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Environmental thermal challenges trigger the brain to coordinate both autonomic and behavioural responses to maintain optimal body temperature 1 , 2 , 3 – 4 . It is unknown how temperature information is precisely stored and retrieved in the brain and how it is converted into a physiological response. Here we investigated whether memories could control whole-body metabolism by training mice to remember a thermal challenge. Mice were conditioned to associate a context with a specific temperature by combining thermoregulatory Pavlovian conditioning with engram-labelling technology, optogenetics and chemogenetics. We report that if mice are returned to an environment in which they previously experienced a 4 °C cold challenge, they increase their metabolic rates regardless of the actual environmental temperature. Furthermore, we show that mice have increased hypothalamic activity when they are exposed to the cold, and that a specific network emerges between the hippocampus and the hypothalamus during the recall of a cold memory. Both natural retrieval and artificial reactivation of cold-sensitive memory engrams in the hippocampus mimic the physiological responses that are seen during a cold challenge. These ensembles are necessary for cold-memory retrieval. These findings show that retrieval of a cold memory causes whole-body autonomic and behavioural responses that enable mice to maintain thermal homeostasis. Cold-sensitive engrams contribute to learned thermoregulation in mice that are returned to an environment in which they previously experienced a cold challenge, through a network formed between the hippocampus and hypothalamus that enables the recall of cold-related memories.

Social buffering occurs when the presence of a companion attenuates the physiological and/or behavioral effects of a stressful or fear-provoking event. It represents a way in which social interactions can immediately and potently modulate behavior. As such, social buffering is one mechanism by which strong social support increases resilience to mental illness. Although the behavioral and neuroendocrine impacts of social buffering are well studied in multiple species, including humans, the neuronal underpinnings of this behavioral phenomenon remain largely unexplored. Previous work has shown that the infralimbic prefrontal cortex (IL-PFC) is important for processing social information and, in separate studies, for modulating fear and anxiety. Thus, we hypothesized that socially active cells within the IL-PFC may integrate social information to modulate fear responsivity. To test this hypothesis, we employed social buffering paradigms in male and female mice. Similar to prior studies in rats, we found that the presence of a cagemate reduced freezing in fear- and anxiety-provoking contexts. In accordance with previous work, we demonstrated that interaction with a novel or familiar conspecific induces activity in the IL-PFC as evidenced by increased immediate early gene (IEG) expression. We then utilized an activity-dependent tagging murine line, the ArcCreERT2 mice, to express channelrhodopsin (ChR2) in neurons active during the social encoding of a new cagemate. We found that optogenetic reactivation of these socially active neuronal ensembles phenocopied the effects of cagemate presence in male and female mice in learned and innate fear contexts without being inherently rewarding or altering locomotion. These data suggest that a social neural ensemble within the IL-PFC may contribute to social buffering of fear. These neurons may represent a novel therapeutic target for fear and anxiety disorders.

Animals rely on innate and learned behavior to respond to their environment, but how the brain balances hardwired responses with adaptive flexibility remains unclear. Here, we demonstrate that innate looming stimulus responses in Mus musculus can be attenuated via repeated unreinforced presentation. This attenuation is long-lasting and generalizing, but is rapidly recovered when the stimulus is paired with an electric foot-shock. Fiber photometry recordings reveal attenuation of responses to visual looming stimuli in the SC and PAG, which do not recover following recovery of behavioral responses. Analysis of c-Fos expression uncovered a ventral CA1 (vCA1) ensemble that is active during both innate and learned looming fear responses. We report that this vCA1 engram is not necessary for innate defensive behavior but is necessary for learned fear responses. These findings reveal a novel role of the hippocampus in adapting to looming stimuli, and provide a platform for understanding the interaction of memory and instinct.

Aglajidae is a family of tropical and temperate marine Cephalaspidea gastropod slugs regarded as active predators. In order to better understand their food habits and trophic interactions, we have studied the diet of all genera through the examination of gut contents. Specimens were dissected for the digestive tract and gut contents were removed and identified by optical and scanning electron microscopy. Our results confirmed that carnivory is the only feeding mode in aglajids and showed a sharp preference for vagile prey (94% of food items). We suggest that the interaction between crawling speed, presence of sensorial structures capable of detecting chemical signals from prey, and unique features of the digestive system (e.g. lack of radula, eversion of the buccal bulb, thickening of gizzard walls) led aglajid slugs to occupy a unique trophic niche among cephalaspideans, supporting the hypothesis that dietary specialization played a major role in the adaptive radiation of Cephalaspidea gastropods.

