Social interactions are essential for neuronal development and emotional behavior. In particular, play behavior during adolescence facilitates neural and social development, whereas social isolation is detrimental and increases stress vulnerability in rodents. Furthermore, stress exposure during the juvenile and adolescent periods increases the risk of post-traumatic stress disorder in adulthood. Adolescent male rats emit 50-kHz ultrasonic vocalizations that reflect positive affect induced by rough-and-tumble play or tickling. We previously demonstrated that tickling, which mimics play behavior, induces positive affect and modulates fear-related behaviors as well as sympathoadrenal stress responses. Building on these findings, the present study investigated whether positive emotional experiences induced by this tickling procedure during adolescence can mitigate with long-term alterations in stress vulnerability following early-life stress exposure at weaning. Male Fischer rats were reared under three conditions from postnatal day 21: group-housed (three per cage), isolated (one per cage), or tickled (isolated and receiving 5 min of daily tickling stimulation). In adulthood, animals were subjected to a battery of behavioral tests, including the open-field, elevated plus-maze, forced swim, and fear conditioning tests. In rats that were socially isolated after weaning, repeated tickling incorporating handling during adolescence was associated with fewer behavioral alterations induced by juvenile foot-shock exposure and social isolation, particularly in the forced swim and fear conditioning tests. These findings suggest an association between positive experiences during adolescence and more favorable emotional outcomes following early-life stress.
BackgroundGambling disorder (GD) is a behavioral addiction characterized by impaired impulse control and fronto-limbic cortical dysfunction. EEG theta cordance, which integrates absolute and relative power to index regional cerebral perfusion and metabolism, has not previously been combined with directional predictive modeling in behavioral addiction research.ObjectiveTo compare regional resting-state theta cordance between GD patients and healthy controls (HCs), and to examine directional predictive associations between cortical cordance and clinical severity indices.MethodsIn this retrospective observational study, 28 male patients with DSM-5 GD and 29 male HCs underwent 21-channel resting-state EEG (eyes-closed, 3-min artifact-free epochs; 4–8 Hz). Theta cordance was computed using the Leuchter algorithm and averaged into eight regions of interest. Clinical measures included the South Oaks Gambling Screen (SOGS), Beck Depression Inventory-II, Beck Anxiety Inventory, and illness duration. Group differences were tested with independent-samples t-tests (with Bayesian complements) and Pearson correlations; an exploratory vector autoregressive (VAR)-based directional predictive framework was applied to cross-sectional observations.ResultsGD patients showed significantly lower central (0.03 ± 1.18 vs. 1.25 ± 1.23; t(55) = −3.79, p < 0.001, d = −1.00) and higher left parietal cordance (t(55) = 2.12, p = 0.039, d = 0.56), with trend-level occipital (p = 0.058) and left temporal (p = 0.067) differences. No cordance–clinical correlations were significant (all p > 0.10). VAR-based analysis identified asymmetric predictive associations: prefrontal (F = 4.60, p = 0.042) and frontocentral cordance (F = 6.65, p = 0.017) with SOGS; central cordance with illness duration (F = 5.77, p = 0.024) and right temporal cordance (F = 5.53, p = 0.027); and reciprocal clinical-to-cortical associations (SOGS→central, F = 4.82, p = 0.038; duration→right temporal, F = 4.53, p = 0.044). HCs showed temporo-occipital directional patterns without clinical correlates.ConclusionCortical theta cordance and clinical severity in GD appear reciprocally associated within an exploratory directional framework. Findings are preliminary given the modest, male-only, single-site sample and cross-sectional design, and require longitudinal confirmation.
Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by social communication deficits and restricted, repetitive behaviors, often accompanied by motor, cognitive, and anxiety-related alterations. Although ASD is diagnosed more frequently in males than females, females remain underrepresented in preclinical studies, limiting understanding of sex-dependent phenotypes. The BTBR T+ Itpr3tf/J (BTBR) mouse strain is a widely used animal model of ASD, yet its sex-specific behavioral profiles across functional domains remain incompletely characterized. Here, we conducted a systematic, multi-domain behavioral assessment in male and female BTBR mice and wild-type (WT) controls, examining action control, motor learning, social behavior, and anxiety-related exploration. Despite normal acquisition of instrumental responding, BTBR mice exhibited altered action control characterized by reduced habitual responding and persistent sensitivity to action-outcome contingencies following extended habit training, with effects being more pronounced in females. In the accelerating rotarod task, BTBR mice displayed impaired motor learning that was more prominent in males, whereas performance under constant-speed conditions indicated largely preserved baseline motor coordination. Social impairments were dimension-specific: BTBR males showed delayed initiation of social investigation, whereas BTBR females exhibited reduced social engagement. In the elevated plus maze (EPM), overall genotype effects were modest; However, sex-dependent differences emerged within BTBR strain, suggesting altered exploratory behavior and risk-assessment strategies rather than generalized anxiety-like behavior. Together, these findings identify domain- and sex-specific alterations in action selection, motor learning, social behavior and anxiety-related exploration in BTBR mice. These results highlight the importance of sex-stratified analyses in preclinical ASD research and provide a behavioral framework for investigating the mechanisms underlying ASD-relevant phenotypes.
BackgroundAlthough cognitive impairment (CI) is common in multiple sclerosis (MS), conventional cognitive rehabilitation is often limited by accessibility and adherence challenges. Telerehabilitation offers an accessible alternative, but its efficacy across different CI severity levels remains unclear. The present prospective, single-center, single-arm interventional study with repeated measures aimed to identify changes in cognitive and psychosocial outcomes following a home-based cognitive telerehabilitation program with weekly synchronous coaching in MS patients with mild versus moderate CI, and to explore whether baseline impairment severity was associated with differences in change over time.MethodsSixty-six MS patients (34 mild CI; 32 moderate CI) completed a 12-week home-based cognitive telerehabilitation program (five sessions/week), supported by weekly Skype coaching. Outcomes were assessed at baseline (T0), post-intervention (T1), and 3-month follow-up (T2). Cognitive and emotional-behavioral functioning were investigated using standardized, validated instruments in the MS population. Changes over time and between-group differences were analyzed using linear models.ResultsAt T1, both groups improved in attention, verbal memory, and subjective cognitive perception (all p < 0.05). Processing speed improved only in mild CI (p < 0.001), whereas executive function improved only in moderate CI (p = 0.007). At T2, mild CI further improved in attention and verbal memory (p = 0.003–0.035), while moderate CI improved only in processing speed (p = 0.006). Emotional-behavioral outcomes improved in both groups at T1 (anxiety p = 0.002; depression p = 0.023; fatigue p < 0.001) and were largely maintained at T2, with no statistically significant between group differences. Mental quality of life improved over time, whereas physical quality of life remained unchanged.ConclusionFollowing the intervention, both groups showed improvements in cognitive and emotional-behavioral outcomes, with larger and more sustained changes in mild CI. These findings should be confirmed in randomized controlled studies.
IntroductionThe brain’s white matter is responsible for communication across the brain and because attention relies on coordinated communication among distributed brain networks, white matter dysfunction may contribute to attentional impairment. Attention problems are among the most common long-lasting cognitive symptoms of mild traumatic brain injury (mTBI) and as attention is fundamental to many aspects of cognition, the effects of attentional impairment can be broad. mTBI-induced effects on oligodendrocytes and myelin contribute to cognitive deficits following injury and myelin plasticity is a potential mechanism for functional recovery. The aims of this work were to investigate the effects of mTBI and inhibition of oligodendrogenesis on attention in mice, and evaluate the contribution of newly generated oligodendrocytes to behavioral recovery following injury.MethodsThis study used the Myrf conditional knockout mouse model, in which the Myrf gene, required for oligodendrocyte precursor cell (OPC) differentiation into mature myelinating oligodendrocytes, is deleted from OPCs following tamoxifen injection, thereby halting oligodendrogenesis. Mice were trained on the 5-Choice Serial Reaction Time (5-CSRT) task before receiving tamoxifen followed by three mTBI or sham procedures. Attention was probed on the 5-CSRT task with decreasing stimulus duration at four timepoints following injury out to 12 weeks.ResultsWhile no mTBI-induced attentional impairment was observed, OPC-MyrfKO mice showed lower accuracy (β = −4.26%, pBonf = 0.003) across injury groups, timepoints and stimulus durations, and fewer premature trials at the later timepoints (genotype-by-timepoint interaction pBonf = 0.03; β = −4.8%, p = 0.017 at 8 weeks and β = −5.19%, p = 0.027 at 12 weeks), suggesting that active oligodendrogenesis is required for sustained attention and task engagement.ConclusionThese results suggest that myelin plasticity in adulthood may contribute to attention and complex task performance. The mouse model of mTBI used did not impact attention as measured by the 5-CSRT task, thus further research is required to elucidate the role of oligodendrogenesis in post-mTBI cognitive recovery.
