (60, 120 mg) or placebo (soymilk powder) daily for 4 wk on the basis of their current antidepressant medications. Results showed that chronic supplementation with low dose of caffeine (60 mg) produced rapid antidepressant action by reduction of depressive scores. Furthermore, low dose of caffeine improved cognitive performance in depressed patients. However, caffeine did not affect sleep as measured by overnight polysomnography. Moreover, chronic caffeine consumption elicited inhibition of hypothalamic-pituitary-adrenal axis activation by normalization of salivary cortisol induced by Trier social stress test., Conclusions: These findings indicated the potential benefits of further implications of supplementary administration of caffeine to reverse the development of depression and enhance the outcome of antidepressants treatment in major depressive disorder., (© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)