Introduction: Animal models play a central role in the experimental study of cognitive dysfunction. The development of specific behavioral tools allows for detailed analysis of the mechanisms involved in spatial learning and memory. The three-tower maze (3T) was designed as an original device for sequential analysis of orientation, decision-making, and memory abilities. Valproic acid, a molecule widely used in neurology, is suspected of impairing cognitive functions through neurotoxic mechanisms. Objective: Experimentally validate the 3T maze as a tool for detecting memory deficits after subchronic exposure to valproic acid in Wistar rats. Methods: Forty-eight Wistar rats of both sexes were randomly divided into three experimental groups: a control group and two groups treated with valproic acid at doses of 200 and 400 mg/kg. The drug was administered orally once a day for 30 days. At the end of the protocol, the animals were subjected to the three-tower maze test. Performance was quantified using parameters combining spatial orientation, cognitive efficiency, decision latency, route errors, and locomotor activity. Results: Animals exposed to valproic acid showed a progressive deterioration in learning and memory abilities, reflected in a significant increase in path errors, longer reward access times, and decreased overall cognitive efficiency. In addition, an increase in avoidance and vigilance behaviors was recorded, suggesting an emotional impact associated with cognitive deficits. Conclusion: The three-tower maze appears to be a relevant experimental tool for the integrated study of memory and behavioral disorders induced by valproic acid. It offers a complementary approach to conventional cognitive exploration tests in rats.

Introduction: Current models lack a detailed neurocircuitry account of how acute stress transitions into impulsive action and, subsequently, guilt-driven repair.

Method: We present a novel theoretical model of stress-mediated PFC–Basal Ganglia dysregulation that unfolds within a dynamic environmental context and is critically shaped by the individual's learned history. The process is triggered by salient environmental stimuli, which the amygdala appraises based on past associative learning. This triggers acute anger, activating the SAM/HPA axes and elevating neurochemicals that suppress PFC activity. Because of this reduced PFC activity, the Basal Ganglia cannot receive its critical input for the proper anticipation of consequences. The striatum then chooses an action based primarily on the immediate stimulus due to the lack of integrative PFC input. This decision is further biased by amygdala-driven salience and reinforced behavioral patterns from the individual's past (e.g., a learned tendency toward verbal aggression). As neurochemicals clear and PFC function restores, its renewed projections evaluate the impulsive act against internalized social rules. This mismatch generates guilt, which subsequently biases the striatum toward a reparative action (e.g., apology) informed by learned strategies for social reconciliation.

Results: This model is supported by the following: Pharmacological evidence that high levels of catecholamines impair prefrontal cortex (PFC) cognitive regulation via alpha-1 adrenergic and D1 dopaminergic receptors, a deficit reversed by adrenergic blockade (Arnsten, 2009); connectivity analyses demonstrating decreased functional coupling between the medial PFC and emotion-processing regions (amygdala/striatum) during anger provocation, which correlates with reactive aggression (Klaassens et al., 2018); and neuroimaging studies identifying a distributed neural signature of guilt centered on the dorsomedial PFC and anterior midcingulate cortex, which predicts the motivation for reparative behavior (Yu et al., 2019).

Conclusion: This model offers a comprehensive framework linking acute stress neurochemistry to observable behavioral shifts, potentially informing future experimental designs and therapeutic targets for impulse-related psychopathology.

Introduction: The "Paradox of Altruism" questions why individuals incur personal risk to aid non-kin strangers—a behavior not fully explained by traditional evolutionary or psychological models centered on kinship or reciprocity.

Method: We developed a theoretical neurobiological framework through a synthesis of established literature. We propose that altruism is driven by the imperative to avoid acute stress, mediated by a subcortical circuit involving the Hypothalamic–Pituitary–Adrenal (HPA) axis, the Sympathetic–Adreno–Medullar (SAM) axis, the prefrontal cortex (PFC), and the basal ganglia.

Results: The model posits that a high-distress stimulus triggers acute HPA and/or SAM axis activation, inducing a rapid reduction in prefrontal cortex (PFC) activity—a stress-induced executive impairment well-documented in the literature (Arnsten, 2009). Due to this diminished PFC function, individuals cannot engage in future-oriented consequence anticipation of their action. With top-down control suspended, the basal ganglia—a structure central to habit formation and action selection under motivational drive (Graybiel,2005)—selects the most immediate and efficient action to terminate the internal aversive signal via negative reinforcement, a process supported by dopaminergic signaling linked to aversive state relief (Redgrave et al., 2010). The altruistic intervention is thus executed as the optimal action for immediate stress relief. This mechanism, evolved for kin-protection in ancestral small groups, is now activated indiscriminately by vulnerable human stimuli, constituting an evolutionary mismatch (Li et al., 2018).