IntroductionOxytocin (OXT) has emerged as a key neuromodulator of social cognition, yet the precise neural circuits underlying its role in social memory remain poorly defined. In this study, we identify a specific mechanism by which OXT regulates social memory encoding through the lateral entorhinal cortex (LEC), a critical gateway to the hippocampus.MethodsUsing whole-cell patch-clamp recordings in mouse brain slices, we examined the effects of OXT on stellate neurons in the superficial layers of the LEC. Behavioral analyses were performed to determine the role of intra-LEC OXT signaling in the encoding and retrieval of social memory. Pharmacological blockade of OXTRs in the LEC was used to assess its effects on social recognition memory and spatial memory performance.ResultsOXT excited stellate neurons in the superficial layers of the LEC via activation of oxytocin receptors (OXTRs). This excitation was mediated by membrane depolarization and enhanced excitatory synaptic transmission, as evidenced by an increased amplitude of miniature excitatory postsynaptic currents. Intra-LEC OXT signaling was essential for the encoding, but not the retrieval, of social memory. Pharmacological blockade of OXTRs in the LEC selectively impaired social recognition memory without affecting spatial memory performance. Furthermore, inhibition of OXTRs during the recall phase did not disrupt memory expression, indicating a specific role in memory formation.DiscussionThese findings establish the LEC as a critical node for OXT-dependent modulation of social memory and suggest that OXT enhances the flow of social information to the hippocampus via direct excitation of LEC stellate neurons. This circuit-specific action provides a mechanistic basis for the selective influence of OXT on social cognition and highlights the LEC–hippocampal pathway as a potential target for therapeutic intervention in social memory deficits associated with neuropsychiatric disorders.
Social touch, provided by body tactile stimulation (TS), is known to trigger appeasement behavior and social stability in mammals. Recent studies have shown that TS also plays a role in regulating social interactions in fish by reducing aggression between individuals. While this effect may stem from decreased aggression in dominants, the potential contribution of increased appeasement behavior in subordinates has been overlooked. Here, we investigated whether TS facilitates the onset of appeasement behavior in the cichlid fish Geophagus iporangensis, a species that exhibits clear dominance-subordination relationships. Isolated individuals were assigned to one of two treatments, either with TS (provided by plastic sticks lined with silicone bristles) or without it for 21 days. Then, each fish was paired with a socially experienced dominant individual to enable rapid hierarchy resolution. Initial appeasement scores did not differ between treatments. However, individuals who experienced TS exhibited significantly higher appeasement scores during the final 5 min of the contest than the control group. Additionally, fish under TS showed an increase in the appeasement score after 10 min of agonistic interaction, while it did not change in the treatment without TS. Overall, this study provides the first evidence that TS can mitigate aggressive interactions by intensifying subordinates’ appeasement behavior, thereby affecting social dynamics similarly to mammals.
