Frontiers in Behavioral Neuroscience最新文献

Early life adversity (ELA) increases risk for multiple psychiatric disorders that are characterized by reward-related dysfunction. Disrupted reward-related processes are commonly observed in humans and rodents following ELA. Rodent studies have shown sex differences in response to natural and drug rewards at baseline, following ELA, and in rodent models of psychiatric diseases that are potentiated by ELA. Yet, less is known regarding the development of ELA-induced alterations in reward-related responses, including how these may differ by sex. To this end, we tested behavioral responses to consummatory and social rewards in control and scarcity-adversity male and female rats using sucrose preference, palatable food consumption, and social play tests during peripuberty and adolescence. Our results suggest no impact of early life scarcity-adversity during peripuberty, but sex- and reward-dependent adolescent effects in which females display reduced sucrose preference whereas males display lower levels of social play solicitations (i.e., dorsal contacts). These findings suggest age-, sex-, and reward-specific effects of early life scarcity-adversity in response to consummatory and social rewards, which appear to emerge during adolescence.

Introduction: The case of the Texas shooter is an event that marked human history, as an 18-year-old young man cold-bloodedly murdered 21 victims.

Objective: To analyze the psychological factors that could explain the antisocial behavior of the case under study.

Methodology: Through clinical behavioral analysis and data collection from the case, a psychological profile was constructed to identify specific factors that provide greater clarity regarding the risk factors associated with the violent act, which enabled the development of this perspective article.

Results: The study delves into several factors that could be considered determining and causal to the antisocial behavior in this case, including child abuse, family violence, bullying, animal cruelty, the impact of maltreatment on brain development, and the relationship between antisocial behavior and the use of violent video games.

Discussion: The analysis concludes by emphasizing the need to identify the causal factors of antisocial behavior in the early stages of human development. Additionally, it highlights the importance of implementing early interventions that can positively influence the factors described in this article.

Recent breakthroughs in marker-less pose-estimation have driven a significant transformation in computer-vision approaches. Despite the emergence of state-of-the-art keypoint-detection algorithms, the extent to which these tools are employed and the nature of their application in scientific research has yet to be systematically documented. We systematically reviewed the literature to assess how pose-estimation techniques are currently applied in rodent (rat and mouse) models. Our analysis categorized each study by its primary focus: tool-development, method-focused, and study-focused studies. We mapped emerging trends alongside persistent gaps. We conducted a comprehensive search of Crossref, OpenAlex PubMed, and Scopus for articles published on rodent pose-estimation from 2016 through 2025, retrieving 16,412 entries. Utilizing an AI-assisted screening tool, we subsequently reviewed the top ∼1,000 titles and abstracts. 67 papers met our criteria: 30 tool-focused reports, 28 method-focused studies, and nine study-focused papers. Publication frequency trend has accelerated in recent years, with more than half of these studies published after 2021. Through a detailed review of the selected studies, we charted emerging trends and key patterns, from the emergence of new keypoint-detection methods to their integration into behavioral experiments and adoption in various disease contexts. Despite significant progress in marker-less pose-estimation technologies, their widespread application remains limited. Many laboratories still rely on traditional behavioral assays, under-using advanced tools. Establishing standardized protocols is the key step to bridge this gap, which will ultimately realize the full potential of marker-less pose-estimation and even greater insight into preclinical behavioral science.

Sound influences motor functions and sound perception is conversely modulated by locomotion. Accumulating evidence supports an interconnection between the auditory system and the basal ganglia (BG), which has functional implications on the interaction between the two systems. Substantial evidence now supports auditory cortex and auditory thalamus inputs to the tri-laminar region of the tail of the striatum (tTS) in rodents. Thalamic input modulates the response gain of striatal neurons, whereas cortical input shapes their frequency tuning. Only recently has our understanding of BG projections to the auditory system advanced. GABAergic neurons in the tTS, which receive input from the auditory cortex, project to the posterior globus pallidus external segment (GPe). Posterior GPe, in turn, sends strong GABAergic projections to the non-lemniscal auditory thalamus (NLAT) and moderate projections to the cuneiform nucleus (CnF). The BG and auditory system are thus interconnected at multiple levels, forming a loop circuit in which the auditory system projects to the striatum and receives BG output via the NLAT. This circuit may mediate BG influence on auditory processing; however, the absence of motor cortex input to the tTS raises questions about its role in movement-related modulation of auditory responses. Given that the NLAT serves as a neural substrate for sound-cued aversive associative learning, BG output to the NLAT may influence learning processes. The pathway connecting the auditory system and CnF via the BG may underlie rhythmic entrainment in healthy individuals and therapeutic effects of rhythmic cues on gait in Parkinson's disease.

