Frontiers in Behavioral Neuroscience最新文献

Slow-wave sleep (SWS) plays a pivotal role in memory consolidation, and electroencephalography (EEG) has provided critical insights into the neural mechanisms underlying these processes. In this mini-review, we discuss how SWS supports the processing of both declarative and procedural memory, in addition to higher cognitive functioning. We focus on the latest evidence from human EEG studies that examine temporal regularities alongside those that have demonstrated the coordinated interplay between slow oscillations, sleep spindles, and hippocampal ripples. We discuss how the precise temporal coupling of these oscillatory events facilitates memory transfer from the hippocampus to the neocortex, enhancing neuronal reactivation and optimizing long-term memory consolidation. We also examine how disruptions to SWS-due to lifestyle factors, ageing, neurological disorders, or pharmacological agents-can impair slow-wave activity and spindle dynamics, leading to memory deficits. Further, we highlight emerging neuromodulation techniques, such as transcranial direct current stimulation and closed-loop auditory stimulation, which harness EEG-based insights to enhance SWS and improve memory outcomes. These findings collectively demonstrate the potential of integrating EEG methodologies with targeted therapeutic interventions to restore SWS, optimize memory consolidation and enhance cognitive health. Finally, we recommend directions for future research aimed at refining these approaches, evaluating their long-term efficacy across diverse populations, and exploring new strategies to preserve memory function in the context of healthy ageing and neurological disease.

Despite miniature brains, insects exhibit flexible, adaptive, and goal-directed responses. Behaviors indicating rule abstraction and complex decision-making challenge the long-standing view of insects as rigid organisms limited to fixed reflexes. Here, we propose a new perspective: interpreting insect behavior through the lens of executive functions (EF). EF refers to a set of cognitive processes enabling behavioral control in situations requiring goal-directed action or adaptation to demanding conditions. Central among EF are inhibition (suppressing automatic, task-irrelevant responses), shifting (switching between strategies or rules), and updating (maintaining and revising relevant information), yet working memory, attention, planning, decision-making, and metacognition are also related to a widely understood set of EF. We argue that insect cognition can be productively reconsidered using the EF framework. Many behaviors documented in the literature align with EF components, even if not explicitly labeled as such. Others can be reinterpreted as EF-driven. Importantly, we show that EF-based interpretations support testable predictions: if executive control is involved, behavior should follow developmental trajectories, exhibit trade-offs between speed and accuracy, and adapt to changing contexts-patterns not expected from fixed heuristics or reflexes. Nonetheless, applying EF concepts to insects comes with challenges. Standard EF paradigms were originally developed to test human participants and often rely on language and explicit task instructions. Moreover, superficially flexible behaviors may still result from specialized, domain-specific routines rather than general cognitive control. Nevertheless, when used carefully, the EF perspective provides a structured, functional framework for studying insect cognition, enabling precise comparison across species with well-established concepts.

Introduction: Current rates of obesity and eating disorders have been steadily increasing, highlighting the importance of understanding the neural circuits of eating. This study explores the potential role of an understudied brain region, the septohypothalamic nucleus (SHy), in feeding control. Based on a serendipitous observation, we hypothesized that central injections of gamma-aminobutyric acid (GABA) receptor antagonists in the SHy would elicit feeding.

Method: Adult male Sprague-Dawley rats (n = 39) were microinjected with a vehicle or GABA_A receptor antagonists (bicuculline or picrotoxin) or a GABA_B receptor antagonist (2-(S)-(+)-2-hydroxy-saclofen [2-OH saclofen]). Food and water intakes were measured at 1, 2, 3, and 24 h after injection, and behavioral responses (sleeping, resting, locomotor activity, vigorous activity, and grooming) were measured for 1 h.

Result: Results showed increased food intake after bicuculline (p < 0.001) and picrotoxin (p = 0.03) injections during the 2nd and 3rd hours compared to controls. In addition, we found increased food intake 1 hour after 2-OH saclofen injections (p < 0.001). As for other behaviors, all three of the drugs suppressed resting (bicuculline: p < 0.001; picrotoxin: p < 0.001; 2-OH saclofen: p < 0.01) and increased locomotor activity (bicuculline: p < 0.001; picrotoxin: p < 0.001; 2-OH saclofen: p = 0.02).

Discussion: Our findings suggest that GABA_A or GABA_B receptor deactivation by antagonists elicited eating with a delayed effect and increased general arousal in rats. These findings collectively suggest that SHy neurons expressing GABA_A and/or GABA_B receptors are elements of a neurocircuit that participates in the regulation of feeding.