Killing is the most extreme behavior that an animal can perform toward another. Rodents are one of the best examples of evolutionary adaptation, being the mammals with the highest number of species and having developed an impressive variety of forms and behaviors, which allow them to live and thrive in the most disparate habitats across all continents except for Antarctica. Moreover, rodents are the most widely employed animal model in biological research. An appropriate knowledge of the ethology of rodents is of particular importance both for basic science and for the employment of these animals as animal models. Since they are common targets of both terrestrial and aerial predators, rodents are frequently viewed merely as prey animals. Nevertheless, it is less known that rodents can also be proficient killers. In fact, most rodents are opportunistic predators. Additionally, rodents perform several non-predatory killing behaviors. However, due to historical reasons (according to the early traditional views, rodents were considered small, exclusively herbivorous animals lacking killing instincts), the killing behaviors of rodents have long been overlooked. In this article, we present an overview of rodent killing behaviors, considering a wide variety of species and genera. Killing behaviors are classified into four major categories: predation (upon invertebrates, fish, amphibians, reptiles, birds and mammals), antipredatory killing, social competition-induced killing (intraspecific and interspecific), and infanticide (non-parental and parental). Notably, killing behaviors are present in the majority of rodent species and can be found in all five rodent suborders (Myomorpha, Sciuromorpha, Hystricomorpha, Castorimorpha, and Anomaluromorpha). The present work is the first in which these diverse types of rodent killing behaviors are described together. This not only allows a synoptical view of killing behaviors, but can also aid in identifying the boundaries between the different categories, making the classification of the specific killing behaviors easier. In the final section, we discuss ethical issues related to research on rodent killing behaviors, and we propose methodological options for addressing such issues in future investigations of these behaviors.
The platform-mediated active avoidance (PMA) task has been used as a rodent model of decision-based active avoidance in which rats learn to avoid a tone-signaled shock. Prior studies utilizing the PMA task have primarily investigated avoidance, freezing, and food-seeking behaviors, but few studies have thoroughly assessed darting behavior, a more recently identified measure of fear that has been largely explored in conditional fear paradigms. Here, we investigated the properties of darting that occur during the PMA task, in which rats either acquired the PMA task alone or with a social partner. We found that rats undergoing solitary PMA produced significantly more darting bouts, whereas rats undergoing social partner PMA produced darts that were faster and shorter in duration. We also found that darting in solitary PMA was predominantly concentrated at the platform, whereas darting in social partner PMA occurred more often outside of the platform and lever zones. Analysis of darting trajectories, which included movements surrounding each darting bout, revealed that darting was embedded in a broader spatially-organized movement between the platform and lever zones, especially during solitary PMA, and this pattern increased across training days. These findings suggest that darting between the platform (safety) and lever (reward) zones reflects transitions between defensive and reward-seeking behaviors, a pattern that strengthens across training and is modulated by social partner condition.
Sleep bruxism is a prevalent sleep-related motor phenomenon characterized by rhythmic masticatory muscle activity that ranges from physiological behavior to a condition with clinically significant craniofacial consequences. Existing models emphasize multifactorial risk factors and centrally mediated dysregulation but lack a unified mechanistic account linking neural regulation, autonomic physiology, airway function, craniofacial biomechanics, and the temporal organization of rhythmic masticatory muscle activity. In this Hypothesis and Theory article, we outline a Free Energy Principle (FEP) – informed framework in which sleep bruxism is interpreted as an expression of predictive regulation and active inference within nested craniofacial, autonomic, and respiratory systems, explicitly as a theoretical account rather than as an empirically established mechanism. Within this framework, we introduce the construct of homeostatic latency, defined conceptually as the temporally extended window over which polysomnographic and electromyographic indices of sleep bruxism frequency, intensity, and inter-episode intervals reflect the efficiency of recovering a quasi-stable equilibrium after arousal-related perturbations. From this, we derive testable hypotheses regarding: (i) clustering of rhythmic masticatory muscle activity around micro-arousals and respiratory events, (ii) characteristic autonomic signatures preceding episodes, (iii) homeostatic latency profiles derived from EMG timing measures, (iv) airway-related phenotypes and responses to mandibular advancement devices, and (v) differentiated profiles across stress-related, arousal-related, respiratory – airway protective, and neuromodulatory sleep bruxism endotypes. In addition, we briefly indicate how an FEP-informed ontological framework for SB could, in future work, be extended into a domain-specific, knowledge-graph – based representation to support integration of multimodal data and hypothesis-driven computational modeling, while emphasizing that such tools are not developed or validated in the present article. Overall, the framework aims to reconcile sleep bruxism as both behavior and condition, in line with contemporary consensus views, and to generate falsifiable predictions for future empirical studies.
