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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]

A range of emotional and motivation impairments have long been clinically documented in people with schizophrenia, and there has been a resurgence of interest in understanding the psychological and neural mechanisms of the so-called "negative symptoms" in schizophrenia, given their lack of treatment responsiveness and their role in constraining function and life satisfaction in this illness. Negative symptoms comprise two domains, with the first covering diminished motivation and pleasure across a range of life domains and the second covering diminished verbal and non-verbal expression and communicative output. In this review, we focus on four aspects of the motivation/pleasure domain, providing a brief review of the behavioral and neural underpinnings of this domain. First, we cover liking or in-the-moment pleasure: immediate responses to pleasurable stimuli. Second, we cover anticipatory pleasure or wanting, which involves prediction of a forthcoming enjoyable outcome (reward) and feeling pleasure in anticipation of that outcome. Third, we address motivation, which comprises effort computation, which involves figuring out how much effort is needed to achieve a desired outcome, planning, and behavioral response. Finally, we cover the maintenance emotional states and behavioral responses. Throughout, we consider the behavioral manifestations and brain representations of these four aspects of motivation/pleasure deficits in schizophrenia. We conclude with directions for future research as well as implications for treatment.

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]

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]

An argument is developed for the conclusion that certain neurological conditions and disorders are directly relevant for understanding the self 's embodiment and the ownership of conscious experience enjoyed by such an embodied self. Since these neurological conditions and disorders provide evidence that there can be shifts of, and compromises to, ownership, they help identify neural substrates and realizers of such ownership. However, even if recent neuroimaging and neuropsychological nominees for neural substrates of ownership unity are core realizers of ownership, they are not its total realizers. Implications of the distinction between core and total realizers are discussed. [ABSTRACT FROM PUBLISHER]

Abstract: The rabbit nictitating membrane (NM) preparation was developed in 1962 by Gormezano as a model system for classical conditioning. It had many features that made it ideal for use in exploring the laws of this conditioning paradigm, including easily obtainable subjects, good control of stimulus delivery and precise response specifications. Most importantly, the preparation evidenced very low spontaneous response rates and showed no evidence of nonassociative effects of sensitization and pseudoconditioning and had highly predictable learning functions. In contrast, previous human and animal models that had been utilized to explore the features of classical conditioning, such as the dog salivary model were far less easy to use, showed high spontaneous response rates, and had high nonassociative components. Over the ensuing years, Gormezano and his students characterized most of the parametric characteristics of classical conditioning with the use of the preparation. In 1970, Richard Thompson began exploring the use of the rabbit NM preparation in his laboratory as a model system with which to explore the brain substrates of classical conditioning. At the time, his work was centered around exploring the neural substrates of sensitization and habituation in spinal reflexes. Soon, however, he turned his attention to the brain substrates of classical conditioning almost exclusively, and produced an impressive amount of data detailing the neural underpinnings of classical conditioning. His work has generated perhaps the most detailed and complete picture of the neural mechanisms of learning currently available, and has led to countless other research efforts in the area of brain and behavior. Current understandings of neural mechanisms of associative learning owe much to Thompson and his various colleagues. [Copyright &y& Elsevier]

Adolescence reflects a period of increased rates of anxiety, depression, and suicide. Yet most teens emerge from this period with a healthy, positive outcome. In this article, we identify biological factors that may increase risk for some individuals during this developmental period by: (1) examining changes in neural circuitry underlying core phenotypic features of anxiety as healthy individuals transition into and out of adolescence; (2) examining genetic factors that may enhance the risk for psychopathology in one individual over another using translation from mouse models to human neuroimaging and behavior; and (3) examining the effects of early experiences on core phenotypic features of anxiety using human neuroimaging and behavioral approaches. Each of these approaches alone provides only limited information on genetic and environmental influences on complex human behavior across development. Together, they reflect an emerging field of translational developmental neuroscience in forming important bridges between animal models of neurodevelopmental and neuropsychiatric disorders. Depression and Anxiety, 2011. © 2011 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

A central part of the brain's limbic system, the amygdala is crucial for emotional learning, aversive conditioning, and response to fear and other emotions. Although the amygdala is a vibrant area of study in the neurosciences, it is virtually ignored in criminology. Here, we review the anatomical location, connectivity, and functions of the amygdala, explore its role in James Blair and colleagues' recently advanced theory of psychopathy, explicate amygdala abnormalities in diverse populations, and explore genetics research relating to amygdala functioning. Because of its role in the regulation of fear and other emotional memory and response, the amygdala is importantly related to psychopathy; callous-unemotional traits; and the vibrant, neuroscience-based investigations of the etiology of antisocial behavior. [ABSTRACT FROM AUTHOR]

