Kainate (KA)-induced status epilepticus hyperexcites neurons and activates ionotropic glutamate receptors, including NMDAR, AMPAR, and GluR6. These receptors physically interact with postsynaptic density protein 95 (PSD95) which acts as a scaffolding protein at the postsynaptic membrane. PSD95 activation and its interaction with NMDARs are mediated by Src kinases* which drive hyperexcitability and neurodegeneration. Hyperexcited neurons activate both microglia and astrocytes to induce the expression of inducible nitric oxide synthase (iNOS)* and Src kinase*. The products of these enzymes, and many other proteins, exacerbate hyperexcitability, and activate neuroinflammation and neurodegeneration pathways. Thus, the hypothesis is that PSD95 blocking peptide (PSD95BP; Tat-NR2B9c) and the iNOS inhibitor 1400W will impact KA-induced changes. *Note: The starred proteins were not detected in the present study.

The downstream effect of the interaction between microtubule-associated protein tau and Src family non-receptor tyrosine kinase Fyn was investigated with a tau/Fyn double KO mouse. We demonstrate that tau has a Fyn-independent role in glutamate-induced calcium response and that MAP2 can compensate for tau in interacting with Fyn in dendrites.

Cell-based drug delivery is a promising approach for future neuroprotective therapies. We infected human mesenchymal stem cells to overexpress BDNF and differentiated them to chondrocytes to hypothetically improve their vitality and survival in a delivery matrix. The BDNF-overexpressing hMSCs protect neurons significantly better from degeneration than native MSCs. This finding has a high potential for future clinical application of hMSCs in human neuronal disorders therapy.

The motor role in phonological processing is weighted by the nature of the language tasks, and the consequent task load relative to the target (LIFGop) modulates tDCS effects. Improved performance following cathodal tDCS, for example, in categorical perception, suggests that compensatory mechanisms occur when tasks involve complex neuronal networks.

Antibodies raised against keyhole limpet hemocyanin (KLH) label thousands of peripheral neurons in snails, including those in the eye and sensory epithelium at the base of the tentacles (left) with a high magnification view of the sensory epithelium (right).