Building a Service Corps: Using Capacity Building Strategies to Promote Service-Learning and Social Entrepreneurship Within a Higher Education Consortium

This article entails a case analysis of a sample of schools from a higher education network or consortium in partnership with The Algernon Sydney Sullivan Foundation.  The Foundation seeks to empower students and communities through civic engagement and social entrepreneurship.  A primary mechanism for doing so is by developing and cultivating a network of 70 colleges and universities, thereby enabling the Foundation’s capacity to educate and prepare nearly 250,000 collegians for life-long and intentional careers in social change-making.  To assist with this endeavor, the Foundation commissioned this study to assess the existing service corps and social entrepreneurship framework of its partner institutions.  Using a capacity-building framework, the study includes findings from a survey of existing service-learning and social entrepreneurship programs and initiatives as well as recommendations for strengthening the Sullivan network or higher education consortium to provide more formal service-learning and social entrepreneurial experiences for collegians.

Reductions in synaptic proteins and selective alteration of prepulse inhibition in male C57BL/6 mice after postnatal administration of a VIP receptor (VIPR2) agonist

RATIONALE: An abundance of genetic and epidemiologic evidence as well as longitudinal neuroimaging data point to developmental origins for schizophrenia and other mental health disorders. Recent clinical studies indicate that microduplications of VIPR2, encoding the vasoactive intestinal peptide (VIP) receptor VPAC2, confer significant risk for schizophrenia and autism spectrum disorder. Lymphocytes from patients with these mutations exhibited higher VIPR2 gene expression and VIP responsiveness (cAMP induction), but mechanisms by which overactive VPAC2 signaling may lead to these psychiatric disorders are unknown. OBJECTIVES: We subcutaneously administered the highly-selective VPAC2 receptor agonist Ro 25-1553 to C57BL/6 mice from postnatal day 1 (P1) to P14 to determine if overactivation of VPAC2 receptor signaling during postnatal brain maturation affects synaptogenesis and selected behaviors. RESULTS: Western blot analyses on P21 revealed significant reductions of synaptophysin and postsynaptic density protein 95 (PSD-95) in the prefrontal cortex, but not in the hippocampus in Ro 25-1553-treated mice. The same postnatally-restricted treatment resulted in a disruption in prepulse inhibition of the acoustic startle measured in adult mice. No effects were observed in open-field locomotor activity, sociability in the three-chamber social interaction test, or fear conditioning or extinction. CONCLUSION: Overactivation of the VPAC2 receptor in the postnatal mouse results in a reduction in synaptic proteins in the prefrontal cortex and selective alterations in prepulse inhibition. These findings suggest that the VIPR2-linkage to mental health disorders may be due in part to overactive VPAC2 receptor signaling during a critical time of synaptic maturation