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Social recognition, the ability to recognize individuals that were previously encountered, requires complex integration of sensory inputs with previous experience. Here, we use a variety of approaches to discern how oxytocin-sensitive neurons in the PFC exert descending control over a circuit mediating social recognition in mice. Using male mice with Cre-recombinase directed to the oxytocin receptor gene (), we revealed that oxytocin receptors (OXTRs) are expressed on glutamatergic neurons in the PFC, optogenetic stimulation of which elicited activation of neurons residing in several mesolimbic brain structures. Optogenetic stimulation of axons in the BLA arising from OXTR-expressing neurons in the PFC eliminated the ability to distinguish novel from familiar conspecifics, but remarkably, distinguishing between novel and familiar objects was unaffected. These results suggest that an oxytocin-sensitive PFC to BLA circuit is required for social recognition. The implication is that impaired social memory may manifest from dysregulation of this circuit. Using mice, we demonstrate that optogenetic activation of the neurons in the PFC that express the oxytocin receptor gene () impairs the ability to distinguish between novel and familiar conspecifics, but the ability to distinguish between novel and familiar objects remains intact. Subjects with autism spectrum disorders (ASDs) have difficulty identifying a person based on remembering facial features; however, ASDs and typical subjects perform similarly when remembering objects. In subjects with ASD, viewing the same face increases neural activity in the PFC, which may be analogous to the optogenetic excitation of oxytocin receptor (OXTR) expressing neurons in the PFC that impairs social recognition in mice. The implication is that overactivation of OXTR-expressing neurons in the PFC may contribute to ASD symptomology.
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http://dx.doi.org/10.1523/JNEUROSCI.2944-18.2019 | DOI Listing |
Neuropsychopharmacology
September 2025
Neuroscience Center, HiLIFE, University of Helsinki, Helsinki, Finland.
Chronic treatment with fluoxetine, a widely prescribed selective serotonin reuptake inhibitor (SSRI), is known to promote neural plasticity. The role of fluoxetine in plasticity has been particularly tied to parvalbumin-positive interneurons, a key population of GABAergic neurons that regulate inhibitory tone and network stability. While our previous studies have highlighted fluoxetine-induced plasticity in the visual cortex and hippocampus, its cell-type-specific effects in the prefrontal cortex (PFC) remain unclear.
View Article and Find Full Text PDFInt J Eat Disord
September 2025
Department of Physiology, Monash University, Clayton, Victoria, Australia.
Objective: Converging evidence from neuroimaging studies and genome-wide association study (GWAS) suggests the involvement of prefrontal cortex (PFC) and striatum dysfunction in the pathophysiology of anorexia nervosa (AN). However, identifying the causal role of circuit-specific genes in the development of the AN-like phenotype remains challenging and requires the combination of novel molecular tools and preclinical models.
Methods: We used the activity-based anorexia (ABA) rat model in combination with a novel viral-based translating ribosome affinity purification (TRAP) technique to identify transcriptional differences within a specific neural pathway that we have previously demonstrated to mediate pathological weight loss in ABA rats (i.
Recent advances in neuroscience enable recording neuronal signals across hundreds of channels while subjects perform complex tasks involving multiple stimulus dimensions. In this study, we developed a novel encode-decode-classify framework employing a gated recurrent variational autoencoder (VAE) to decode decision-making processes from over 300 simultaneously recorded neuronal channels in the prefrontal cortex and basal ganglia of monkeys performing a multidimensional feature-learning task. Using hierarchical stratified sampling and balanced accuracy, we trained and evaluated the model's ability to predict behavioral choices based on neuronal population dynamics.
View Article and Find Full Text PDFJ Cogn Neurosci
September 2025
Neuroscience and Neuroengineering Research Laboratory, Biomedical Engineering Department, School of Electrical Engineering, Iran University of Science and Technology (IUST), Narmak, Tehran, Iran.
Neocortical circuits consist of multiple neuronal cell types, each likely playing distinct roles in flexible behavior. However, studies of decision-making have often overlooked these cell types, limiting our understanding of their specific contributions to local circuit functions. To address this, we simultaneously recorded neuronal activity from the frontal eye field (FEF), lateral PFC, and lateral intraparietal area (LIP) in a macaque monkey performing a visuomotor decision-making task.
View Article and Find Full Text PDFBrain Behav Immun
August 2025
Department of Psychology and Neuroscience, University of Colorado Boulder, Boulder, CO 80301, USA.
Exposure to stressors elevates glucocorticoid (GC) levels in the periphery and brain, directly impacting neurogenesis, neuronal morphology and function, as well as neuroinflammatory processes. The ability to exert behavioral control over an adverse event prevents many of the sequelae of stressor exposure; however, extensive evidence indicates that this protection occurs without concomitant reductions in hypothalamic-pituitary-adrenal (HPA) axis activity. Given that brain GC levels can be regulated independently of changes in HPA output, we investigated whether controllability might alter corticosterone (CORT) levels and CORT-sensitive gene expression in rat brain, even though it does not modulate peripheral CORT.
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