Topic: chronic social defeat stress

Mood disorders are characterized by behavioral changes arising from network-level alterations, with the amygdala (AMY)-ventral hippocampus (vHPC) pathway being a central component. Anhedonia, the reduced ability to feel pleasure, is a core feature of mood disorders. However, how stress-induced changes in motivation to seek and consume rewards are represented in the activity patterns in the AMY and vHPC remains unclear. Furthermore, how these activity patterns can inform pathway-specific manipulations to rescue anhedonic behavior remains to be explored. Here, we used Neuropixels probes to recor

Serotonin (5-hydroxytryptamine; 5-HT) plays an important role in a wide range of mental abilities, including modulation of emotions, motivation, and impulse control. Pathological changes in serotonin levels are associated with mental disorders such as depression, anxiety, and aggression. Chronic stress or traumatic experiences are thought to trigger the development of depression. However, only a subset of individuals experiencing chronic stress or traumatic life events develop depressive-like behavior (susceptible), while others remain resilient. In order to investigate multiple aspects of dep

Despite its critical importance to social animals, the mechanisms underlying the establishment of new social interactions remain largely unknown. We identified a role for neurons expressing neuropeptide B/W receptor-1 (NPBWR1) in the central amygdala (CeANpbwr1 neurons) in this process. CeANpbwr1 neurons were activated only during physical interactions with unfamiliar mice, but not with familiar mice. Manipulations of the neuronal circuit comprising CeANpbwr1 neurons suggested that this excitation was essential for sustaining physical interactions with novel conspecifics. Remarkably, stimulati

The basolateral amygdala (BLA) is increasingly recognized as a key regulator of depression and anxiety-like behaviors. However, the specific contribution of individual BLA neurons to these behaviors remains poorly understood. Building on our previous study, which demonstrated increased activity in glutamatergic BLA neurons in response to aversive stimuli and that enhancing inhibition in the BLA can alleviate depressive-like behaviors, we investigated the role of individual GABAergic neurons (BLAGABA) in depressive and anxiety-like phenotypes. Our findings indicate that BLAGABA neurons show dec

The stress response serves as a protective mechanism to address daily challenges, yet it's crucial for it to cease when the threat subsides, as prolonged stress engagement links to higher vulnerability to neuropsychiatric disorders.Lysine Specific Demethylase 1 (LSD1) is an epigenetic enzyme participating in the CoREST/HDAC2 corepressor complex regulating neuronal plasticity-related gene transcription. In the mammalian brain, LSD1 activity is modulated by its neurospecific splicing isoform neuroLSD1, lacking co-repressive activity as long as the ability to recruit corepressor partners. Numerou

Environmental stress plays a key role in the development of psychiatric disorders, and also has a negative impact on sleep integrity. Insomnia and sleep disturbances are core symptoms observed in patients with stress-related disorders. However, stress reactivity is the result of a combination of genetic and environmental influences that ultimately impacts one’s physiology and behavior in a variety of ways. In this project we will focus on stress susceptibility and how it could trigger psychiatric diseases in a peculiar gene-environment interaction.Studying glutamatergic neurotransmission, we d

Chronic psychosocial stress is a significant risk factor for the development of stress-associated psychiatric disorders, including major depressive disorder, which causes profound debilitation and has increasing worldwide prevalence. Pre-clinical and clinical studies have linked peripheral immune system alterations to stress-related disorders, such as elevated levels of proinflammatory immune cells and cytokines in circulation. Endothelial cells are critical components of the blood-brain barrier (BBB), as they interface directly with immune cells and their released factors, which can enter the

Aims: Investigation of differences in synaptic inputs from ventral tegmental area (VTA), ventral hippocampus (VH) and basolateral amygdala (BLA) on anterior cingulate cortex(ACC) neurons across all cortical layers between stress susceptible (SS) and stress resilient (SR) mice. Methods: Projections from VTA, VH and BLA excitatory neurons were labeled with cyan, green and yellow pre-eGRASP and ACC pyramidal neurons were labeled with post-eGRASP and TagRFP-T. Three weeks later, 10 mice were exposed to chronic social defeat stress for 10 days and on 11th day mice were divided into SS and SR groups