ObjectiveThis study aimed to investigate the mechanisms underlying impaired sustained attention under positive acceleration stress.MethodsWe used a lower body negative pressure model to simulate positive acceleration stress and employed electroencephalography (EEG) to observe changes in brain function.ResultsEEG results indicated that sustained attention exhibited a dissociation effect between early and late stages of processing following positive acceleration stress. The latency of the P2 component induced by non-target stimuli at the Cz electrode was significantly reduced under lower body negative pressure conditions, suggesting enhanced early perceptual processing of visual stimuli under acceleration stress. The amplitude of the P300 component induced by non-target stimuli at the Pz and Cz electrodes was significantly lower than that at baseline, suggesting impaired late-stage response selection processes. These findings indicate that individuals exhibit adaptive capacity under cerebral ischemia induced by acceleration stress, whereby enhanced early perceptual processing may partially compensate for impairments in the late-stage response selection phase.ConclusionThe dissociation between the early and late stages of visual attention processing reflects the body’s adaptive adjustment ability in response to acceleration stress.
Background:Aquatic exercise combines structured physical activity, sensorimotor training, and social participation, and may be an acceptable adjunctive intervention for children with autism spectrum disorder (ASD). However, existing trials are limited by small samples, heterogeneous outcomes, and complex data structures. Objective:To evaluate the effects of aquatic exercise on ASD-related symptoms or behaviors, motor or physical function, autism severity, stereotyped behaviors, social function, and other outcomes in children with ASD. Methods:Controlled studies comparing structured aquatic exercise with passive or active controls were included. Hedges' g was calculated using post-intervention values, with positive values favoring aquatic exercise. Random-effects models were fitted using restricted maximum likelihood with Knapp-Hartung confidence intervals. For outcomes with only 2 studies, fixed-effect sensitivity analyses were also reported. Change-score analyses and sensitivity analyses using different pre-post correlation assumptions were performed. Multiple motor outcomes from the same study were combined within study. Results:Six studies involving 159 children were included for overall ASD-related symptoms or behaviors. Aquatic exercise showed a favorable effect compared with control conditions (g = 1.31, 95% CI 0.63-1.99, p = 0.004; I 2 = 45.5%), and the result remained stable in leave-one-out and change-score sensitivity analyses. Four studies involving 119 children were included for broad motor or physical function. The pooled effect favored aquatic exercise but did not reach statistical significance and showed very high heterogeneity (g = 2.35, 95% CI -0.11 to 4.80, p = 0.056; I 2 = 90.2%). After excluding the study with estimated data, the effect decreased to g = 1.60 (95% CI -0.71 to 3.91). CARS/CARS-2, stereotyped behaviors, and social function each included only 2 studies, with unstable model-based inferences. Subgroup analyses did not identify significant differences by control type, intervention duration, or training frequency. Conclusion:Aquatic exercise may improve overall ASD-related symptoms or behaviors in children with ASD. Evidence for motor function and other specific outcomes remains limited, heterogeneous, and exploratory. Systematic review registration:https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420261436475.
A multitude of studies have confirmed the essential role of the hippocampus in the acquisition and updating of associative experience. In rodents, spatial memories are dependent on hippocampal information processing and encoding. The role of the dorsal hippocampal pole is well documented, but information about the roles of the intermediate and ventral hippocampus in spatial learning are few and often contradictory. Here, we used fluorescence in situ hybridization (FISH) to identify nuclear expression of the immediate early (IEG) gene, Homer1a, that was triggered by specific spatial learning events in hippocampal neurons of adult male rats. We compared IEG expression in the cornu ammonis (CA) and dentate gyrus (DG) along the proximodistal and dorsoventral hippocampal axis, triggered by novel learning about spatial constellations of large (macroscale), or partially concealed (microscale) objects within a familiar environment. We observed that the dorsal hippocampus predominates with regard to the neuronal encoding of both forms of spatial content information, whereby the distal CA1 (dCA1) and proximal CA3 (pCA3) preferentially encode microscale spatial location. The infrapyramidal blade of the DG, as well as pCA3, encode macroscale information. The intermediate CA shows increased IEG expression in dCA1 triggered by novel microscale information, but the DG of neither the intermediate, nor ventral, hippocampus encode macroscale information. The ventral hippocampus exhibits IEG expression patterns that are unique in comparison to the other two structures: here, both CA1 (proximal and distal) and pCA3 encode macroscale information. Taken together, these findings suggest that the intermediate and ventral hippocampus support spatial memory encoding, but may do so in support of differentiated and distinct aspects of associative learning.
