Inside Silicon Research Articles

Measurement of High Voltage Stress Induced Traps Inside Thin Silicon Oxide Films

ABSTRACTAfter thin silicon oxide films were stressed at high voltages, two changes occurred in the current-voltage and transient current characteristics of the films. The low-level, pre-tunneling current rose and the transient decay of the current after removal of a voltage pulse changed from an exponential RC time constant decay to a very long decay that was characterized by a 1/t time dependence. Using an extension of the tunneling front discharge model, previously developed to describe the transient changes in the threshold voltages of transistors after avalanche injection or irradiation, the 1/t time dependence was derived. This 1/t transient discharge current was used to determine the density and distribution of the traps inside of the oxide after the high voltage stress. The technique and model used for determining the trap densities and distributions from the transient currents will be described. The model was used to describe the charging of traps in the oxide.

Nerve cables formed in silicone chambers reconstitute a perineurial but not a vascular endoneurial permeability barrier

The passage of molecules into the endoneurial environment of the axons of normal peripheral nerve is regulated by two permeability barriers, the perineurial-nerve barrier and the endoneurial blood-nerve barrier. These barriers exist because of the presence of tight junctions between adjacent perineurial cells and adjacent endothelial cells. In the present study we investigated whether permeability barriers form in nerve cables, which develop inside silicone chambers. The sciatic nerves of adult rats were cut, and the proximal and distal ends sutured into opposite ends of silicone chambers that were filled with dialyzed plasma. The presence of barriers was determined with the tracer horseradish peroxidase (HRP), which was injected intravenously and detected histochemically in tissues by light and electron microscopy. At four weeks, a regenerated nerve cable extended across the 10 mm length of each chamber. However, no permeability barriers were present since the reaction product for HRP was visible throughout the cable. At twenty-six weeks, all the axons in cables were gathered into minifascicles. Each minifascicle of axons was surrounded by perineurial cells. Blood vessels were excluded from the minifascicles by the perineurial cells and the vessels were permeable to HRP, thus indicating that their endothelial cells had not formed tight junctions. Despite the leakage of HRP from the excluded vessels, the tracer did not reach the axons because the perineurial cells encircling the minifascicles developed tight junctions. In some animals, the chambers were removed at four weeks to determine whether the chamber influenced barrier development. This manipulation had no effect since cables, with or without chambers, exhibited similar findings at twenty-six weeks. Our results indicate that nerve cables regenerate a perineurial but not an endoneurial permeability barrier. We conclude that axons in long-term cables are protected by only a perineurial permeability barrier.