The study was led by Alexei Morozov of the Fralin Biomedical Research Institute at VTC, who has long been interested in how the brain converts environmental warnings into behavior. Scientists have documented for decades that animals cluster together when confronted with acute threats such as predators, a phenomenon sometimes described as collective defense. Far less understood is whether a conditioned stimulus, a neutral signal that has acquired meaning through experience, can recruit the same kind of social pulling-together. The Virginia Tech team designed their experiments specifically to separate the learned nature of the threat from its immediate physical presence, asking whether memory alone could reshape social positioning.

The experimental logic was straightforward but demanding. Each mouse was first trained alone to associate a particular tone with a short, mild foot shock, a standard conditioning procedure that reliably produces a lasting memory of the sound as a predictor of harm. One to two days later, when that memory had consolidated but the shock was long past, the researchers placed the mice in pairs and played the tone again. The animals that had previously lived together drew measurably closer to one another when the tone sounded, while mice paired with unfamiliar partners showed no consistent change in the distance between them. The contrast between the two conditions was the central result: familiarity determined whether the warning signal produced social approach.

Importantly, the tendency to draw closer was not simply a byproduct of freezing, the well-known fear response in which mice become motionless when they detect danger cues. The researchers found no link between how much an animal froze and whether it moved toward its partner, indicating that companion-seeking and freezing are distinct behavioral outputs generated by the same warning signal. This dissociation matters for how scientists interpret fear conditioning experiments more broadly, because it suggests that a single conditioned cue can split into multiple parallel behavioral streams, one expressed through body posture and stillness and the other through deliberate spatial reorientation toward a trusted individual.

What the familiar pairs did was subtle rather than theatrical. The team did not observe overt comforting behaviors such as grooming or huddling of the kind sometimes described in other social species. Instead, their quantitative measure was a decrease in the distance between the animals’ snouts, showing that the familiar mice not only closed the physical gap between them but also oriented their bodies and heads toward one another. That orientation detail is significant, because it implies a directed social engagement rather than random crowding. The animals appeared to be monitoring and positioning themselves relative to a specific, recognized individual, which is precisely the kind of behavior a social-memory system would be expected to regulate.

Morozov framed the stranger result in terms of the ecology of the species. Mice are territorial animals, and an unfamiliar mouse of the same sex can read more like an intrusion than an ally, so a danger cue that would drive a resident toward a known cagemate produces no such effect with a stranger. He drew a parallel to human behavior, noting that people, too, may be less inclined to cooperate with groups they do not know, and that learning about one another can help dissolve that barrier and make collective responses to shared threats easier. The analogy is suggestive rather than direct, but it points to why the researchers believe the circuitry they identified could have relevance well beyond rodent behavior, particularly for neuropsychiatric conditions in which social approach is impaired.

The mechanistic core of the study lies in a specific connection between two of the brain’s most intensively studied structures. The basolateral amygdala is essential for processing threatening cues and attaching emotional significance to sensory signals, while the ventral hippocampus is deeply involved in social memory, the storage and retrieval of information about specific individuals. The researchers temporarily suppressed neuronal communication along the pathway running from the basolateral amygdala to the ventral hippocampus. When that projection was disrupted, the mice no longer moved closer to their familiar companions upon hearing the tone, even though their freezing responses were unchanged. The result cleanly separates the threat-detection side of the circuit from the social-approach side: the animals still recognized the tone as dangerous, but the signal no longer translated into proximity-seeking.

A second line of evidence implicated oxytocin, the neuropeptide famous for its roles in social recognition, bonding and affiliative behavior across mammals. When the team blocked receptors for oxytocin, the overall proximity response disappeared as well. Intriguingly, the researchers have not yet determined exactly where in the brain oxytocin acts to influence this particular behavior, leaving an open question that the group considers a priority for future work. Together, the two manipulations sketch a circuit-level model in which the amygdala, having identified a threat, recruits the hippocampus to coordinate a social response, while the hippocampus simultaneously acts as a gatekeeper, permitting that coordination only between animals with an established social history.