Abstract: Although the brainstem plays an important role in breathing–swallowing coordination (BSC), the role of suprabulbar structures is ill defined. Given the known decrease in global cerebral activity during sleep, the sleep–wake paradigm was used to elucidate suprabulbar influences. Non-nutritive BSC of 10 healthy human infants was monitored longitudinally during wakefulness and sleep from birth to 1 year of age. Time-locked recordings of submental muscle activity, nasal airflow, and thyroid acoustics enabled the categorization of swallows depending on the preceding and following respiratory phase. In contrast to the change in the overall pattern of BSC with age, and despite well-known marked postnatal cortical development over this time, no arousal-related differences were seen during the first year of life. This most likely reflects complete brainstem control of non-nutritive BSC in infants. [Copyright &y& Elsevier]

Abstract: A single session of footshocks in rats causes long-lasting sensitisation of behavioural, hormonal and autonomic responses to subsequent novel stressful challenges as well as altered pain sensitivity. These changes mimic aspects of post-traumatic stress disorder in humans. Our aim was to identify neuropeptide substrates in the central nervous system involved in stress sensitisation. Male Wistar rats were exposed to ten footshocks in 15 min (preshocked) or placed in the same cage without shocks (control). Two weeks later, rats were placed in a novel cage, subjected to 5 min of 85 dB noise, and returned to their home cage. Rats were killed either before or 1 h after noise and their brains processed for in situ hybridization for neuropeptide Y (NPY) and beta-preprotachykinin-I (PPT) mRNA. Additional groups of rats were killed under basal conditions and brains processed for NPY and neurokinin receptor binding with radiolabelled ligands. Two weeks after footshock treatment NPY mRNA expression was increased in the basolateral amygdala and showed preshock×noise interaction in the locus coeruleus (down after noise in controls, lower basal and unchanged after noise in preshocked). PPT expression in the lateral parabrachial nucleus also showed preshock×noise interaction (up after noise in controls, higher basal and down after noise in preshocked), and was increased after noise in the periaquaeductal grey. NK1 receptor binding in the agranular insular cortex and arcuate nucleus of the hypothalamus and NK2 receptor binding in the amygdala was lower in preshocked rats than in controls. Altered expression of NPY in the basolateral amygdala and locus coeruleus could contribute to or compensate for behavioural and autonomic sensitisation in preshocked rats. Altered PPT expression in the parabrachial nucleus may be involved in the altered pain processing seen in this model. Lower NK1 and NK2 receptor numbers in cortex, hypothalamus and amygdala may reflect secondary adaptations to altered neuropeptide release. These long-term changes in brain neuropeptide systems could offer novel leads for pharmacological modulation of long-term stress-induced sensitisation. [Copyright &y& Elsevier]

This study was designed to examine the correlations between resting-state brain glucose metabolism (CMRglc), as measured with Positron Emission Tomography and performance on executive function tasks in Alzheimer's disease (AD), while taking into account the severity of cognitive deterioration. We addressed this issue in 50 AD patients, classified as very mild (n = 22) and mild (n = 28) AD on the basis of an extensive neuropsychological battery. Thirteen healthy subjects were selected as controls for the neuropsychological measures. Statistical Parametric Mapping (SPM) was used to examine voxel-wise correlations between CMRglc and scores on selected cognitive tests of executive functions: the Stroop Test, the Trail Making Test, the Dual Task and the Phonemic Fluency, while correcting for age and global CMRglc. All analyses were done separately for the two AD subgroups. The very mild AD patients showed significant associations between Stroop and Trail Making Test scores and prefrontal regions metabolism, whereas the mild AD patients exhibited more widely distributed cognitive–metabolic correlations extending to the posterior brain regions. These data suggest that a large cortical network is implicated in executive dysfunction in AD, and that the pattern of cognitive–metabolic correlations varies according to disease severity. [ABSTRACT FROM AUTHOR]

Abstract: Virtual environments have been frequently used for training and skill improvement. However, do real and virtual worlds engage the same brain states in human perceivers? We measured brain activity using functional magnetic resonance imaging (fMRI) while adults watched movie and cartoon clips, simulating real and virtual visual worlds, respectively. Relative to baselines using random static images, the medial prefrontal cortex (MPFC) and the cerebellum were activated only by movie clips of other humans. In contrast, cartoon clips of human and non-human agents activated the superior parietal lobes, while movie clips of animals also activated the superior parietal lobes. Our fMRI findings suggest that the perception of real-world humans is characterised by the involvement of MPFC and the cerebellum, most likely for on-line representation of the mental states of others, whereas the perception of virtual-world agents engages the parietal cortex in attention to actions. [Copyright &y& Elsevier]

Research has shown that individuals with autism and Asperger syndrome are impaired in humor appreciation, although anecdotal and parental reports provide some evidence to the contrary. This paper reviews the cognitive and affective processes involved in humor and recent neurological findings. It examines humor expression and understanding in autism and Asperger syndrome in the context of the main psychological theories (Theory of Mind, Executive Functions, Weak Central Coherence and Laterization models) and associated neural substrates. In the concluding sections, examples of humor displayed by individuals with autism/Asperger syndrome which appear to challenge the above theories are analyzed and areas for further research are suggested. [ABSTRACT FROM AUTHOR]

