Sensory neurobiology: Muscles power pheromone sensation.

While we understand how the five main sensory organs enable and facilitate stimulus detection, little is known about how the vomeronasal organ enables pheromone sensation. A new study finds specialized muscles poised to coordinate stimulus delivery, dynamics, and arousal.

Neurobiological mechanisms and therapeutic impact of electroconvulsive therapy (ECT).

Electroconvulsive therapy (ECT) is an efficient therapeutic resource for psycho-pharmacotherapeutic resistant forms of depression. ECT is a form of electrical brain stimulation involving the induction of a controlled seizure, clinically similar to an epileptic seizure, that is initiated in the prefrontal region of the brain and spreads to the cortex and subcortex, including the diencephalic structures. This is achieved by creating a transcranial electric field and synchronously depolarizing neuronal membranes. The mechanisms of action of ECT are not yet fully understood, but several hypotheses have been proposed to explain how it affects the brain: neurotransmitter changes, neuroplasticity, network connectivity, endocrine system regulation and changes in regional cerebral blood flow and regional metabolism.

Common and distinct cortical thickness alterations in youth with autism spectrum disorder and attention-deficit/hyperactivity disorder.

BACKGROUND: Autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD) are neurodevelopmental disorders with overlapping behavioral features and genetic etiology. While brain cortical thickness (CTh) alterations have been reported in ASD and ADHD separately, the degree to which ASD and ADHD are associated with common and distinct patterns of CTh changes is unclear. METHODS: We searched PubMed, Web of Science, Embase, and Science Direct from inception to 8 December 2023 and included studies of cortical thickness comparing youth (age less than 18) with ASD or ADHD with typically developing controls (TDC). We conducted a comparative meta-analysis of vertex-based studies to identify common and distinct CTh alterations in ASD and ADHD. RESULTS: Twelve ASD datasets involving 458 individuals with ASD and 10 ADHD datasets involving 383 individuals with ADHD were included in the analysis. Compared to TDC, ASD showed increased CTh in bilateral superior frontal gyrus, left middle temporal gyrus, and right superior parietal lobule (SPL) and decreased CTh in right temporoparietal junction (TPJ). ADHD showed decreased CTh in bilateral precentral gyri, right postcentral gyrus, and right TPJ relative to TDC. Conjunction analysis showed both disorders shared reduced TPJ CTh located in default mode network (DMN). Comparative analyses indicated ASD had greater CTh in right SPL and TPJ located in dorsal attention network and thinner CTh in right TPJ located in ventral attention network than ADHD. CONCLUSIONS: These results suggest shared thinner TPJ located in DMN is an overlapping neurobiological feature of ASD and ADHD. This alteration together with SPL alterations might be related to altered biological motion processing in ASD, while abnormalities in sensorimotor systems may contribute to behavioral control problems in ADHD. The disorder-specific thinner TPJ located in disparate attention networks provides novel insight into distinct symptoms of attentional deficits associated with the two neurodevelopmental disorders. TRIAL REGISTRATION: PROSPERO CRD42022370620. Registered on November 9, 2022.

After the trans brain: a critique of the neurobiological accounts of embodied trans* identities.

This paper critically analyses three main neurobiological hypotheses on trans* identities: the neurobiological theory about the origin of gender dysphoria, the neurodevelopmental cortical hypothesis, and the alternative hypothesis of self-referential thinking and body perception. In this study I focus then the attention on three elements: the issue of (de)pathologisation, the idea of the trans brain, and the aetiology of trans* identities. While the neurobiological theory about the origin of gender dysphoria and the neurodevelopmental cortical hypothesis claim the existence of the trans brain, each offering its own neurobiological depiction, the hypothesis of self-referential thinking and body perception doesn't postulate a distinctive neurobiological trait for all trans* people. I problematize both portrayals of the trans brain departing from the findings and conceptualizations of the paradigm shifting brain mosaicism. Unlike the hypothesis of self-referential thinking and body perception that keeps the question of causation open, both the neurobiological theory about the origin of gender dysphoria and the neurodevelopmental cortical hypothesis situate the origin of trans* identities in the neurobiological domain. I challenge the biological deterministic framework in which this aetiology is inscribed from a dynamic processual entanglement perspective. Finally, concerning the issue of (de)pathologisation of trans* identities, an evolution can be seen in each of the hypothesis and among them, from the least to the most depathologising. However, I question their complete departure from a pathologising framework.

Clinical Psychology in the Era of Research Diagnostic Criteria (RDoC): Reconciling Individually-Focused Practice with a Broader Biopsychosocial Context.