That gatekeeper role is what Morozov sees as the most conceptually interesting aspect of the findings. In his view, the amygdala recognizes the threat and the hippocampus holds the social memories, and the conjunction of the two determines whether danger produces approach or indifference. He has suggested that studying hippocampal activity during these experiments will help uncover how that gate actually operates at the cellular level, a question that touches on one of the central puzzles in social neuroscience: how the brain tags specific individuals as safe or unsafe and then uses those tags to bias behavior in real time. The current study provides the behavioral assay and the first circuit-level leverage points for answering it.

Michael Friedlander, Virginia Tech’s vice president for health sciences and technology and executive director of the Fralin Biomedical Research Institute, emphasized the translational promise of the work. In his assessment, the experiments by Morozov and his team represent far more than the exploration of a basic mechanism; they begin to deliver the kind of mechanistic understanding that will be essential for developing precise therapies for neuropsychiatric disorders in which adaptive social interactions in humans are compromised. Conditions ranging from autism spectrum disorder to social anxiety involve difficulties in deciding whom to approach and under what circumstances, and a defined amygdala-hippocampus circuit gated by oxytocin offers a concrete biological target for that broader clinical effort.

The study was conducted by Wataru Ito and Alexei Morozov of the Fralin Biomedical Research Institute, where Morozov is a faculty member of the Center for Neurobiology Research and also holds an appointment in the Department of Psychiatry and Behavioral Medicine at the Virginia Tech Carilion School of Medicine. The research was published as an experimental study in Neuropsychopharmacology under the title describing proximity in mice induced by an auditory-conditioned stimulus, with an article publication date of 15 July 2026. Funding came from the National Institutes of Health and the Seale Innovation Fund, and the authors declared no competing interests. For a field that has long treated fear conditioning as a story about individual animals and their internal states, the work adds a distinctly social dimension: the brain’s alarm system, it seems, does not merely command the body to freeze or flee, but also checks who is standing nearby before deciding whether closeness is a comfort worth seeking.

Subject of Research: Learned threat cues driving familiarity-dependent social proximity in mice through amygdala-hippocampal circuitry and oxytocin signaling

Article Title: When danger is about, mice look to their friends

Article References: When danger is about, mice look to their friends. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: mice, social behavior, fear conditioning, amygdala, hippocampus, oxytocin, neuropsychopharmacology, threat response, social memory, Virginia Tech, behavioral neuroscience, proximity

Earlier animal work had already hinted that overexposure to digital-style stimulation very early in life, before weaning, could produce hyperactivity, social deficits and disrupted neuroplasticity. What remained unclear was whether the childhood period, after pups are weaned but before adolescence, carries a similar risk. This matters because human screen exposure frequently intensifies during exactly this stage, when children begin choosing their own content and spending longer stretches with tablets, televisions and gaming devices. The Iranian team, led by Amirreza Hosseinzadeh and corresponding author Monireh Mansouri, together with Hamidreza Pouretemad and Mozhan Parsa, designed their experiment to test that specific post-weaning window under tightly controlled laboratory conditions.

The experimental protocol was deliberately simple in concept but rigorous in execution. Male rats, beginning at postnatal day 22, the point of weaning, were placed in front of a display presenting colored lights paired with cartoon sounds for six hours every single day, continuing until postnatal day 52, which corresponds roughly to adolescence in the rat. This sustained regimen of excessive audiovisual stimulation, abbreviated EAVS by the authors, was intended to model, in a controlled fashion, the kind of high-intensity, fast-paced sensory input that digital media delivers to developing children. The animals were then put through a battery of standard behavioral assays designed to probe the domains most commonly affected in autism spectrum disorder: social interaction, repetitive behavior, and activity levels.

The behavioral results were unambiguous. Rats that had experienced the daily audiovisual overstimulation showed markedly increased repetitive behaviors, one of the diagnostic hallmarks of autism spectrum conditions. They also demonstrated impaired social interaction, engaging less and differently with conspecifics than their normally reared peers. In addition, the exposed animals were hyperactive, moving with an intensity and persistence not seen in controls. Together, the three behavioral changes map onto the classic triad that researchers look for when building animal models of autism-like phenotypes, and their co-occurrence after a purely environmental manipulation is the most provocative aspect of the study.