Introduction: Traumatic brain injury is the leading cause of death and disability in individuals under 40 years old. It induces various neuropathological outcomes, including cognitive, emotional, and physiological deficits, likely linked to early neuroinflammatory processes. In an animal model, mild traumatic brain injury (mTBI) has been shown to elevate oxidative stress biomarkers, such as advanced oxidation protein products (AOPP) and malondialdehyde (MDA), which persist for over a week. Despite extensive research on anti-inflammatory and neuroprotective therapies, most preclinical and clinical studies report limited efficacy. Synthetic glucocorticoids offer potential for early treatment of TBI-induced neuroinflammation, but clinical use is hindered by adverse effects and poor central nervous system biodistribution. Triamcinolone possesses anti-inflammatory, anti-angiogenic, and microglial inhibitory properties, although it has poor solubility and limited blood-brain barrier (BBB) penetration. Lipid nanocapsules (LNCs) may enhance TR solubility, bioavailability, BBB permeation, and intracellular delivery. This study aimed to evaluate the efficacy of triamcinolone-loaded LNCs (NT) on oxidative stress and cognitive-emotional outcomes following mTBI.

Methods: Adult male Wistar rats were subjected to closed-head mTBI via a 45 g weight-drop method, under anesthesia. Animals received NT, conventional triamcinolone, or empty LNCs, 15 minutes and 24 hours post-injury. They were sacrificed 24 hours, 1 or 7 days later for biochemical analysis of AOPP, MDA, and antioxidant enzymes (catalase and superoxide dismutase) activity in the hippocampus, prefrontal, and motor cortices. Separate cohorts underwent behavioral tests assessing memory (novel object recognition, Y-maze, and fear conditioning), 7 days after mTBI.

Results: mTBI induced significant impairments in recognition memory and fear retention, as well as increased AOPP, MDA, and CAT activity. SOD levels peaked at 24 h and normalized by day 7. NT, but not conventional TR, effectively prevented behavioral deficits and normalized OS markers. Importantly, early NT treatment reduced CAT overactivation at 7 days.

Discussion: This study provides the first evidence of the efficacy of NT in mitigating cognitive and emotional sequelae following mTBI, likely through enhanced brain delivery and early modulation of oxidative stress pathways.

Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interaction and restricted, repetitive behaviors (RRBs). These symptoms may stem from cognitive flexibility deficits, with dysfunction in the prefrontal cortex (PFC) and related neural circuits proposed as underlying mechanisms.

Objectives: This study examined whether transcranial direct current stimulation (tDCS) could enhance PFC activity and functional connectivity, thereby improving cognitive flexibility in a valproic acid (VPA)-induced ASD rat model.

Methods: Pregnant Sprague-Dawley rats were administered VPA (600 mg/kg, E12.5) or saline. VPA-exposed offspring exhibiting curved tails received tDCS and underwent behavioral tests, including the three-chamber social interaction test and cross-maze rule-shifting task, while local field potentials (LFPs) were recorded. Immunohistochemistry was performed to evaluate microglial activation (Iba1 +) and synaptic density (PSD95).

Results: Valproic acid -exposed offspring displayed significant social interaction deficits and impaired cognitive flexibility, alongside disrupted functional connectivity in frontal-striato-hippocampal circuits. Neuroinflammatory analysis revealed elevated Iba1+ microglial density (p < 0.05) and increased PSD95 expression (p < 0.05). After tDCS intervention, VPA rats exhibited restored sociability and cognitive performance, normalized functional connectivity, and significantly reduced microglial activation (p < 0.05), though PSD95 levels were unaffected.

Conclusion: Our results indicate that tDCS ameliorates ASD-like phenotypes in VPA rats, potentially through microglial suppression and PFC network synchronization. These findings support neuromodulation as a promising therapeutic approach for ASD-related cognitive dysfunction.

Major depressive disorder (MDD) is a complex neuropsychiatric condition whose multifactorial etiology remains incompletely explained by neuron-centric and neurotransmitter hypotheses alone. This review addresses that gap by positioning microglia-the CNS's resident immune cells-as central drivers of MDD pathogenesis. We organize current evidence around five interrelated themes: hypothalamic-pituitary-adrenal (HPA) axis dysfunction, monoaminergic and kynurenine pathway imbalances, neuroinflammatory overactivation, synaptic and white-matter integrity disruption, and gut-brain axis perturbations. In MDD, microglia shift from a surveillant resting state to either an overactivated or functionally inhibited phenotype, exacerbating pathology via aberrant cytokine release, dysregulated synaptic pruning and impaired myelin support. These changes are modulated by genetic susceptibility, sex differences, environmental stressors and microbiome alterations. We then survey translational advances-traditional and novel therapeutics that modulate microglial polarization, emerging blood- and imaging-based biomarkers, and strategies to harness microglia-oligodendrocyte cross-talk for remyelination-and highlight integrative platforms for stratifying inflammation-driven versus non-inflammatory subtypes. Our principal takeaway is that microglia represent a unifying nexus and actionable target for precision interventions tailored to individual biological profiles.

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.