Frontiers in Behavioral Neuroscience最新文献

It is now well-accepted that differing frequencies of neuro-oscillations support the selection, quantising, and pacing of information around different circuits in the brain. Another related function of neuro-oscillations, for which the frequency of oscillation is again critical, is to allow for integration of neural activity across differing spatial scales. In this short review, we discuss the degree to which human scalp-recorded EEG occurring in the theta-range (4-8 Hz) can be used to infer activation of mnemonic circuits involving the hippocamps and diencephalon (Papez loops), as well as in the neocortical areas the activity is directly recorded from. We also discuss the potential role of theta-range frequency modulation in the selection of specific mnemonic circuits. In light of the foregoing, we suggest that the frequency at which theta is occurring within and between cognitive tasks should be reported more thoroughly than it generally is. Finally, we suggest that assessing disruptions in frequency modulation of theta-range oscillations is a potentially valuable biomarker for disorders such as Alzheimer's disease.

Approximately 20% of adolescents report experiencing anhedonia, conferring high risk for the onset of adolescent depression. Early life adversity (ELA) is associated with anhedonia, and individual differences in reward motivation may inform this association. The current study examined whether reward-seeking behaviors moderated the prospective association between ELA and anhedonia 12-months later among adolescents. During a baseline visit, 74 participants, aged 11-17, completed the Balloon Analogue Risk Task (BART) to measure reward-seeking behaviors via adjusted average balloon pumps. Indeed, participation in the BART has been shown to activate the fronto-striatal neural circuits known to subserve reward-seeking. ELA was assessed continuously via parent-report using a 9-item Adverse Childhood Experiences questionnaire, with scores reflecting cumulative exposures to adversity prior to enrollment; interaction effects were subsequently probed at low, average, and high values for interpretation. At baseline and 12-months later, participants completed the anhedonia subscale within the Reynolds Adolescent Depression Scale 2nd Edition. Adolescents with greater ELA reported more anhedonia 12-months later (b = 0.97, SE = 0.46, p = 0.04), suggesting that ELA confers risk for developing anhedonia. Reward-seeking behavior moderated this association, such that adolescents with more experiences of ELA and low (b = 2.35, SE = 0.61, p < 0.01) and average reward seeking-behavior (b = 0.95, SE = 0.43, p = 0.03), but not high reward-seeking behavior (b = -0.45, SE = 0.60, p = 0.45), were at the greatest risk for increasing severity of anhedonia across the subsequent 12-months. Reward-seeking behaviors may aid in distinguishing which youth with ELA are at risk for depression. Additionally, results from this study may help to inform more specific interventions by increasing reward-seeking behaviors to mitigate the risks of developing anhedonia.

Standardized immobilization of zebrafish larvae is crucial for consistent behavioral assays such as optokinetic response, feeding, and tail-movement analyses, but traditional agarose embedding methods remain labor-intensive and variable. We developed the Agarose Stamped Device (ASD), a low-cost platform that imprints larva-sized wells into agarose, enabling rapid and reproducible alignment of multiple larvae while preserving viability. Customizable designs permit immobilization while maintaining eye, mouth, or tail freedom-achieved far more easily than with traditional embedding and post-processing. We demonstrate that the ASD sufficiently stabilizes larvae for high-resolution eye tracking, feeding assays, and tail-movement analyses. By combining standardized positioning with behavioral flexibility, the ASD broadens the range of feasible zebrafish experiments and lowers barriers to high-throughput behavioral neuroscience.

Introduction: Sleep plays a crucial role in memory consolidation, not only stabilizing newly encoded information but also potentially supporting forgetting. Yet it remains unclear how sleep prioritizes what is retained or discarded when multiple salience cues, such as emotional valence and top-down instructional goals, compete for consolidation.

Methods: In two studies, we examined how emotional content and intentional memory instruction interact to shape memory performance across a 12 h interval that included either nocturnal sleep or wakefulness. Participants completed a directed forgetting paradigm with neutral and negatively valenced words, followed by immediate recognition and delayed free recall.

Results: In both Study 1 (online) and Study 2 (in-lab), behavioral results showed that instruction to remember significantly enhanced recognition and recall, whereas emotion alone did not produce consistent benefits; however, sleep condition did not impact memory performance. In Study 2 (in-lab), which included overnight EEG monitoring, physiological markers of sleep revealed meaningful correlates of memory performance. Specifically, sleep spindle activity predicted recall for negative remember-cued words, while Slow Wave Sleep (SWS) and delta power were negatively correlated with total recall, suggesting a trade-off between deep sleep and memory accessibility. REM theta power was associated with increased false recall of emotionally negative foils, consistent with emotional memory generalization.