Conclusion: Altruism toward strangers is reconceptualized as deterministic, self-directed physiological regulation. This model generates novel, falsifiable predictions; for example, it suggests a precise temporal sequence in which an acute stress spike via the SAM axis (upon encountering a threatened non-kin human) precedes a reduction in prefrontal activity and the subsequent selection of helping actions—provided the altruistic act reduces stress relative to that individual's perspective. This framework offers a new lens through which to dissect the proximate causes of paradoxical helping behavior.

Conflicts of interest: None declared.

This paper investigates chaotic conditions that organizations face, emphasizing the necessity of adopting new technologies and strategic thinking. The focus is on behavioral sciences, particularly the relationship between brain functionality, neurological processes and managerial behavior. This research delves into analysis of brain wave activity, especially Alpha Waves, using a blend of theoretical and experimental methods to understand influences on decision-making in uncertain environments. Vital questions are posed, such as how knowledge of brain wave activity can enhance decision-making and the implications of these findings for psychology and model resilience against adversarial attacks. Through empirical exploration and use of EEG, this study links behavioral research with computational models, highlighting impact of brain functionality on behavior and advocating for rethinking of decision-making processes. Ultimately, this research aims to develop robust models that reshape managerial strategies, thereby emphasizing importance of neuroscience in addressing management challenges. This paper poses key questions regarding interpretability of models based on brain activity and resilience to biases and adversarial attacks. Some of these are as follows: How does understanding brain wave activity enhance the comprehension of decision-making in environments? In what ways can organizations implement findings to improve decision-making? What implications do these findings have for future research in psychology? How might adversarial attacks influence development of decision-making models using brain data? Through empirical exploration, via EEG’s role in enhancing decision-making and involving a small respondent sample, this study seeks to bridge behavioral research with computational models to enhance understanding of cognitive dynamics in managerial contexts. This paper advocates for rethinking decision-making foundations by proposing alternative frameworks to better comprehend decision problems in practical applications. This paper contributes valuable insights toward developing more robust and interpretable models that can radically transform managerial strategies. Consequently, the recommendations put forth urge a re-evaluation of decision-making frameworks, reinforcing relevance of neuroscience in practical management issues.

This study addresses the complex nature of human cognition within a dynamically complex interplay of distributed neural networks, oscillatory activity, and subjective experiential phenomena. Although computational models have made a rich addition to our understanding of memory, attention, and decision-making processes, it is often the case that these models neglect the phenomenological dimensions that make up the lived experience of thought. Accordingly, in the present paper, a neuro-phenomenological framework that synergistically couples EEG-based neural oscillation analysis with first-person cognitive narratives is introduced for mapping the architecture of consciousness and cognition in a more integrative way. Employing EEG recordings taken during conditions of both rest and task performance, the present study addresses the issue of correlations between oscillatory signatures (i.e., alpha, theta, and gamma bands) and self-reported body variable cognitive states of attention, working memory load, and perceptual switching. These empirical relationships are then interpreted in the context of predictive processing, and explain how the brain builds internal world models and how departures from these world models can bring about cognitive dissonance or attention drift. One or two secondary objectives are to explore the possibility of using artificial intelligence models of intelligence, especially architectures of deep learning style, trained on multimodal data, to simulate or approximate the aforementioned cognitive states. By combining human EEG signatures, and the internal state of representation of artificial neural networks, this work attempts to narrow down the gap between biological and computational understanding. The findings add to the emerging field of discussion in computational cognitive neuroscience, embodied cognition, and cognitive modeling that insists that future brain–behavior mapping efforts do not solely focus on the neural correlates of thought but also its structural and phenomenological "feel". This integrative way of thinking has very important implications for cognitive training, neuroadaptive interfaces, and diagnostics for mental health.

Behavioral phenotyping represents a central pillar of contemporary behavioral neuroscience, offering a functional readout of neural integrity that cannot be captured solely through molecular or histological markers. In Alzheimer’s disease (AD), where cognitive decline, emotional dysregulation, and disruptions in adaptive behavior emerge long before overt neuropathology is detectable, behavioral assays provide an indispensable tool for characterizing therapeutic potential. This study underscores the critical role of behavioral testing in evaluating ten phytochemical extracts derived from Rubus fruticosus(FT,LT,FH,LH,PFH,PLH), Abutilon pannosum(A2), Abutilon grandifolium(A1), Rheum palmatum(R), and Zingiber officinale(G) in the 5xFAD transgenic mouse model, integrating in silico predictions with multidimensional behavioral outcomes.

