A Student-Centered, Entrepreneurship Development (ASCEND) Undergraduate Summer Research Program: Foundational Training for Health Research.

Increasing the participation of students of African descent and other minoritized populations in the scientific workforce is imperative in generating a more equitable biomedical research infrastructure and increasing national research creativity and productivity. Undergraduate research training programs have shown to be essential tools in retaining underrepresented minority (URM) students in the sciences and attracting them into STEM and biomedical careers. This paper describes an innovative approach to harness students' entrepreneurial desire for autonomy and creativity in a Summer Research Institute (SRI) that has served as an entry point into a multiyear, National Institutes of Health Building Infrastructure Leading to Diversity (NIH BUILD)-funded research training program.

Student Affect During an HBCU Summer Research Program.

The popularity and effectiveness of intensive summer research programs to increase student self-efficacy is known. The Summer Research Institute (SRI) training experience, as part of undergraduate student training in Morgan State University's NIH BUILD program, uses an entrepreneurial approach to prepare students for careers in health-related research. Bandura's self-efficacy theory's (1977) four antecedents are represented in the SRI curriculum, which provides multiple opportunities for mastery experiences and for moments of roused feelings.

Early Life Stress Alters Adult Inflammatory Responses in a Mouse Model for Depression.

Increased levels of pro-inflammatory cytokines and hypothalamic pituitary axis (HPA) activity are strongly associated with depression. Childhood stress and trauma predispose individuals for increased inflammatory tone and major depression in later life, suggesting that early life reprogramming of the stress/immune axis may be involved in the pathogenesis of depression. In this study, we are using a short duration neonatal maternal separation stress (MS) paradigm in mice to test if early life stress can impact plasma and brain inflammatory tone into adulthood.

Effects of brief stress exposure during early postnatal development in balb/CByJ mice: I. Behavioral characterization.

Early life stress has been linked to the etiology of mental health disorders. Rodent models of neonatal maternal separation stress frequently have been used to explore the long-term effects of early stress on changes in affective and cognitive behaviors. However, most current paradigms risk metabolic deprivation, due to prolonged periods of pup removal from the dam.

Neonatal dopamine depletion induces changes in morphogenesis and gene expression in the developing cortex.

The mesocorticolimbic dopamine (DA) system is implicated in mental health disorders affecting attention, impulse inhibition and other cognitive functions. It has also been involved in the regulation of cortical morphogenesis. The present study uses focal injections of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle of BALB/c mice to examine morphological, behavioral and transcriptional responses to selective DA deficit in the fronto-parietal cortex.

Neonatal serotonin depletion alters behavioral responses to spatial change and novelty.

Multiple brain disorders that show serotonergic imbalances have a developmental onset. Experimental models indicate a role for serotonin as a morphogen in brain development. To selectively study the effects of serotonin depletions on cortical structural development and subsequent behavior, we developed a mouse model in which a serotonin neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), is injected into the medial forebrain bundle (mfb) on the day of birth.

Modeling early cortical serotonergic deficits in autism.

Autism is a developmental brain disorder characterized by deficits in social interaction, language and behavior. Brain imaging studies demonstrate increased cerebral cortical volumes and micro- and macro-scopic neuroanatomic changes in children with this disorder. Alterations in forebrain serotonergic function may underlie the neuroanatomic and behavioral features of autism.

Prenatal exposure to the acetylcholinesterase inhibitor methanesulfonyl fluoride alters forebrain morphology and gene expression.

Methanesulfonyl fluoride (MSF) is a CNS-selective acetylcholinesterase (AChE) inhibitor, currently being developed and tested for the treatment of symptoms of Alzheimer's disease. We have previously confirmed that a single in utero exposure to MSF at clinically appropriate doses inhibits AChE activity in fetal rat brain by 20%, and when administered throughout gestation, MSF achieves a 40% level of inhibition. Here, we show that rats chronically exposed in utero to MSF display marked sex-specific differences in morphological development of the cerebral cortical layers compared with controls at 7 days of age.

Sex-specific development of cortical monoamine levels in mouse.

Several mental health disorders exhibit sex differences in monoamine levels associated with dimorphic cortical ontogeny. Studies in rodents support the notion that monoamines can profoundly modulate morphogenesis. Here, we show significant sex and hemisphere differences in BALB/cByJ mice on postnatal day 3 for dopamine (DA) and serotonin (5-TH), supporting the notion that sex differences in early monoaminergic ontogeny may result in dimorphic cortical development.

A morphogenetic role for acetylcholine in mouse cerebral neocortex.

Recently, cholinergic afferents to cerebral cortex have met renewed attention regarding the regulation of plasticity as well as cognitive processing. My laboratory has developed a mouse neonatal basal forebrain lesion paradigm that has contributed considerably to the understanding of cholinergic mechanisms in cortical development. We have shown that transient cholinergic deafferentation, beginning at birth, precipitates alterations in neuronal differentiation and synaptic connectivity that persist into maturity, and contribute to altered cognitive behavior.

Neonatal electrolytic lesions of the basal forebrain stunt plasticity in mouse barrel field cortex.

Previous studies have shown that neonatal electrolytic lesions of basal forebrain cholinergic projections in mice lead to a transient cholinergic depletion of neocortex and to permanent alterations in cortical cytoarchitecture and in cognitive performance. The present study examines whether neonatal electrolytic lesions of the basal forebrain modify neocortical plasticity. Using cytochrome oxidase histochemistry, we compared cross-sectional areas of individual barrels in the barrel field of four groups of postnatal day 8 (P8) old mice that on P1 received either (1) right electrolytic lesions of the basal forebrain, (2) left C row 1-4 whisker follicle ablations, (3) combined lesion treatments or (4) ice anesthesia only.