Behavior alone, however, does not explain mechanism, so the team turned to quantitative neuroanatomy. Using three-dimensional stereological measurement, a technique that allows unbiased estimation of structure volumes and cell numbers from systematically sampled tissue sections, the researchers examined the amygdala, the almond-shaped complex in the medial temporal lobe that assigns emotional significance to sensory input and is heavily implicated in social behavior. What they found was significant enlargement of the amygdala overall, along with an increased number of neurons in two of its key subregions: the basolateral nucleus, which integrates sensory and cortical information feeding into the amygdala, and the central nucleus, which serves as the main output station driving emotional and autonomic responses.

This pattern of structural plasticity is technically significant because the amygdala occupies an unusual position in autism research. Human neuroimaging studies of autism spectrum disorder have variously reported amygdala enlargement in young children with the condition, and altered connectivity between the amygdala and social brain networks is a recurring finding. The fact that a purely environmental input, six hours per day of colored lights and cartoon sounds, was sufficient to drive both volume increases and neuron number increases in the basolateral and central subregions suggests that developmental sensory overstimulation can push the amygdala along a growth trajectory that mirrors, at least superficially, the structural differences observed in clinical populations. The authors are careful, however, to frame this as an autism-like phenotype rather than a model of autism itself.

That caution is important and the researchers state it explicitly. Rodents do not voluntarily choose their media, so the model cannot capture the motivational and behavioral complexity of human device use, where children actively seek out screens and their exposure patterns vary enormously. What the model does offer is experimental control: a defined stimulus, a defined duration, a defined developmental window, and a homogenous genetic background. Within those constraints, the study isolates the neurobiological consequences of sensory overstimulation per se, free from the confounds of family environment, socioeconomic status, or pre-existing developmental differences that complicate every human screen-time study. It is precisely this control that human correlational research can never achieve.

The timing of the manipulation also carries an implicit message about brain development. Postnatal day 22 to 52 in the rat encompasses a period of intense experience-dependent plasticity, when circuits in the limbic system and cortex are being refined by environmental input. The amygdala, in particular, continues to mature through this window, and the increased neuron counts observed in the basolateral and central nuclei indicate that the overstimulation did not merely alter existing neurons but was associated with changes in neuronal population size, whether through altered neurogenesis, altered survival, or shifts in the timing of developmental cell loss. Untangling which of those mechanisms is responsible will be a natural target for follow-up work, as will determining whether the effects persist into adulthood or can be reversed by returning the animals to normal environments.

For the broader public conversation about children and screens, the study does not say that tablets cause autism. Autism spectrum disorder is a strongly heritable, multifactorial condition, and no single environmental exposure can be called its cause. What the research does support is a narrower and still consequential claim: that the developing brain, through at least the childhood years, is structurally and behaviorally responsive to the intensity and character of its sensory environment, and that sustained, excessive exposure to fast, colorful, noisy audiovisual input can bias that development toward patterns of behavior and brain structure that resemble aspects of autism. Previous work had established this vulnerability for the pre-weaning period; this study extends it into the post-weaning phase, closing a gap that parents and pediatricians had every reason to wonder about.

The study was funded by the Iran Cognitive Sciences and Technologies Council and approved by the Ethics Committee of Shahid Beheshti University, conducted in accordance with the National Institutes of Health Guide for the Care and Use of Laboratory Animals. Its publication as an open-access article ensures that the full methods, stereological protocols and raw behavioral data are available for scrutiny and replication. As debate over childhood screen exposure continues to intensify worldwide, work of this kind provides the kind of mechanistic, experimentally controlled evidence that observational studies alone cannot supply, and it will likely fuel further research into how the timing, duration and content of sensory stimulation interact to shape the social and emotional brain during development.

Subject of Research: Effects of post-weaning excessive audiovisual stimulation on autism-like behavior and amygdala structure in rats

Article Title: Post-weaning audiovisual overstimulation induces autism-like phenotypes and amygdala structural plasticity in rats

Article References: Hosseinzadeh, A., Mansouri, M., Pouretemad, H., & Parsa, M. (2026). Post-weaning audiovisual overstimulation induces autism-like phenotypes and amygdala structural plasticity in rats. BMC Neuroscience. https://doi.org/10.1186/s12868-026-01041-2

Image Credits: AI Generated

DOI: 10.1186/s12868-026-01041-2

Keywords: autism spectrum disorder, audiovisual overstimulation, amygdala, brain development, rats, screen exposure, behavioral neuroscience, stereology, social interaction, repetitive behavior, hyperactivity, childhood