There is growing consensus that diagnostic labels are insufficient to describe the individual child's psychiatric profile, much less inform the precise combination of interventions that will minimize the impact of risk and/or bolster protective factors over the course of a particular child's development. Moreover, investigations of neurobiological and genetic mechanisms associated with psychopathology have revealed considerable cross-diagnostic overlap, undermining the validity of models that propose a 1:1 relationship between risk and psychiatric disorder. Accordingly, recent publications have advocated for neurodevelopmental models that utilize trait-based measurement, as well as increased emphasis on integration of biological and experiential mechanisms. Despite an expanding body of literature supporting this conceptual shift, the practical implications remain unclear. In this special issue, we compile a collection of novel empirical research papers and reviews that build on the trans-diagnostic principles of the RDoC framework.

Daniel Kronauer.

Daniel Kronauer explores the behavioral genetics and neurobiology of ants, tracing their evolution from solitary ancestors to supremely social insects. In this interview with Neuron, he discusses his lab's efforts to develop a new ant model species and describes how his passion for natural history inspires his research.

Neuroscience-informed classification of prevention interventions in substance use disorders: An RDoC-based approach.

Neuroscience has contributed to uncover the mechanisms underpinning substance use disorders (SUD). The next frontier is to leverage these mechanisms as active targets to create more effective interventions for SUD treatment and prevention. Recent large-scale cohort studies from early childhood are generating multiple levels of neuroscience-based information with the potential to inform the development and refinement of future preventive strategies. However, there are still no available well-recognized frameworks to guide the integration of these multi-level datasets into prevention interventions. The Research Domain Criteria (RDoC) provides a neuroscience-based multi-system framework that is well suited to facilitate translation of neurobiological mechanisms into behavioral domains amenable to preventative interventions. We propose a novel RDoC-based framework for prevention science and adapted the framework for the existing preventive interventions. From a systematic review of randomized controlled trials using a person-centered drug/alcohol preventive approach for adolescents, we identified 22 unique preventive interventions. By teasing apart these 22 interventions into the RDoC domains, we proposed distinct neurocognitive trajectories which have been recognized as precursors or risk factors for SUDs, to be targeted, engaged and modified for effective addiction prevention.

Evolution, biomechanics, and neurobiology converge to explain selective finger motor control.

Humans use their fingers to perform a variety of tasks, from simple grasping to manipulating objects, to typing and playing musical instruments, a variety wider than any other species. The more sophisticated the task, the more it involves individuated finger movements, those in which one or more selected fingers perform an intended action while the motion of other digits is constrained. Here we review the neurobiology of such individuated finger movements. We consider their evolutionary origins, the extent to which finger movements are in fact individuated, and the evolved features of neuromuscular control that both enable and limit individuation. We go on to discuss other features of motor control that combine with individuation to create dexterity, the impairment of individuation by disease, and the broad extent of capabilities that individuation confers on humans. We comment on the challenges facing the development of a truly dexterous bionic hand. We conclude by identifying topics for future investigation that will advance our understanding of how neural networks interact across multiple regions of the central nervous system to create individuated movements for the skills humans use to express their cognitive activity.

Treatment of dissociative identity disorder: leveraging neurobiology to optimize success.

INTRODUCTION: Dissociative identity disorder (DID) is a treatable mental health condition that is associated with a range of psychobiological manifestations. However, historical controversy, modern day misunderstanding, and lack of professional education have prevented accurate treatment information from reaching most clinicians and patients. These obstacles also have slowed empirical efforts to improve treatment outcomes for people with DID. Emerging neurobiological findings in DID provide essential information that can be used to improve treatment outcomes. AREAS COVERED: In this narrative review, the authors discuss symptom characteristics of DID, including dissociative self-states. Current treatment approaches are described, focusing on empirically supported psychotherapeutic interventions for DID and pharmacological agents targeting dissociative symptoms in other conditions. Neurobiological correlates of DID are reviewed, including recent research aimed at identifying a neural signature of DID. EXPERT OPINION: Now is the time to move beyond historical controversy and focus on improving DID treatment availability and efficacy. Neurobiological findings could optimize treatment by reducing shame, aiding assessment, providing novel interventional brain targets and guiding novel pharmacologic and psychotherapeutic interventions. The inclusion of those with lived experience in the design, planning and interpretation of research investigations is another powerful way to improve health outcomes for those with DID.

Insect neurobiology: Oviposition crowd control.

A new study examines how Helicoverpa armigera females detect chemicals released by conspecific eggs in order to avoid laying more eggs on the same substrate. This work opens new avenues for basic research inquiries and offers a potential strategy for controlling insect pests.

