A feasibility and pilot trial of the Brief Educational Guide for Individuals in Need (BEGIN): Psychoeducation for individuals at risk for psychosis.

Individuals at clinical high risk for psychosis (CHR) report a strong desire for psychoeducation, and clinical guidelines recommend psychoeducation in early psychosis care. Although several CHR psychoeducation models have been developed, additional research is needed to establish the effectiveness of these models. The goal of this study was to conduct a pilot trial of the Brief Educational Guide for Individuals in Need (BEGIN). BEGIN is a brief structured psychoeducation intervention designed to educate CHR individuals on symptoms and treatment options. We conducted a feasibility and pilot study of 25 CHR individuals (60% female, Mage = 20.6, 64% non-White, 52% Hispanic/Latino) identified via the Structured Interview for Psychosis Risk Syndromes. Qualitative interviews were administered to learn about their experience and analyzed using iterative thematic analysis. Participants (n = 12) completed pre- and post-BEGIN self-report measures to assess factors that influence treatment engagement, including CHR knowledge and motivation for therapy. Data were analyzed using Hedges' g effect sizes and paired samples t tests. The intervention completion rate (83%) and therapeutic alliance were high. Qualitative themes and quantitative measures converged on similar results showing how CHR individuals were impacted by receiving psychoeducation via BEGIN, including increased CHR knowledge (g = 1.37), competence to monitor symptoms (g = 0.53), hope (g = 0.87), and motivation for therapy (g = 0.46). This study demonstrated the feasibility, acceptability, and potential benefits of the BEGIN CHR psychoeducation model, including enhancing motivation for treatment. The flexible but standardized format can facilitate BEGIN's implementation and dissemination.This pilot study found that the Brief Educational Guide for Individuals in Need (BEGIN), a standardized five-session psychoeducation intervention for individuals at clinical high risk for psychosis (CHR), was feasible, acceptable, and enhanced mental health literacy and motivation for subsequent treatment. Clinicians can utilize the BEGIN intervention to ensure the empathic provision of psychoeducation when disclosing patients' CHR status. Future research with a larger sample will establish efficacy and the development of a clinician training to facilitate implementation (PsycInfo Database Record (c) 2024 APA, all rights reserved).

A dual-pathway architecture enables chronic stress to promote habit formation.

Chronic stress can change how we learn and, thus, how we make decisions by promoting the formation of inflexible, potentially maladaptive, habits. Here we investigated the neuronal circuit mechanisms that enable this. Using a multifaceted approach in male and female mice, we reveal a dual pathway, amygdala-striatal, neuronal circuit architecture by which a recent history of chronic stress shapes learning to disrupt flexible goal-directed behavior in favor of inflexible habits. Chronic stress inhibits activity of basolateral amygdala projections to the dorsomedial striatum to impede the action-outcome learning that supports flexible, goal-directed decisions. Stress also increases activity in direct central amygdala projections to the dorsomedial striatum to promote the formation of rigid, inflexible habits. Thus, stress exerts opposing effects on two amygdala-striatal pathways to promote premature habit formation. These data provide neuronal circuit insights into how chronic stress shapes learning and decision making, and help understand how stress can lead to the disrupted decision making and pathological habits that characterize substance use disorders and other psychiatric conditions.

Neural mechanisms of comforting: Prosocial touch and stress buffering.

Comforting is a crucial form of prosocial behavior that is important for maintaining social unity and improving the physical and emotional well-being of social species. It is often expressed through affiliative social touch toward someone in distress, providing relief for their distressed state. In the face of increasing global distress, these actions are paramount to the continued improvement of individual welfare and the collective good. Understanding the neural mechanisms responsible for promoting actions focused on benefitting others is particularly important and timely. Here, we review prosocial comforting behavior, emphasizing synthesizing recent studies carried out using rodent models. We discuss its underlying behavioral expression and motivations, and then explore both the neurobiology of prosocial comforting in a helper animal and the neurobiology of stress relief following social touch in a recipient as part of a feedback loop interaction.

insomniac links the development and function of a sleep-regulatory circuit.

Although many genes are known to influence sleep, when and how they impact sleep-regulatory circuits remain ill-defined. Here, we show that insomniac (inc), a conserved adaptor for the autism-associated Cul3 ubiquitin ligase, acts in a restricted period of neuronal development to impact sleep in adult Drosophila. The loss of inc causes structural and functional alterations within the mushroom body (MB), a center for sensory integration, associative learning, and sleep regulation. In inc mutants, MB neurons are produced in excess, develop anatomical defects that impede circuit assembly, and are unable to promote sleep when activated in adulthood. Our findings link neurogenesis and postmitotic development of sleep-regulatory neurons to their adult function and suggest that developmental perturbations of circuits that couple sensory inputs and sleep may underlie sleep dysfunction in neurodevelopmental disorders.

Early life trauma increases threat response of peri-weaning rats, reduction of axo-somatic synapses formed by parvalbumin cells and perineuronal net in the basolateral nucleus of amygdala.

Early life trauma is a risk factor for life-long disorders related to emotional processing, but knowledge underlying its enduring effect is incomplete. This study was motivated by the hypothesis that early life trauma increases amygdala-dependent threat responses via reduction in inhibition by parvalbumin (PV) interneurons and perineuronal nets (PNN) supporting PV cells, thus increasing excitability of the basolateral amygdala (BLA). From postnatal day (PN) 8-12, rat pups of both sexes were reared under normal bedding or under insufficient nest-building materials to induce maternal-to-infant maltreatment trauma (Scarcity-Adversity Model, SAM). At weaning age of PN23, the SAM group exhibited increased threat responses to predator odor. The SAM-induced increase in threat response was recapitulated in normally reared PN22-23 rats that were unilaterally depleted of PNN in the BLA by the enzymes, chondroitinase-ABC plus hyaluronidase at PN19-20. Light and electron microscopic analysis of the BLA revealed that anterior-to-mid levels of SAM group's BLAs exhibited decreased PNN intensity and decreased axo-somatic synapses between PV-to-principal pyramidal-like neurons and PV-to-PV. PV and PNN densities (cells/mm2 ) in the BLA of both control (CON) and SAM groups were still low at PN12 and SAM delayed the ontogenetic rise of PV intensity and PNN density. Moreover, PV cell density in the anterior-to-mid BLA correlated negatively with threat response of CON animals, but not for SAM animals. Thus, reduction of PNN-supported, PV-mediated somatic inhibition of pyramidal cells provides a mechanistic support for the enduring effect of early life maltreatment manifested as increasing innate threat response at weaning.