Humor is a uniquely human quality whose neural substrates remain enigmatic. The present report combined dynamic, real-life content and event-related functional magnetic resonance imaging (fMRI) to dissociate humor detection (“getting the joke”) from humor appreciation (the affective experience of mirth). During scanning, subjects viewed full-length episodes of the television sitcoms Seinfeld or The Simpsons. Brain activity time-locked to humor detection moments revealed increases in left inferior frontal and posterior temporal cortices, whereas brain activity time-locked to moments of humor appreciation revealed increases in bilateral regions of insular cortex and the amygdala. These findings provide evidence that humor depends critically upon extant neural systems important for resolving incongruities (humor detection) and for the expression of affect (humor appreciation). [Copyright &y& Elsevier]

This communication provides an update of our understanding of the neurological bases for the close association between balance control and anxiety. New data suggest that a vestibulo-recipient region of the parabrachial nucleus (PBN) contains cells that respond to body rotation and position relative to gravity. The PBN, with its reciprocal relationships with the extended central amygdaloid nucleus, infralimbic cortex, and hypothalamus, appears to be an important node in a primary network that processes convergent vestibular, somatic, and visceral information processing to mediate avoidance conditioning, anxiety, and conditioned fear responses. Noradrenergic and serotonergic projections to the vestibular nuclei also have parallel connections with anxiety pathways. The coeruleo-vestibular pathway originates in caudal locus coeruleus (LC) and provides regionally specialized noradrenergic input to the vestibular nuclei, which likely mediate effects of alerting and vigilance on the sensitivity of vestibulo-motor circuits. Both serotonergic and nonserotonergic pathways from the dorsal raphe nucleus and the nucleus raphe obscurus also project differentially to the vestibular nuclei, and 5-HT2A receptors are expressed in amygdaloid and cortical targets of the PBN. It is proposed that the dorsal raphe nucleus pathway contributes to both (a) a tradeoff between motor and sensory (information gathering) aspects of responses to self-motion and (b) a calibration of the sensitivity of affective responses to aversive aspects of motion. This updated neurologic model continues to be a synthetic schema for investigating the neurological and neurochemical bases for comorbidity of balance disorders and anxiety disorders. [Copyright &y& Elsevier]

Attention is a complex process whose disturbance is considered a core deficit in a number of disorders [e.g., Attention Deficit Hyperactivity Disorder (ADHD), schizophrenia]. In 1956, Rosvold and colleagues [J. Consult. Psychol. 20 (1956) 343.] demonstrated that the continuous performance test (CPT) as a measure of sustained attention was highly sensitive to brain damage or dysfunction. These findings have been replicated with various populations and with various versions of the CPT. The CPT is now cited as the most frequently used measure of attention in both practice and research. Across studies, results are consistent with models of sustained attention that involve the interaction of cortical (frontal, temporal, parietal), subcortical (limbic, basal ganglia), and functional systems including the pathways between the basal ganglia, thalamus, and frontal lobes. Right hemisphere involvement (asymmetric response) is also evident across multiple studies. As such, the CPT demonstrates sensitivity to dysfunction of the attentional system whether this is due to diffuse or more focal damage/dysfunction or in conjunction with any specific disorder. CPT performance can be viewed as symptom specific (attentional disturbance), but it is not disorder specific (e.g., ADHD). Implications for neuropsychological interpretation of CPT results are presented. [Copyright &y& Elsevier]

We studied the electrodermal skin conductance responses (SCRs) of 36 subjects with well-characterized lesions in various regions of the cerebral hemispheres. Several lesion loci were consistently associated with defective electrodermal responding: the ventromedial frontal region (right and left), the right inferior parietal region, and the anterior cingulate gyrus (right and left). Our findings provide direct information regarding neural correlates of skin conductance responses in bumans. [ABSTRACT FROM AUTHOR]

Recent water maze experiments suggest that rats performing place navigation primarily use the geometric information provided by a set of landmarks, and neglect the featural information provided by the identities of the landmarks. Here, I develop a model that explains how an animal may perform place navigation by relying only on geometric information. The core of the model is the representation of places as panoramas defined by circular bar-codes embodying the relative bearings and apparent sizes of the landmarks, irrespective of their identities. There are two stages in the model. During the first stage, the animal freely explores its environment in order to acquire spatial information at the local level. During the second stage, the animal uses the information previously memorized to perform place navigation towards the goal it intends to reach. The possible role of two brain areas in place navigation is discussed within this framework. Beyond their primary role in landmark-based representations of places, hippocampal place cells may be involved in computing the current distances to the landmarks. Beyond their primary role in landmark-based representations of headings, post-subicular head-direction cells may be involved in computing the “compass bearings” of the landmarks. [ABSTRACT FROM AUTHOR]