Introduction: Dopamine system dysfunction is closely associated with nervous system diseases such as Parkinson's disease and psychiatric disorder. Current research is limited to the individual application of dopamine D1 and D2 receptor-related agents, and the systematic effects of combined dopamine D1/D2 receptor inhibition on neural function remain unclear. In this study, we aimed to investigate the dose-dependent effects of co-DR1/2I (combined administration of dopamine receptor 1 inhibitor SCH39166 and dopamine receptor 2 inhibitor raclopride) on oxidative stress, learning, memory, emotion, and motor function in the substantia nigra, striatum, and hippocampus of mice.

Methods: After administering varying doses of co-DR1/2I through gastric tubes to male C57BL/6 mice, we used enzyme-linked immunosorbent assay to measure monoamine oxidase B (MAO-B), reactive oxygen species (ROS), and superoxide dismutase (SOD) activity. Behavioral changes were assessed, using open field, rotarod, and water maze tests. Tyrosine hydroxylase positive neurons were labeled with immunofluorescence, and tyrosine hydroxylase levels were detected by Western blot (WB) assay.

Results: Low-dose co-DR1/2I significantly increased MAO-B and ROS levels (p < 0.01) and decreased SOD activity (p < 0.01) in the substantia nigra, striatum, and hippocampus. MAO-B activity positively correlated with ROS (r = 0.916, p < 0.001) and negatively correlated with SOD (r = -0.685, p < 0.001), whereas ROS negatively correlated with SOD (r = -0.661, p < 0.001) in co-DR1/2I-treated mice. The medium- and high-dose groups exhibited spatial memory impairment (longer escape latency, p < 0.05) in the water maze and more anxiety-like behavior (reduced central zone time, p < 0.01) in the open field test; however, no abnormalities in motor coordination were observed in the rotarod test (p > 0.05). Immunofluorescence and WB confirmed a reduction in the dopaminergic neuron count after co-DR1/2I.

Conclusion: This is the first study to demonstrate that co-DR1/2I triggers cognitive and emotional dysfunction by exacerbating oxidative stress and dopaminergic neuronal damage, thereby advancing our understanding of the neurotoxic mechanisms of dopamine receptor antagonists. Future studies are needed to explore targeted antioxidant therapies and receptor-selective modulation strategies to reduce the side effects.

Risk decision-making is a fundamental cognitive process that involves distributed neural circuits, with impairments observed across various psychiatric conditions. This systematic review synthesizes current evidence on the neurobiological substrates underlying maladaptive risk processing, highlighting three key findings. First, frontostriatal dysregulation is identified as a central feature, characterized by prefrontal hypoactivation and striatal hyperreactivity, particularly prominent in bipolar disorder and addiction. Second, disorder-specific neural signatures are noted, such as insular dysfunction in anxiety disorders, ventral striatal blunting in depression, and orbitofrontal-insula decoupling in schizophrenia. Third, computational modeling reveals distinct alterations in risk sensitivity, loss aversion, and reward valuation parameters across different diagnostic categories. This review also evaluates principal assessment methodologies and therapeutic interventions. Future research should prioritize the integration of computational psychiatry with multimodal biomarkers to advance both theoretical models and clinical applications.

Disruptions in sleep are common across clinical populations, particularly those with neurological and psychiatric disorders, making restorative sleep and sustained wakefulness a public health priority. Sleep is essential for brain function, impacting cognition in addition to serving as a critical factor in memory consolidation and healthy aging. Neuromodulation via transcranial photobiomodulation (t-PBM) increases cerebral mitochondrial activity and blood flow. These effects may underlie improvements in sleep quality and wakefulness observed after t-PBM. In this systematic review, we summarize the current literature across clinical and healthy populations, which describes t-PBM's potential to improve sleep, wakefulness, and cognition. The scope of this review also includes t-PBM's effect on the brain's glymphatic system and blood flow, the potential of this strategy to augment alertness, wakefulness, and associated cognitive processes, and the suggestion for targeted t-PBM application for future research based on the underlying neurobiological mechanisms of t-PBM and wakefulness across diverse clinical populations.

