Building Ethnically Diverse Digital Collections

Building ethnically diverse collections has always been challenging -- either because minority communities do not see traditional institutions as keepers of their histories or librarians/archivists are not embedded sufficiently in the communities to recognize the value of their materials. And lastly, when communities do donate physical materials, processing and enabling access to these collections can often be slow, due to a myriad of reasons. The perception of a lack of public interest may lead to low processing priority, which only increases the potential for loss. Minority communities\u27 motivation may be negatively impacted, furthering mistrust of traditional institutions and harming any potential momentum in acquiring materials. Open access platforms provide libraries and librarians with new opportunities to develop ethnically diverse collections without donors having to donate and gift items. It also allows the nonspecial collection library from needing the required archival space and requirements to properly house physical materials. At the Cultural Heritage Center at San Jose State University (SJSU), we have been digitizing community and university materials from our race/ethnic communities. SJSU faculty, students, and alumni have been pleased with the discoveries of these collections, which include graduation programs and student publications. Most libraries have access to the common hardware and software that can offer a more inclusive perspective than the traditional Special Collections archives. We will demonstrate how a team of individuals can make libraries\u27 digital collections more inclusive and ethnically rich and diverse

Gβγ and the C Terminus of SNAP-25 Are Necessary for Long-Term Depression of Transmitter Release

Short-term presynaptic inhibition mediated by G protein-coupled receptors involves a direct interaction between G proteins and the vesicle release machinery. Recent studies implicate the C terminus of the vesicle-associated protein SNAP-25 as a molecular binding target of Gβγ that transiently reduces vesicular release. However, it is not known whether SNAP-25 is a target for molecular modifications expressing long-term changes in transmitter release probability.This study utilized two-photon laser scanning microscopy for real-time imaging of action potential-evoked [Ca(2+)] increases, in single Schaffer collateral presynaptic release sites in in vitro hippocampal slices, plus simultaneous recording of Schaffer collateral-evoked synaptic potentials. We used electroporation to infuse small peptides through CA3 cell bodies into presynaptic Schaffer collateral terminals to selectively study the presynaptic effect of scavenging the G-protein Gβγ. We demonstrate here that the C terminus of SNAP-25 is necessary for expression of LTD, but not long-term potentiation (LTP), of synaptic strength. Using type A botulinum toxin (BoNT/A) to enzymatically cleave the 9 amino acid C-terminus of SNAP-25 eliminated the ability of low frequency synaptic stimulation to induce LTD, but not LTP, even if release probability was restored to pre-BoNT/A levels by elevating extracellular [Ca(2+)]. Presynaptic electroporation infusion of the 14-amino acid C-terminus of SNAP-25 (Ct-SNAP-25), to scavenge Gβγ, reduced both the transient presynaptic inhibition produced by the group II metabotropic glutamate receptor stimulation, and LTD. Furthermore, presynaptic infusion of mSIRK, a second, structurally distinct Gβγ scavenging peptide, also blocked the induction of LTD. While Gβγ binds directly to and inhibit voltage-dependent Ca(2+) channels, imaging of presynaptic [Ca(2+)] with Mg-Green revealed that low-frequency stimulation only transiently reduced presynaptic Ca(2+) influx, an effect not altered by infusion of Ct-SNAP-25.The C-terminus of SNAP-25, which links synaptotagmin I to the SNARE complex, is a binding target for Gβγ necessary for both transient transmitter-mediated presynaptic inhibition, and the induction of presynaptic LTD