Pharmacokinetic and target-prediction analyses suggested favorable absorption, strong blood–brain barrier permeability, and potential engagement with pathways implicated in synaptic plasticity and neuroprotection. However, behavioral assays were essential for determining whether these theoretical properties translated into meaningful functional effects. A comprehensive battery was employed to probe complementary cognitive and affective domains: Y-Maze for working memory, Novel Object Recognition for recognition memory, Radial Arm Maze for spatial learning, Open Field and Elevated Plus Maze for locomotion and anxiety-like behavior, and Forced Swimming for depressive-like responses.

Behavioral outcomes revealed extract-specific signatures that were not predictable from computational data alone. Most extracts displayed an inverse dose-dependent pattern, with lower doses producing more pronounced improvements in memory performance and emotional regulation, often surpassing the effects of the reference treatment. In contrast, other extracts followed a classical dose-response profile, enhancing cognition at higher doses and increasing exploratory behavior at lower doses.

These findings highlight the irreplaceable value of behavioral testing as a functional bridge between in silico predictions and neurobiological mechanisms. By capturing complex, systems-level outcomes, behavioral assays remain essential for identifying promising neuroactive compounds and for advancing translational research in AD.

Introduction: Current explanations of motivated behavior remain theoretically fragmented across neuroscience, psychology, evolutionary biology, etc. The Proximal Chemical Mandate Principle addresses this fragmentation by proposing that all motivated behavior can be reduced (for unification) to two invariant neurobiological objectives: reward neurochemicals maximization (R↑) (e.g., Dopamine, Opioid , Oxytocin, and more) and/or stress neurochemicals minimization (S↓) (e.g., Norepinephrine, Cortisol, and more).

Methods: We developed this novel theoretical reductionist framework by synthesizing direct evidence from decades of behavioral neuroscience literature, including intracranial self-stimulation, conditioned avoidance paradigms, fiber photometry, and optogenetic studies. The model establishes causal relationships with specific neurochemical signals to motivated behaviors and its ultimate outcome.

Results: Direct experimental evidence demonstrates the following:

Compulsive reward maximization via intracranial self-stimulation, whereby rats repeatedly press levers to stimulate reward pathways despite physiological exhaustion (Olds & Milner, 1954).

Immediate subsecond dopamine encoding of reward value, with nucleus accumbens transients driving motivated action (R↑) within 150–300 ms (Hamid et al., 2021; Mohebi et al., 2024).

Learned stress minimization through conditioned avoidance behaviors (by prediction) that trigger immediately and persist even without immediate threat.

Rapid-onset threat processing via specialized amygdala circuits that detect threats within 120 ms and initiate defensive responses (S↓) within 200 ms (Li et al., 2022).

Real-time instantaneous value–threat integration through prefrontal–striatal circuits that resolve decision conflicts (S↓) within 400–600ms (Zhou et al., 2023).

Conclusions: These findings support a unified novel, testable framework that potentially resolves apparent behavioral paradoxes—including altruism (S↓via altruistic act), addiction (R↑via supernormal stimuli), suicide (S↓), and voluntary childlessness—by demonstrating how identical (R↑,S↓) mandates produce divergent outcomes through contextual implementation. The principle provides testable predictions (if direct mesolimbic dopamine self-stimulation ever stops voluntarily without any other strong environment stimuli, the theory is falsified) for behavioral neuroscience and psychiatry.

Conflicts of interest: None

Introduction

Catatonia is a serious yet often underdiagnosed neuropsychiatric condition marked by disturbances in motor behavior, speech, and responsiveness. Despite its clinical significance, limited tools exist for reliably assessing catatonia outside traditional in-person psychiatric evaluations. The need for remote and standardized assessment tools is urgent in underserved areas where face-to-face consultations may not be feasible. The Bush-Francis Catatonia Rating Scale (BFCRS) [Bush, et al. Acta Psychiatrica Scandinavica, 1996;93:129-136] offers a structured, validated approach to quantifying catatonia symptoms that may be adaptable for remote use.

Methods

As part of an ongoing project [Kadubandi, et al. Development of a rating instrument to identify catatonia by virtual viewing of motor assessments. Zenodo, V3, 2025. https://doi.org/10.5281/zenodo.16061703], a team of eight raters trained in the BFCRS independently viewed and scored videos of motor assessment of a male identified only by age and sex. All assessments were based solely on observed motor behavior. Consensus discussions to agree on a score for each item were conducted after individual ratings were submitted to the organizing committee. Statistical analysis, including inter-rater reliability using Fleiss’ Kappa, was conducted using R software.