Discussion: Importantly, these findings extend prior nap-based research by demonstrating that full-night sleep physiology reflects selective consolidation mechanisms even in the absence of overt behavioral effects. Overall, results underscore the primacy of top-down instruction over emotional salience in shaping memory, and highlight the utility of sleep physiology for understanding selective memory consolidation.

Nitrogen detoxification pathways in the central nervous system supply a range of neurotransmitters, ranging from long-appreciated examples like nitric oxide and agmatine, to emergent neurotransmitters including spermidine, spermine, and polyamine-derived GABA. This review summarizes specialized nitrogen detoxification pathways in the brain, and evidence supporting several of these pathways' metabolites as co-transmitters in neurons and glia. Known functional roles of these nitrergic co-transmitters in learning, sleep, addiction, and other neurological disorders will be discussed to elucidate the adaptive value of nitrergic co-transmission, with a particular focus on nitrergic modulation of coincidence detection at NMDA receptors. Finally, this review sums up with a discussion of how nitrogen homeostasis in the brain serves as a coordinating locus for the control of these nitrergic neurotransmitters, and approaches for identifying bona fide co-transmitter effects of these metabolites in future work.

Neurosteroids are critical regulators of brain function, exerting profound effects on neurodevelopment, emotional regulation, cognition, and resilience to stress across the lifespan. Synthesized endogenously in the brain and peripheral tissues, neurosteroids modulate neural circuits through both genomic and non-genomic mechanisms. This review synthesizes current evidence on the roles of neurosteroids from fetal development through advanced biological aging, emphasizing their involvement in neuronal plasticity, synaptic modulation, myelination, and neurogenesis. We explore how neurosteroid dysregulation contributes to mood and cognitive disorders and highlight age- and sex-related changes in neurosteroid synthesis which may impact risk. Lifestyle factors including diet, exercise, and mindfulness are also examined for their ability to modulate neurosteroidogenesis and promote brain health. By integrating findings across developmental stages and physiological states, we underscore the functional roles of neurosteroids as modulators of emotional and cognitive states across the lifespan, and advocate for deeper investigation into neurosteroid-based intervention for across indications and throughout the lifespan.

Homosexuality is an intricate and multifactorial phenomenon affected by the interaction of biological, genetic, neurological and environmental factors. This paper examines the interplay of homosexuality determinants. Biological determinants such as the role of androgen levels, the fraternal birth order effect and maternal immune response contribute to shaping sexual orientation. Additionally, genetic influences are also assessed. These include the potential role of X chromosome, the possible link of fragile X mental retardation neighbor gene (FMR1) to sexual orientation, the function of genetic variants such as COMT an MTHFR, as well as connection with chromosomes 7, 8, 13 and 14. Furthermore, neurologic factors such as the role of the hypothalamus are assessed to highlight their contribution to sexual preference and attraction mediation. Lastly, childhood gender nonconformity and early exposure to traumatic events are among the environmental influences that contribute to the development of homosexuality. By incorporating various perspectives, this paper seeks to present a thorough overview of the multiple factors influencing sexual orientation, while emphasizing the importance of ongoing interdisciplinary research in this area.

Introduction: Emerging evidence suggests that exercise-induced fatigue negatively affects nervous system function, yet effective mitigation strategies are limited. This study aimed to determine whether intranasal methylene blue (MB) could prevent neurological deficits induced by exhaustive exercise in a rat model.

Methods: We utilized a rat exhaustive exercise training paradigm. Animal body weight was monitored, and a battery of behavioral tests was conducted to evaluate locomotor activity, anxiety-like behaviors, and spatial learning and memory. At the cellular level, we assessed neuron loss, apoptosis, synaptic proteins, myelin sheath, gliosis, and mitochondrial morphology in the hippocampal CA1 region and the striatum.

Results: Rats subjected to exhaustive exercise exhibited reduced locomotor activity, increased anxiety-like behaviors, and impaired spatial memory. This was associated with significant neuron loss, activation of apoptotic pathways, loss of synaptic proteins and myelin sheath, gliosis, and compromised mitochondrial morphology in the hippocampus and striatum. Notably, intranasal MB treatment significantly rescued these neuronal damages and improved performance in behavioral tests.

Discussion: Our findings demonstrate the neuroprotective effects of intranasal MB against exhaustive exercise-induced neurological deficits. This suggests that MB is a promising therapeutic agent for preventing the adverse neurological consequences of extreme physical exertion.