Effects of lockdowns on neurobiological and psychometric parameters in unipolar depression during the COVID-19 pandemic.

Defying the COVID-19 pandemic required restriction measures of unprecedented scale, that may induce and exacerbate psychiatric symptoms across the population. We aimed to assess in vivo dynamic effects of mitigation strategies on human brain neurobiology, neuroplastic as well as psychometric parameters. Three structural magnetic resonance imaging measurements, serum brain-derived neurotrophic factor (sBDNF) analyses, and psychometric assessments (Beck Depression Inventory-II and Perceived Stress Questionnaire-20) were performed in healthy individuals and patients with a recurrent major depressive disorder in the period from September 2020 to July 2021. Group differences and changes over time in structural imaging, neuroplastic and psychometric parameters were assessed with linear mixed models. Analysis of data from 18 patients with a recurrent major depressive disorder and 28 healthy individuals showed clinically relevant scores for depression and stress in the patient group as well as significant cross-sectional differences in depression scores (F = 30.89, p < 0.001) and three subscales of the Perceived Stress Questionnaire (Worries: F = 19.19, p < 0.001, Tension: F = 34.44, p < 0.001, Joy: F = 12.05, p = 0.001). Linear mixed models revealed no significant changes over time in cortical thickness of the prefrontal cortex, anterior cingulate cortex, hippocampus, and amygdala (F = 0.29, p > 0.1) and no interaction with group (F = 0.28, p > 0.1). Further, analysis revealed no main effect of time and no interaction of time x group in depressive symptoms, perceived stress subscales, and sBDNF (all p > 0.1). Despite the limited sample size, the strength of this investigation lies in the multimodal assessment of peri-pandemic lockdown effects. Nine months of varying restrictions measures did not result in observable changes in brain morphology nor impact depressive symptoms in either psychiatric patients with a recurrent major depressive disorder or healthy individuals. While these neurobiological and psychometric data stand in contrast to initial expectations about the effects of restriction measures, they might inform future investigations of longitudinal effects of restriction measures on mental health.

Neurobiology of numerical learning.

Numerical abilities are complex cognitive skills essential for dealing with requirements of the modern world. Although the brain structures and functions underlying numerical cognition in different species have long been appreciated, genetic and molecular techniques have more recently expanded the knowledge about the mechanisms underlying numerical learning. In this review, we discuss the status of the research related to the neurobiological bases of numerical abilities. We consider how genetic factors have been associated with mathematical capacities and how these link to the current knowledge of brain regions underlying these capacities in human and non-human animals. We further discuss the extent to which significant variations in the levels of specific neurotransmitters may be used as potential markers of individual performance and learning difficulties and take into consideration the therapeutic potential of brain stimulation methods to modulate learning and improve interventional outcomes. The implications of this research for formulating a more comprehensive view of the neural basis of mathematical learning are discussed.

Ascorbate and its transporter SVCT2: The dynamic duo's integrated roles in CNS neurobiology and pathophysiology.

Ascorbate is a small antioxidant molecule essential for the proper development and function of the brain. Ascorbate is transported into the brain and between brain cells via the Sodium vitamin C co-transporter 2 (SVCT2). This review provides an in-depth analysis of ascorbate's physiology, including how ascorbate is absorbed from food into the CNS, emphasizing cellular mechanisms of ascorbate recycling and release in different CNS compartments. Additionally, the review delves into the various functions of ascorbate in the CNS, including its impact on epigenetic modulation, synaptic plasticity, and neurotransmission. It also emphasizes ascorbate's role on neuromodulation and its involvement in neurodevelopmental processes and disorders. Furthermore, it analyzes the relationship between the duo ascorbate/SVCT2 in neuroinflammation, particularly its effects on microglial activation, cytokine release, and oxidative stress responses, highlighting its association with neurodegenerative diseases, such as Alzheimer's disease (AD). Overall, this review emphasizes the crucial role of the dynamic duo ascorbate/SVCT2 in CNS physiology and pathology and the need for further research to fully comprehend its significance in a neurobiological context and its potential therapeutic applications.

The potassium channels: Neurobiology and pharmacology of tinnitus.