IntroductionNeural development is regulated by several spatiotemporally changing factors, which are essential for enabling neurons to develop functional networks, during early developmental stages. Additionally, external physical stimuli, like scanning prenatal ultrasound (US) examination, may influence neural development. Aim of our study is to examine potential consequences of diagnostic level ultrasound exposure during the early phase of hippocampal CA1 neural network development by using computational models.MethodsUsing in silico modelling, this study explores and compares multiple features of intraneuronal dendritic signal propagation in US-treated and control CA1 pyramidal neurons to look for possible alterations caused by US. We used morphological data of CA1 neurons based on previous morphometric datasets and built high-fidelity subthreshold passive and active segmental cable models of these neurons in the NEURON simulator. To simulate dendritic signalling either a current was injected or a synapse was activated at hundreds of dendritic points of model neurons, eliciting local postsynaptic potentials (PSPs), and multiple descriptors of dendritic impulse propagation between dendritic points and soma were computed.ResultsOur computer models predict that diagnostic level US treatment does not induce changes in specific membrane resistance and capacitance of neuronal membrane. Correlative analyses of simulated dendritic impulse propagation in US treated (UT) and non-treated control neurons (NT) revealed minor differences in attenuations and delays of somatopetally propagating PSPs in the passive model, and these alterations became even less pronounced when hyperpolarization-activated cyclic nucleotide-gated (HCN) cation channels and A-type potassium (KA) channels were inserted into the model. Synaptic input pattern recognition between UT and NT neurons showed no significant alterations.DiscussionWe conclude that subthreshold somatopetal signalling properties of US-treated CA1 neuronal membranes remain predominantly at the level of non-treated cells. This conservation is due primarily to HCN channels, contributing to net membrane conductance at rest in an inhomogeneous manner over the somato-dendritic surface. The HCN channels balance the effects of US-induced morphological alterations on dendritic signalling. Conservation of signalling properties align with our independent prediction on the conservation of synaptic integration and input pattern recognition in UT neurons.
Coping factors, such as perceived or actual behavioral control over some aspect of an adverse event, are associated with resilience and are often argued to help optimize or even dampen glucocorticoid responses to stressors. Interestingly, when coping responses (i.e., stressor controllability) are experimentally manipulated in animals, controllable and uncontrollable stressors produce identical peripheral glucocorticoid responses despite eliciting markedly different behavioral outcomes. However, these studies have been conducted exclusively in male rats. In the present study, we investigated corticosterone (CORT) levels in female rats using the same controllability parameters that have been shown to produce differences in behavioral outcomes. Replicating previous studies, both controllable [escapable shock (ES)] and uncontrollable [inescapable shock (IS)] stress produced equivalent elevations in CORT levels in male rats. In contrast, in female rats, IS produced a greater increase in CORT levels than ES. We further assessed in the same animals whether initial controllability alters the CORT response to a future challenge. In male rats, but not female rats, prior IS (Time 1) sensitized the CORT response to subsequent IS (Time 2), an effect blocked by prior ES. Finally, in a separate cohort, the female controllability difference in the acute plasma CORT response was not observed in medial prefrontal cortex or striatal regions. Prefrontal expression of 11β-hydroxysteroid dehydrogenase type 1, an enzyme that regulates local concentrations of CORT, was increased in female rats exposed to ES relative to those exposed to IS. These results support the growing evidence that stress-induced differences in peripheral CORT are not necessarily reflected in brain structures that support behavioral outcomes, potentially due to regulatory mechanisms at the local tissue level.
Stroke is a leading cause of death and disability, affecting over 15 million people each year. Developing effective therapies depends on accurate, scalable methods to assess sensorimotor recovery in preclinical models. Standard motor tests like grid walking and ladder tests rely on manual scoring, limiting objectivity and throughput. To address this, we compared a commercially available automated ladder test with a newly developed deep learning-based grid walking test using DeepLabCut (DLC) in a photothrombotic stroke model in mice. Our results show that the automated ladder test system failed to detect significant unilateral deficits in stroke animals. It did not capture the expected increase in missteps in the affected forepaw after stroke, even though motor cortex infarcts were confirmed histologically, and the functional impairment was apparent with manual scoring in the grid walking test. In contrast, our DLC-based grid walking model provided fully automated quantification of this widely used test. It achieved millimeter-scale tracking accuracy and detected a ∼3-fold increase in foot faults in stroke-affected mice compared to controls, clearly differentiating between affected and unaffected forepaws for at least 2 weeks post-stroke. These findings expose the limitations of the commercial automated ladder test and demonstrate that the DLC-based pose-estimation-assisted misstep quantification in grid-walk test provides greater sensitivity for detecting motor deficit.