Results

Six separate assessments were conducted across five video sessions. Each of the seven raters independently scored 23 BFCRS items. Fleiss' Kappa was used to evaluate inter-rater reliability. The calculated Fleiss’ Kappa values across the six assessments were 0.375, 0.556, 0.576, 0.667, 0.590, and 0.578. The average Fleiss’ Kappa was 0.557, indicating moderate inter-rater agreement, which supports the reliability of the BFCRS when used remotely.

Conclusions

The preliminary application of the BFCRS in a remote assessment framework suggests potential for standardizing catatonia evaluations beyond traditional settings. If validated by further statistical analysis, this approach could improve access to timely diagnosis and intervention, particularly in areas with limited psychiatric resources.

Background:

Stereotyped behaviors are a hallmark of neurodevelopmental disorders, but are often difficult to quantify in real-time, especially in remote clinical settings. These repetitive, non-goal-directed movements can provide critical diagnostic information, yet no dedicated tool currently exists for structured assessment via telehealth. In response, we utilized the Timed Stereotypies Rating Scale (TSRS) [Brašić JR. Treatment of movement disorders in autism spectrum disorders. In: Hollander E (Editor). Autism Spectrum Disorders. Volume 24 of the Medical Psychiatry Series. ISBN 0-8247-0715-X, Marcel Dekker, Inc., New York. 2003;273-346] to identify and rate these behaviors in a patient with hypokinetic catatonia.

Objectives:

As part of an ongoing project [Kadubandi, et al. Development of a rating instrument to identify catatonia by virtual viewing of motor assessments. Zenodo, V3, 2025. https://doi.org/10.5281/zenodo.16061703], we tested the feasibility of applying the TSRS during remote clinical assessments using video recordings shared via teleconferencing platforms.

Methods:

Archived video recordings of a male displaying markedly reduced movements were shown to trained clinical raters during online meetings. The session host shared the screen to present each video. Raters independently used the TSRS to assess the presence, frequency, and severity of stereotyped motor behaviors. After individual ratings, consensus scores were discussed and documented for each video segment.

Results:

Fifteen valid observations were included in the analysis utilizing R. The internal consistency of the TSRS was high, demonstrated by a Cronbach’s alpha of 0.838 across 7 items. Inter-rater reliability was also strong. The Intraclass Correlation Coefficient (ICC) for average measures was 0.804 (95% CI: 0.611–0.923, p < 0.001), indicating excellent agreement among raters when averaging scores. The ICC for single measures was 0.370 (95% CI: 0.183–0.631, p < 0.001), suggesting fair reliability for individual raters.

Conclusions:

Preliminary application of the TSRS in remote settings shows promise as a structured method for evaluating catatonic behaviors virtually.

Introduction: Hypoxic stress disrupts homeostatic balance, triggering neuroendocrine and oxidative responses that manifest as behavioural impairments and biochemical alterations. Elevated corticosterone and oxidative damage are hallmark features of such stress-induced pathology. Solanum campylacanthum, a plant traditionally used as a pest deterrent, lacks empirical evidence supporting its medicinal application. However, its taxonomic synonym Solanum incanum has demonstrated antioxidant activity. This study investigates the potential of ethanol extract of S. campylacanthum leaves (EESC) to counteract hypoxia-induced neurobehavioral and biochemical disturbances in male Wistar rats.

Methods: Acute toxicity was evaluated using Lorke’s method, revealing an oral LD₅₀ exceeding 5000 mg/kg. Rats (150–200 g) were randomized into five orally treated groups (n=6): Group 1—vehicle (10mL/kg, distilled water) without exposure to hypoxia; Groups 2–5—10mL/kg, distilled water, EESC (100, 200, and 400 mg/kg), respectively, one hour before exposure to hypoxia which was induced by placing animals in sealed 450 mL chambers for 20 minutes daily over 14 days. Behavioural assessments (anxiety, depression, memory, and locomotion); serum corticosterone; brain oxidative markers, such as superoxide dismutase (SOD), catalase, glutathione (GSH), and malondialdehyde (MDA); and adrenal weights were evaluated.

Results: Oral administration of EESC significantly alleviated hypoxia-induced behavioural impairments, including anxiety, depressive-like symptoms, motor deficits, and memory decline. Biochemical analysis revealed that treatment with EESC dose-dependently reduced serum corticosterone and brain MDA levels when compared to hypoxic control, indicating suppressed stress and oxidative damage. Concurrently, antioxidant defenses were enhanced, with marked dose-dependent increases in SOD, catalase, and GSH concentrations. Additionally, EESC treatment significantly prevented adrenal gland hypertrophy, suggesting the modulation of the hypothalamic–pituitary–adrenal axis.

Conclusion: These findings collectively indicate that S. campylacanthum extract confers adaptogenic and antioxidant benefits under sustained hypoxic stress, supporting its potential for further pharmacological investigation.