Tinnitus is a widespread public health issue that imposes a significant social burden. The occurrence and maintenance of tinnitus have been shown to be associated with abnormal neuronal activity in the auditory pathway. Based on this view, neurobiological and pharmacological developments in tinnitus focus on ion channels and synaptic neurotransmitter receptors in neurons in the auditory pathway. With major breakthroughs in the pathophysiology and research methodology of tinnitus in recent years, the role of the largest family of ion channels, potassium ion channels, in modulating the excitability of neurons involved in tinnitus has been increasingly demonstrated. More and more potassium channels involved in the neural mechanism of tinnitus have been discovered, and corresponding drugs have been developed. In this article, we review animal (mouse, rat, hamster, and guinea-pig), human, and genetic studies on the different potassium channels involved in tinnitus, analyze the limitations of current clinical research on potassium channels, and propose future prospects. The aim of this review is to promote the understanding of the role of potassium ion channels in tinnitus and to advance the development of drugs targeting potassium ion channels for tinnitus.

The Translational Future of Stress Neurobiology and Psychosis Vulnerability: A Review of the Evidence.

Psychosocial stress is a well-established risk factor for psychosis, yet the neurobiological mechanisms underlying this relationship have yet to be fully elucidated. Much of the research in this field has investigated hypothalamic-pituitary-adrenal (HPA) axis function and immuno-inflammatory processes among individuals with established psychotic disorders. However, as such studies are limited in their ability to provide knowledge that can be used to develop preventative interventions, it is important to shift the focus to individuals with increased vulnerability for psychosis (i.e., high-risk groups). In the present article, we provide an overview of the current methods for identifying individuals at high-risk for psychosis and review the psychosocial stressors that have been most consistently associated with psychosis risk. We then describe a network of interacting physiological systems that are hypothesised to mediate the relationship between psychosocial stress and the manifestation of psychotic illness and critically review evidence that abnormalities within these systems characterise highrisk populations. We found that studies of high-risk groups have yielded highly variable findings, likely due to (i) the heterogeneity both within and across high-risk samples, (ii) the diversity of psychosocial stressors implicated in psychosis, and (iii) that most studies examine single markers of isolated neurobiological systems. We propose that to move the field forward, we require well-designed, largescale translational studies that integrate multi-domain, putative stress-related biomarkers to determine their prognostic value in high-risk samples. We advocate that such investigations are highly warranted, given that psychosocial stress is undoubtedly a relevant risk factor for psychotic disorders.

Historical postmortem studies on catatonia: Close reading and analysis of Kahlbaum's cases and scientific texts between 1800 and 1900.

In the 19th century, postmortem brain examination played a central role in the search for the neurobiological origin of psychiatric and neurological disorders. During that time, psychiatrists, neurologists, and neuropathologists examined autopsied brains from catatonic patients and postulated that catatonia is an organic brain disease. In line with this development, human postmortem studies of the 19th century became increasingly important in the conception of catatonia and might be seen as precursors of modern neuroscience. In this report, we closely examined autopsy reports of eleven catatonia patients of Karl Ludwig Kahlbaum. Further, we performed a close reading and analysis of previously (systematically) identified historical German and English texts between 1800 and 1900 for autopsy reports of catatonia patients. Two main findings emerged: (i) Kahlbaum's most important finding in catatonia patients was the opacity of the arachnoid; (ii) historical human postmortem studies of catatonia patients postulated a number of neuroanatomical abnormalities such as cerebral enlargement or atrophy, anemia, inflammation, suppuration, serous effusion, or dropsy as well as alterations of brain blood vessels such as rupture, distension or ossification in the pathogenesis of catatonia. However, the exact localization has often been missing or inaccurate, probably due to the lack of standardized subdivision/nomenclature of the respective brain areas. Nevertheless, Kahlbaum's 11 autopsy reports and the identified neuropathological studies between 1800 and 1900 made important discoveries, which still have the potential to inform and bolster modern neuroscientific research in catatonia.

Cellular neurobiology of hyperforin.

Hyperforin is a phloroglucinol derivative isolated from the medicinal plant Hypericum perforatum (St John's wort, SJW). This lipophilic biomolecule displays antibacterial, pro-apoptotic, antiproliferative, and anti-inflammatory activities. In addition, in vitro and in vivo data showed that hyperforin is a promising molecule with potential applications in neurology and psychiatry. For instance, hyperforin possesses antidepressant properties, impairs the uptake of neurotransmitters, and stimulates the brain derived neurotrophic factor (BDNF)/TrkB neurotrophic signaling pathway, the adult hippocampal neurogenesis, and the brain homeostasis of zinc. In fact, hyperforin is a multi-target biomolecule with a complex neuropharmacological profile. However, one prominent pharmacological feature of hyperforin is its ability to influence the homeostasis of cations such as Ca2+ , Na+ , Zn2+ , and H+ . So far, the pathophysiological relevance of these actions is currently unknown. The main objective of the present work is to provide an overview of the cellular neurobiology of hyperforin, with a special focus on its effects on neuronal membranes and the movement of cations.