Food cravings (FC) are closely associated with behaviors such as loss of control, binge eating, and emotional eating. Although FC is among the symptoms proposed for food addiction (FA), we argue that the distress associated with eating, managing cravings, and experiencing loss of control may not, in itself, constitute a framework consistent with addiction or addiction-like eating. Grouping these concepts under the FA label may contribute to conceptual confusion, potentially leading to diagnostic inaccuracies. This integrative review aimed to explore the concepts of FA and FC, as well as their interrelations, through methodologies such as self-report questionnaires and visual analog scales. A systematic search without time restrictions yielded 37 original studies for qualitative analysis. The selected investigations examined FA and FC as primary outcomes and were categorized into five thematic sections: (1) genetic factors, (2) neurobiology, (3) behavioral factors, (4) emotional factors, and (5) food cues. The findings indicate that cravings play a mediating role in disordered eating patterns and are associated with excessive consumption or impaired control in individuals exhibiting symptoms attributed to FA. This review addresses three key issues: (i) theoretical and psychometric challenges in the conceptualization of FA, (ii) redundancies among FC, eating-related distress, and self-reported loss of control, and (iii) whether FA is primarily a matter of semantics. Phrases related to constructs of substance use disorders correlate with constructs that are neuropsychopharmacological influenced, and they impose new constructs upon previously established eating behavior patterns, along with their already known neural and neuropsychological correlates (such as emotional eating, dietary restraint, binge eating, and craving). The concept of FA, along with its scale and the new diagnostic questionnaire, also integrates cultural perceptions of food with established psychological constructs, drawing on previously recognized phenomena. Investigating the continuum encompassing (i) cravings, (ii) disordered eating attitudes, and (iii) body image-related distress presents a significant challenge, particularly when researchers overlook the underlying human narratives that define this multifaceted phenomenon. Without a clear theoretical and epistemological framework, the boundaries of FA risk becoming overly broad, diminishing its utility as a diagnostic tool or basis for interventions. The challenges in establishing a consistent and precise definition underscore the need for further research to ensure the concept represents a distinct and scientifically valid phenomenon rather than a generalized reflection of eating-related constructs.

Introduction: Despite the rise in psychiatric disorders worldwide, the underlying brain circuits responsible for these devastating conditions remain elusive. The lateral habenula (LHb) has emerged as a key brain structure in depression studies due to its hyperactive state in both patients and animal models. While this aligns with known roles in driving aversive states and regulating serotonin release, it is still unclear how acute and transient activity changes in the LHb can influence higher order cognitive processes such as learning, memory, and behavioral adaptation. Given the importance of these processes to psychiatric conditions, understanding how LHb activity impacts cognitive function allows novel insights into the neurobiological mechanisms of disorders like depression.

Methods: Towards this goal, we used chemogenetic activation to temporarily excite glutamatergic neurons in the mouse LHb and assessed impacts on associative memory.

Results and discussion: Surprisingly, we found that transient activation of LHb impaired long-term memory, without affecting anxiety or depression-like behaviors. Specifically, post-training activation of LHb glutamatergic neurons disrupted object recognition and reward-based associative long-term memory, while sparing fear associated long-term memory. The memory impairment was restricted to a critical temporal window post-training/conditioning that corresponded with the consolidation stage of long-term memory. Strikingly, pairing LHb glutamatergic neuronal activation with systemic ketamine administration rescued the long-term memory deficits, indicating that LHb glutamatergic neurons modulate consolidation of associative memories via a NMDA-mediated mechanism. Together, these findings support a novel role for LHb glutamatergic neuronal activity in the consolidation of associative long-term memories.

Introduction: Air pollution (AP) has been associated with increased risk for multiple neurodevelopmental disorders. As one of the most abundant contaminants of AP, iron (Fe) is critical to brain function, with both deficiencies and excesses leading to potential neurotoxicity. Our prior studies examining the impact of developmental exposures of mice to inhaled Fe (1.0 μg/m³) alone or in conjunction with sulfur dioxide SO₂ (1.31 mg/m³; FeS) from postnatal days (PND) 4-7 and 10-13 (human 3rd trimester brain equivalent period) revealed alterations in brain neurotransmitter levels at PND14 which had generally recovered by PND60, but which were, nevertheless, followed by behavioral impairments. The current study sought to determine whether subsequent behavioral experience, which requires neurochemical mediation, had unmasked residual deficits in neurotransmitter function in response to developmental FeS or Fe inhalation.

Methods: Consequently, levels of brain neurotransmitters and trans-sulfuration markers were measured in mice that had either behavioral experience (BE) or no behavioral experience (NB) at PND 215 (Fe only) or 357 (FeS).

Results: BE itself markedly increased brain neurotransmitter and trans-sulfuration marker levels, particularly in males. These increases were prevented in males in both frontal cortex and striatum by prior developmental FeS exposures. In females, developmental Fe exposure was associated with residual increases particularly in striatal serotonergic function and levels of homocysteine independently of behavioral experience.

Discussion: Collectively, these findings show the ability of behavioral experience to unmask later life residual consequences of developmental exposures to FeS in males and of latent emerging effects of Fe in females. The collective findings may have relevance to later life neurodegenerative diseases and disorders now increasingly associated with air pollution exposures, and also underscore how understanding how various components of air pollution influence brain is critical to regulatory decisions for public health protection.