The parabrachial nucleus, a compact structure tucked into the dorsolateral pons, has long been recognized as a major relay station for alarm signals traveling from the body and spinal cord up to forebrain circuits. CGRP-expressing neurons in this region project densely to the central amygdala, the bed nucleus of the stria terminalis and other threat-processing hubs, and earlier work established that artificially activating these neurons produces powerful aversive states and widespread fear-like responses. What remained less clear was whether CGRP signaling in the parabrachial nucleus influences not just the intensity of fear, but the specific behavioral form that fear takes, an issue the new study set out to address directly.

To do so, the researchers employed a platform-based active avoidance paradigm, an experimental setup in which a rodent can terminate or avoid an aversive stimulus by moving onto a raised platform. Unlike classical Pavlovian fear-conditioning assays, which measure freezing as the primary output, active avoidance tasks capture the animal’s capacity to translate threat detection into goal-directed escape behavior. This distinction is crucial, because freezing and active avoidance are not simply different intensities of the same response; they represent distinct defensive strategies governed by partially separable neural circuits, and animals typically select between them based on factors such as the distance to the threat, the availability of escape routes and previous experience with the environment.

The central manipulation involved pharmacological or chemogenetic inhibition of CGRP signaling within the parabrachial nucleus. When CGRP activity was suppressed, the researchers observed a striking reorganization of defensive behavior: animals spent less time in the passive, immobile freezing posture that normally dominates their response to learned threat cues, and instead escalated their engagement with the active avoidance strategy, rapidly locating and mounting the escape platform. In other words, dampening CGRP did not blunt fear altogether, as one might naively predict if the peptide were simply a universal fear amplifier. Rather, it redirected the defensive response, channeling the animal’s motivational energy from one stereotyped strategy into another.

This dissociation carries substantial theoretical weight. Classical models of fear conditioning have often treated freezing as the canonical index of conditioned fear, so much so that a pharmacological intervention reducing freezing would conventionally be interpreted as anxiolytic or fear-reducing. The new results challenge that inference. Animals with inhibited parabrachial CGRP signaling were not less afraid; they were differently afraid, mobilizing an active coping strategy in place of an immobile one. The study therefore reinforces an increasingly influential view in behavioral neuroscience: that fear must be measured across a repertoire of adaptive responses, and that single-measure assays can systematically mischaracterize the effects of neural or pharmacological manipulations.

From a mechanistic standpoint, the findings suggest that CGRP neurons in the parabrachial nucleus act as a biasing signal within a distributed defensive decision network. These neurons are well positioned for such a role. They integrate interoceptive alarm signals, including those carried by the spinal trigeminal and lamina I spinothalamic pathways, and broadcast the resulting arousal state to forebrain structures that execute specific defensive programs. Projections to the central amygdala have been implicated in promoting passive defensive reactions, whereas circuits running through the ventrolateral periaqueductal gray and basal ganglia loops are more closely associated with active escape and avoidance. By altering the gain of CGRP signaling at the source, the manipulation appears to rebalance competition between these downstream effectors, tilting the system toward the active option.

The platform-based paradigm proved especially informative because it allowed within-subject quantification of both response types. Rather than relying on separate cohorts of freezing-conditioned and shuttle-box-trained animals, the researchers could observe individual animals distributing their behavior between immobility and platform escape across trials. This design revealed that the shift from freezing to avoidance was not a threshold artifact or a byproduct of altered shock sensitivity; instead, it reflected a genuine reweighting of strategy selection, consistent with a decision-level function for parabrachial CGRP rather than a purely sensory or motor role.

The translational implications are significant, particularly for post-traumatic stress disorder and other trauma- and anxiety-related conditions in which patients exhibit maladaptive defensive postures. Human PTSD is often characterized not only by exaggerated fear responses but by inflexibility in choosing among coping strategies, including a failure to engage active avoidance or escape behaviors that might reduce harm. If CGRP signaling in the parabrachial-amygdala pathway similarly constrains active coping in humans, drugs that modulate CGRP receptors, a class already developed and clinically validated for migraine prophylaxis through gepant compounds, could conceivably be repurposed or re-evaluated for their effects on defensive strategy selection. The new study does not establish such clinical effects, but it provides a rigorous animal-model foundation for asking the question.

