Topic: early-life stress

Early postnatal development is a critical period for the configuration of neural networks that support emotional and socioaffective behaviors. In this sense, children raised in stressful environments are at high risk of developing maladaptive behaviors immediately or later in life, including antisocial and aggressive behaviors. However, the neurobiological bases of such phenomena remain poorly understood. Here, we showed that, in the long-term, maternal separation with early weaning (MSEW) decreased the density of somatostatin (SST) interneurons in the basolateral amygdala (BLA) of females and

Early-life stress alters brain function and increases the risk of suffering psychiatric disorders later in life. Sustained stress affects the response of the mesolimbic dopaminergic (DA) system. That system regulates the activational component of motivated behavior, including effort-based decision-making. The aim of our study was to evaluate the impact of social distancing starting at PND28 (SD - two mice per cage separated by a wall with holes) on the willingness to exert effort during adulthood in an operant procedure. In this task, mice of both sexes were trained in different schedules that

Early-life stress (ELS) disrupts brain development and predisposes sufferers to stress-related disorders and compulsive behaviour in adulthood. Accumulating evidence connects these disorders with neurons within the stress-sensitive, brainstem nucleus incertus (NI), which synthesize the neuropeptides, relaxin-3 (RLN3) and cholecystokinin (CCK). Although NI RLN3 neurons are implicated in stress responses, arousal and drug-seeking behaviour, their vulnerability to stress during development has not been explored, and little is known about NI CCK neurons. Therefore, this study investigated the infl

Alzheimer’s disease (AD) is a highly prevalent age-related neurological disorder, characterized by progressive cognitive decline and accumulation of neuropathological hallmarks in various brain regions. Emerging research highlights early-life stress (ELS) as a significant risk factor in its pathogenesis. We and others have demonstrated in preclinical models that ELS exacerbates both pathology of AD and glial response to amyloid-overexpression. Recently, we demonstrated possible convergence of ELS, AD and mitochondrial dysfunctions, utilizing proteomic analysis of synaptosomes​. Seeking to unde