Background: Oral cancer ranks 16th among the most frequent malignant neoplasms worldwide, with a mortality rate of 54% within the first 5 years after diagnosis. It is crucial to develop strategies to improve cure and survival rates. Objective: To develop, validate, and apply an instrument on beliefs about oral cancer to guide future educational, promotional, and preventive activities for this disease. Methods: Cross-sectional study in 318 adults. Content was validated using Lawshe's criteria, and Confirmatory Factor Analysis was used to assess structural validity. Internal consistency was calculated with Cronbach's Alpha. Mann–Whitney U tests were used to compare medians of dimensions based on demographic variables. Results: The final instrument included 18 items across three dimensions (threat, benefits, and cues to action), with adequate fit indicators: RMSEA: 0.051 (95% CI: 0.038–0.063), CFI: 0.93, TLI: 0.916, SRM: 0.063. Internal consistency was good (Alpha between 0.65 and 0.85). 67.3% of participants were women. Significant differences were observed between men and women ( p  = 0.040) and between participants over and under 40 years old ( p < 0.001), in perceived threat as well as in cues to action ( p < 0.001). Conclusion: The Oral Cancer Belief Instrument demonstrated adequate validity and consistency, making it a reliable tool for promoting health prevention strategies.

Spinocerebellar ataxias (SCAs) are autosomal dominant genetic disorders characterized by progressive cerebellar degeneration and phenotypic variability. MJD/SCA3, the most prevalent form around the world and in Latin America, is also likely the most common hereditary ataxia in Uruguay. Despite its relevance, Uruguay lacks comprehensive epidemiological studies, and molecular diagnostics remain inaccessible in public health systems. This review provides a phenotypic description on genetically confirmed patients with MJD/SCA3 as a first step towards generating knowledge on this matter in our country. A retrospective review of 37 Uruguayan patients with suspected SCA was conducted. Sixteen patients with confirmed molecular diagnosis of MJD/SCA3 were included on this review. Data collected encompassed demographic information, genetic testing results, clinical manifestations, and imaging findings. Patients were evaluated at the Ataxias Polyclinic, Hospital de Clínicas, between 2019 and 2024 by the authors. Statistical analyses were performed using SPSS version 29.0. The mean age of symptom onset was 41.75 years, with gait ataxia as the initial symptom in 87.5% of cases. Clinical findings included appendicular ataxia (100%), dysarthria (90%), and oculomotor alterations (90%), with diverse deep sensitivity impairment in 62.5%. Genetic testing revealed an average of 72.9 CAG repeats in the ATXN3 gene. Cerebellar atrophy was observed in 75% of patients with MRI. Most had a diagnostic delay of 6.5 years and an autosomal dominant family history. Findings align with international descriptions of MJD/SCA3 while highlighting regional characteristics, including a potential genetic link with southern Brazil. The absence of dysautonomia, typically prevalent in MJD/SCA3, suggests underdiagnosis or insufficient evaluation. This study underscores the need for systematic clinical and molecular evaluations in Uruguay and serves as a foundation to understand hereditary ataxias at a national level. Further research is essential for improving diagnosis and management of this complex pathology.

Teaching English to refugees, migrants, and multilingual students from a variety of linguistic and cultural backgrounds presents special challenges for teachers and stakeholders. A significant portion of the U.S population (68.99 million) speaks a language other than English at home which creates emotional and scholastic challenges for newcomers adjusting to a new environment. Addressing these challenges requires culturally sensitive, adaptable pedagogical strategies that promote resilience, equity, and confidence for students and teachers. The proposal project -a workshop for educators and stakeholders- emphasizes in the importance of multilingual teachers in fostering inclusive environments and highlights practical actions such as proving language support, creating multilingual resource, and connecting with families. This research includes a literature review, key definitions, language acquisition theories, and recommendations for best practices.

A threat to survival in the wild is vulnerability to infection. The immune system is essential for defence against foreign species which cause sickness. During infection the brain triggers conserved behaviors, including fever, tiredness and anorexia that support immunity. The immune system stores infection information via adaptive immunity, however it remains unclear whether the brain stores immune-related information as long-term memory engrams. Here we demonstrate that mice form contextual memories for sickness events. Upon sickness-memory recall mice lower whole-body metabolism, and increase coactivation between the hippocampus and sickness regions such as the central amygdala, alongside elevated engram activation. Optogenetic reactivation of sickness engrams decreases metabolism, similar to natural recall. Finally, natural recall and artificial reactivation of a sickness-memory increased genes associated with the acute phase response in the liver. These findings suggest that sickness experiences are encoded as engrams, which upon reactivation trigger coordinated metabolic and innate immune responses.