Romantic love lacks a mechanistic, testable evolutionary account. Prior work notes parallels with mother–infant bonding but leaves the genetic architecture and falsifiable predictions unspecified. We argue that romantic love evolved not through the evolution of new “love genes,” but by altering the regulation of existing genes: changing when, where, and under what physiological conditions these genes are active. This regulatory co-option framework generates several falsifiable predictions: (1) a shared genetic basis between maternal bonding and romantic love, (2) the involvement of non-coding, regulatory DNA regions in the brain, (3) a largely shared genetic architecture between the sexes, with differences in gene expression, and (4) genetic signals localized to specific brain circuits. We outline specific genomic and statistical methods to test these predictions, establishing clear criteria that would support or refute our hypothesis. This work shifts the study of romantic love’s evolution from analogy to a program of empirical inquiry and hopes to shed light on how social monogamy entered the Homo sapiens lineage. Key challenges include the lack of high quality meta-analytic fMRI evidence of romantic love and the scarcity of detailed data from relevant human brain circuits.
IntroductionThe age of the world’s population is continuing to increase, and older individuals are continuing to consume alcohol. Preclinical animal research has demonstrated that aged animals are significantly more sensitive to the effects of alcohol than younger animals and the effect of alcohol in aged animals is often sex dependent.MethodsThe current project investigates if acute alcohol administration produces sex dependent effects in hypothermia and spatial memory impairments in aged female and aged male Sprague Dawley rats.ResultsAcute alcohol administration produced sex dependent effects in that hypothermia in female rats was significantly greater following administration of 1.0 g/kg alcohol but not following 2.0 g/kg alcohol. However, spatial memory impairments were similar between aged female and aged male rats following a 1.0 g/kg alcohol challenge.DiscussionThe current results demonstrate in aged animals that alcohol administration produces sex dependent effects in some tasks and highlight the importance of determining the impact of alcohol in older adults as well as younger subjects.
IntroductionSpatial memory relies on distributed hippocampal–cortical networks that are highly sensitive to modulation of excitability, connectivity, and synaptic plasticity. Transcranial magnetic stimulation (TMS) has emerged as a promising tool to experimentally probe and therapeutically modulate these networks, although its effects on spatial memory remain heterogeneous.MethodsWe conducted a PRISMA-guided systematic review synthesizing evidence from rodent and human studies examining the effects of TMS on spatial memory. A total of 35 studies (23 animal, 12 human) identified through searches of Scopus, Web of Science, and PubMed were included, encompassing a broad range of stimulation protocols, behavioral paradigms, and neurophysiological outcomes.ResultsIn animal models, TMS consistently improved spatial learning and memory under pathological conditions, including neurodegenerative, vascular, stress-related, and injury models. These effects were associated with convergent mechanisms, including restoration of hippocampal long- term potentiation, modulation of neurotrophic signaling, reduced apoptosis and neuroinflammation, enhanced synaptic plasticity, and recovery of hippocampal network function. In contrast, findings in healthy animals were mixed and strongly dependent on stimulation parameters. Human findings were similarly variable. Improvements were observed in some clinical populations, whereas results in healthy individuals were inconsistent and task dependent. Neurophysiological evidence indicated modulation of oscillatory activity and hippocampal–cortical connectivity, although these changes did not always translate into measurable behavioral effects.DiscussionOverall, TMS effects on spatial memory appear to be strongly state-dependent, reflecting interactions between stimulation parameters and underlying circuit integrity. Further research should prioritize multimodal approaches integrating behavioral and neurophysiological measures, particularly in clinical populations, to improve mechanistic understanding and translational applicability.Systematic review registrationhttps://osf.io/, identifier 10.17605/OSF.IO/32VWN.
