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Item CAN WE MAKE AN AXON FROM SEMICONDUCTOR MEMRISTORS?(Office of the Vice Chancellor for Research, 2013-04-05) Mirza, Qurat-ul-Ann; Joglekar, YogeshMemristor, a short for memory resistor, is the fourth fundamental circuit element whose instantaneous resistance depends not only on the voltage, but also on the history of the voltage applied to it. This recently discovered titanium dioxide thin film device has characteristics that are analogous to voltage-gated ion channels in biological membranes. In 1952, Alan Hodgkin and Andrew Huxley (HH) introduced an electrical circuit model that described the behavior of a neuron membrane. The electrical circuit consists of a capacitor which is due to phospholipid bilayer, three resistors that represent each ionic channel, and batteries that drive the ionic currents. The purpose of our research was to investigate the characteristics that are shared by both the biological membranes and the memristors. We introduce a minimal Hodgkin-Huxley model for DC applied stimulus in which the leakage channel, membrane capacitance, and potassium equilibrium voltage are absent. We conclude that spiking requires sodium and potassium channels in Hodgkin-Huxley model and, therefore, we predict that two or more distinct memristor species are necessary to mimic the electrical response of a neuron.Item PEG-PDLLA micelle treatment improves axonal function of the corpus callosum following traumatic brain injury(Mary Ann Liebert, Inc., 2014-07-01) Ping, Xingjie; Jiang, Kewen; Lee, Seung-Young; Cheng, Ji-Xing; Jin, Xiaoming; Department of Anatomy & Cell Biology, IU School of MedicineThe initial pathological changes of diffuse axonal injury following traumatic brain injury (TBI) include membrane disruption and loss of ionic homeostasis, which further lead to dysfunction of axonal conduction and axon disconnection. Resealing the axolemma is therefore a potential therapeutic strategy for the early treatment of TBI. Monomethoxy poly (ethylene glycol)-poly (D, L-lactic acid) di-block copolymer micelles (mPEG-PDLLA) have been shown to restore depressed compound action potentials (CAPs) of spinal axons and promote functional recovery after spinal cord injury. Here, we evaluate the effect of the micelles on repairing the injured cortical axons following TBI. Adult mice subjected to controlled cortical impact (CCI) were treated with intravenous injection of the micelles at 0 h or 4 h after injury. Evoked CAPs were recorded from the corpus callosum of coronal cortical slices at 2 days after injury. The CCI caused significant decreases in the amplitudes of two CAP peaks that were respectively generated by the faster myelinated axons and slower unmyelinated axons. Micelle treatment at both 0 h and 4 h after CCI resulted in significant increases in both CAP peak amplitudes. Injection of fluorescent dye-labeled micelles revealed high fluorescent staining in cortical gray and white matters underneath the impact site. Labeling membrane-perforated neurons by injecting a membrane impermeable dye Texas Red-labeled dextran into lateral ventricles at 2 h post-CCI revealed that immediate micelle injection after CCI did not reduce the number of dye-stained cortical neurons and dentate granule cells of the hippocampus, indicating its ineffectiveness in repairing plasma membrane of neuronal somata. We conclude that intravenous administration of mPEG-PDLLA micelles immediately or at 4 h after TBI allows brain penetration via the compromised blood brain-barrier, and thereby improves the function of both myelinated and unmyelinated axons of the corpus callosum.