The prefrontal cortex (PFC) receives input from all other cortical regions and functions to plan and direct motor, cognitive, affective, and social behavior across time. It has a prolonged development, which allows the acquisition of complex cognitive abilities through experience but makes it susceptible to factors that can lead to abnormal functioning, which is often manifested in neuropsychiatric disorders. When the PFC is exposed to different environmental events during development, such as sensory stimuli, stress, drugs, hormones, and social experiences (including both parental and peer interactions), the developing PFC may develop in different ways. The goal of the current review is to illustrate how the circuitry of the developing PFC can be sculpted by a wide range of pre-and postnatal factors. We begin with an overview of prefrontal functioning and development, and we conclude with a consideration of how early experiences influence prefrontal development and behavior.neural plasticity | dendritic spines | prenatal stress | psychoactive drugs | metaplasticity T he development of the cerebral cortex reflects more than a simple unfolding of a genetic blueprint; rather, it represents a complex dance of experiential and genetic factors that mold the emerging cerebrum. Pre-and postnatal environmental events, such as sensory stimuli, hormones, parent-child relationships, stress, and psychoactive drugs, modify cerebral development and, ultimately, adult behavior. Although all cerebral regions are influenced by early experience, the effects of experience are significantly different in specific cortical regions. The goal of this article is to review the ways in which one specific region, the prefrontal cortex (PFC), is sculpted by a wide range of pre-and postnatal factors. We begin with an overview of the nature and function of the PFC, followed by a review of experience-dependent modification of prefrontal organization and function. What Is the PFC?Kaas (1) proposed that a few basic areas of cerebral cortex are present in all mammals. These include primary and secondary visual and somatosensory areas (i.e., V1, V2, S1, S2), at least one auditory area and one taste area, a motor area, a transitional strip of cortex that relates the amygdala and hippocampus to other cortical areas (i.e., perirhinal cortex, entorhinal cortex), and a region referred to as the PFC. The definition of the sensory regions is relatively straightforward insofar as they receive unimodal input from the sensory receptor systems (e.g., eye, ear, tongue), and the outputs of the motor cortex are ultimately directed via polysynaptic pathways to effector organs. The outputs of all cortical regions are also components of feedback loops through which the cortex and subcortical regions of the brain mutually influence each other. Although there is no universally acceptable definition of the PFC, it can be regarded to be the region of the cortex that receives its principal thalamic inputs from the mediodorsal nucleus of the thalamus (e.g., 2). This cor...

A B S T R AC TThe aim of this integrative review was to identify the protective factors that contribute to family resiliency. Families are comprised of individuals who interact across levels in a socio-ecological system. Family resiliency does not develop through evasion of risk, but through successful application of protective factors to engage in adverse situations and emerge from them stronger. In an effort to move away from pathological labelling, this review provides a foundation for strength-based family interventions. Thirteen peerreviewed databases were searched for articles and information regarding family resiliency. Careful review yielded 24 protective factors that foster resiliency across three distinct but interactive levels: individual, family and community. The protective factors identified in this review of the literature offer an excellent starting point for development of clinical interventions to support family resiliency.

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ObjectiveWhether sex differences contribute to the heterogeneity of mild traumatic brain injury (mTBI) and repeated mTBI (RmTBI) outcomes in adolescents is unknown. Therefore, this study examined changes in, and differences between, male and female rats following single mTBI and RmTBI.MethodsRats were given a single mTBI, RmTBI (i.e., 3x), or sham injuries. Injuries were administered using a lateral impact model that mimics forces common in human mTBI. After the final injury, rats underwent extensive behavioral testing to examine cognition, motor function, and anxiety‐ and depressive‐like behavior. Postmortem analyses investigated gene expression and structural changes in the brain.ResultsMany of the outcomes exhibited a sex‐dependent response to RmTBI. While all rats given RmTBI had deficits in balance, motor coordination, locomotion, and anxiety‐like behavior, only male rats given RmTBI had short‐term working memory deficits, whereas only females given RmTBI had increased depressive‐like behavior. Volumetric and diffusion weighted MRI analyses found that while RmTBI‐induced atrophy of the prefrontal cortex was greater in female rats, only the male rats exhibited worse white matter integrity in the corpus callosum following RmTBI. Sex‐dependent changes in brain expression of mRNA for glial fibrillary acidic protein, myelin basic protein, and tau protein were also observed following injury.InterpretationThese findings suggest that in adolescent mTBI, sex matters; and future studies incorporating both male and females are warranted to provide a greater understanding of injury prognosis and better inform clinical practice.