More broadly, the work exemplifies a shift in how learning and memory research frames threat-related behavior. Instead of treating fear as a unitary internal state read out through a single behavioral channel, contemporary neuroscience increasingly emphasizes a menu of genetically and anatomically specified defensive circuits whose relative activation determines the observable strategy. CGRP neurons in the parabrachial nucleus now appear to be one of the clearest molecularly identifiable control points for that selection process. By demonstrating that inhibition of this specific neuropeptide population reconfigures, rather than diminishes, defensive behavior, the study offers both a conceptual lesson, that fear research must account for strategy switching, and a practical one, that assays capturing active coping are indispensable for interpreting interventions aimed at threat-related circuitry. As attention turns to how upstream inputs and downstream targets partition the freezing-versus-avoidance decision, the parabrachial CGRP system is likely to remain a focal point for understanding how brains choose how to be afraid.

Subject of Research: Role of CGRP neurons in the parabrachial nucleus in selecting between freezing and active avoidance defensive strategies

Article Title: CGRP inhibition in the PBN shifts defensive strategy from freezing to active avoidance in a platform-based active avoidance paradigm

Article References: CGRP inhibition in the PBN shifts defensive strategy from freezing to active avoidance in a platform-based active avoidance paradigm. (n.d.). https://doi.org/10.1038/s41539-026-00453-3

Image Credits: AI Generated

DOI: 10.1038/s41539-026-00453-3

Keywords: CGRP, parabrachial nucleus, active avoidance, freezing, fear conditioning, defensive behavior, threat processing, amygdala, neuropeptides, behavioral neuroscience, PTSD, platform-based avoidance paradigm

The right anterior temporal lobe has emerged over the past decade as a hub of what researchers call socioemotional semantics: the stored knowledge that allows us to understand what emotions are, what they mean, and how they apply to particular people and situations. Whereas the left temporal lobe is dominant for verbal and factual semantic knowledge, the right hemisphere appears to carry a disproportionate share of conceptual knowledge about the social and emotional world. Work by Younes and colleagues, published in Brain in 2022, argued that right temporal degeneration produces a distinctive semantic variant of behavioral frontotemporal dementia in which this socioemotional knowledge base erodes. Patients may retain vocabulary and general facts while losing the ability to grasp the emotional significance of faces, voices, and situations. The consensus statement from the International Working Group on right temporal predominant frontotemporal dementia, published in Communications Medicine in 2025, formalized this clinical picture and highlighted how frequently the condition goes unrecognized in ordinary practice.

That recognition problem is not trivial. A multicenter retrospective cohort study led by Ulugut and colleagues in Alzheimer’s & Dementia in 2024, spanning dozens of memory clinics across Europe and North America, documented how often patients with right anterior temporal predominance receive delayed or incorrect diagnoses. Because their symptoms are emotional and behavioral rather than linguistic, they are frequently mislabeled as having primary psychiatric disorders, and their brain scans may be misread because radiologists are more accustomed to left-sided temporal atrophy patterns. The clinical stakes of understanding exactly what goes wrong in the emotional brain in this variant are therefore high, both for diagnosis and for counseling families about what to expect as the disease progresses.

The Leuven-led study approaches the problem with a methodological twist. Rather than asking simply which brain regions light up when patients view emotional material, the researchers apply pattern expression analysis, a technique refined by Tor D. Wager and collaborators over the past decade. Pattern expression methods rely on multivariate neural signatures: spatial maps of voxel-level activity weights that have been derived in large independent samples and validated as sensitive and specific markers of particular mental states. Among the signatures relevant to this work are a neural signature for picture-induced negative affect developed by Chang and colleagues in PLoS Biology, a distributed signature for the subjective experience of fear described by Zhou and colleagues in Nature Communications, and dissociable signatures of empathic care and empathic distress described by Ashar and colleagues in Neuron. By projecting each patient’s brain activity patterns onto these signatures, the researchers can estimate, on a continuous scale, how strongly a given emotional process is expressed in an individual brain.

