Digital Histology 2.0: An Open Educational Resource

The teaching of histology is increasingly relying on digital resources in lieu of traditional microscope laboratories. For nearly 20 years, health science education at VCU has depended on a Digital Histology curricular resource on CD-ROM, previously licensed by Wiley Publishing. Now facing issues related to accessibility and technological constraints, this resource is being re-designed as a web-based, mobile-friendly, interactive, open educational resource for VCU health science students and all learners across the world. For the past two decades, there has been a steady decline in the use of microscopes in histology instruction (1,2). As a replacement, a number of digital resources have been developed including image collections published along with the major Histology textbooks. However, these packages mostly offer statically labeled images with limited descriptive text. In 1998, faculty in the department of Anatomy and Neurobiology developed a CD-ROM entitled Digital Histology. While cutting edge at the time, this resource served as a digital atlas with on-demand labeling of structures, interactive quizzes, and formative feedback for more than 6000 VCU medical, dental, graduate, and undergraduate students. However, the shift in standards has rendered this program obsolete and inaccessible to modern devices, including Apple and mobile platforms. Additionally, due to its proprietary authoring software, instructional content can no longer be updated

Differential transactivation of sphingosine-1-phosphate receptors modulates NGF-induced neurite extension

The process of neurite extension after activation of the TrkA tyrosine kinase receptor by nerve growth factor (NGF) involves complex signaling pathways. Stimulation of sphingosine kinase 1 (SphK1), the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (S1P), is part of the functional TrkA signaling repertoire. In this paper, we report that in PC12 cells and dorsal root ganglion neurons, NGF translocates SphK1 to the plasma membrane and differentially activates the S1P receptors S1P1 and S1P2 in a SphK1-dependent manner, as determined with specific inhibitors and small interfering RNA targeted to SphK1. NGF-induced neurite extension was suppressed by down-regulation of S1P1 expression with antisense RNA. Conversely, when overexpressed in PC12 cells, transactivation of S1P1 by NGF markedly enhanced neurite extension and stimulation of the small GTPase Rac, important for the cytoskeletal changes required for neurite extension. Concomitantly, differentiation down-regulated expression of S1P2 whose activation would stimulate Rho and inhibit neurite extension. Thus, differential transactivation of S1P receptors by NGF regulates antagonistic signaling pathways that modulate neurite extension

Digital Histology

Digital Histology is an interactive, online, openly licensed histology text and atlas that presents all the topics covered in professional, graduate and undergraduate histology courses. It is organized as a multi-hierarchy outline that reinforces broader histological concepts and parallels the content of most histology textbooks. Digital Histology, featuring on-demand labeling of structures and interactive quizzes with formative feedback, can be used by a diverse group of learners

Novel role of the nociceptin system as a regulator of glutamate transporter expression in developing astrocytes.

Our previous results showed that oligodendrocyte development is regulated by both nociceptin and its G-protein coupled receptor, the nociceptin/orphanin FQ receptor (NOR). The present in vitro and in vivo findings show that nociceptin plays a crucial conserved role regulating the levels of the glutamate/aspartate transporter GLAST/EAAT1 in both human and rodent brain astrocytes. This nociceptin-mediated response takes place during a critical developmental window that coincides with the early stages of astrocyte maturation. GLAST/EAAT1 upregulation by nociceptin is mediated by NOR and the downstream participation of a complex signaling cascade that involves the interaction of several kinase systems, including PI-3K/AKT, mTOR, and JAK. Because GLAST is the main glutamate transporter during brain maturation, these novel findings suggest that nociceptin plays a crucial role in regulating the function of early astrocytes and their capacity to support glutamate homeostasis in the developing brain

Differential proliferative responses of cultured Schwann cells to axolemma and myelin-enriched fractions. II. Morphological studies

Axolemma-enriched and myelin-enriched fractions were prepared from bovine CNS white matter and conjugated to fluorescein isothiocyanate (FITC). Both unlabelled and FITC-labelled axolemma and myelin were mitogenic for cultured rat Schwann cells. Treatment of Schwann cells with the FITC-labelled mitogens for up to 24 h resulted in two distinct morphological appearances. FITC-myelin-treated cells were filled with numerous round, fluorescent-labelled intracellular vesicles, while FITC-axolemma-treated cells appeared to be coated with a patchy, ill-defined fluorescence, primarily concentrated around the cell body but extending onto the cell processes. These observations were corroborated under phase microscopy. Electron microscopy revealed multiple, membrane-bound, membrane-containing phagosomes within myelin-treated cells and to a far lesser extent in axolemma-treated cells. The effect on the expression of the myelin-mediated and axolemma-mediated mitogenic signal when Schwann cells were treated with the lysosomal inhibitors, ammonium chloride and chloroquine, was evaluated. The mitogenicity of myelin was reduced 70–80% by these agents whereas the mitogenicity of axolemma was not significantly altered under these conditions. These results suggest that axolemma and myelin stimulate the proliferation of cultured Schwann cells by different mechanisms. Myelin requires endocytosis and lysosomal processing for expression of its mitogenic signal; in contrast, the mitogenicity of axolemma may be transduced at the Schwann cell surface.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47376/1/11068_2005_Article_BF01200801.pd