This approach matters because univariate activation analysis, the traditional workhorse of functional MRI, is poorly suited to degenerative diseases. Atrophy and signal loss in the damaged tissue can mask genuine changes in how remaining neural circuitry functions, and emotions are represented in distributed, overlapping networks rather than in single blobs of activation. Pattern expression sidesteps some of these limitations by summarizing whole-network geometry. The technical pipeline underpinning the study draws on well-established neuroimaging infrastructure: structural images processed with FreeSurfer and the Desikan gyral parcellation for regional volume estimates, cortical thickness compared against normative data compiled by Potvin and colleagues, and functional images preprocessed with the FMRIPrep pipeline described by Esteban and colleagues in Nature Methods. These choices place the findings on a reproducible, transparent footing that other groups can adopt.

The theoretical backdrop is the idea, articulated most influentially by Mesulam, that large-scale neurocognitive networks encode knowledge through representation, inference, and transcendent encoding across heterogeneous cortical hubs. Within that framework, the right anterior temporal lobe functions as a convergence zone for nonverbal conceptual knowledge, including knowledge of emotions, faces, and social scripts. Hurley and colleagues demonstrated a nonverbal route to conceptual knowledge involving the right anterior temporal lobe, and Lambon Ralph, Jefferies, Patterson, and Rogers provided the computational account of semantic cognition that situates such hubs within a controlled semantic retrieval system. When the hub degenerates, the downstream consequence is not simply local dysfunction but a degradation of the distributed network’s ability to construct emotional meaning from sensory input.

Previous imaging work in frontotemporal degeneration has already hinted at how this cascade unfolds. De Winter and colleagues showed in Cortex that amygdala atrophy alters emotion-related activity in face-responsive cortical regions, demonstrating that structural damage to one node of the emotion network propagates functionally to distant nodes. Marshall and colleagues mapped the functional neuroanatomy of emotion processing across the frontotemporal dementias in Brain, and Lindberg and colleagues documented altered empathy processing in the disease in JAMA Network Open. Rouse, Binney, Patterson, Rowe, and Lambon Ralph proposed a neuroanatomical and cognitive model of impaired social behavior that integrates atrophy in temporal and frontal networks. The new letter extends this line of inquiry by asking not merely where emotional processing falters but how the characteristic spatial patterns of emotional brain activity are expressed, or fail to be expressed, in right temporal variant patients.

The study was conducted in compliance with the Declaration of Helsinki and approved by the ethics committee of University Hospitals Leuven, with written informed consent from all participants, and the authors report no conflicts of interest. Funding for the work was provided in part by the Research Foundation Flanders, KU Leuven, the King Baudouin Foundation, and the Sequoia Fund for Research on Ageing and Mental Health. The data supporting the findings are available on request from the corresponding author but are not publicly accessible, because they contain information that could compromise participant privacy. Corresponding author Jan Van den Stock, whose laboratory has long focused on social and emotional processing in dementia, led the collaboration together with senior co-authors including Mathieu Vandenbulcke and Dartmouth’s Tor D. Wager.

For the field, the significance of this work lies in its convergence of two research programs that have developed largely in parallel: the clinical nosology of right temporal variant frontotemporal dementia, now consolidated by international consensus, and the computational neuroscience of emotion signatures, now mature enough to be applied to individual patients. If validated patterns of emotional brain response can be measured reliably in this patient group, the same metrics could eventually serve as biomarkers for early diagnosis, as targets for interventions aimed at preserving socioemotional competence, and as outcome measures in trials of disease-modifying therapies. For families coping with a disorder that erodes the emotional core of personhood, the study offers something more modest but no less valuable: a rigorous, mechanistic account of what is happening inside the brain when a loved one’s emotional world begins to change, and a demonstration that modern imaging science can now see that change with increasing precision.

Subject of Research: Emotional brain responses and pattern expressions in right temporal variant frontotemporal dementia

Article Title: Emotional brain responses and pattern expressions in right temporal variant frontotemporal dementia

Article References: Emotional brain responses and pattern expressions in right temporal variant frontotemporal dementia. (n.d.). https://doi.org/10.1007/s00415-026-14117-0

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14117-0

Keywords: frontotemporal dementia, right temporal variant, emotional processing, fMRI, pattern expression, neural signatures, amygdala, socioemotional semantics, right anterior temporal lobe, empathy, neurodegeneration, Journal of Neurology