Bentonite is a promising buffer material for high-level radioactive waste (HLW) disposal due to the high nuclides sorption capacity and swelling property. However, bentonite has the potential to generate colloid particles, with small particle sizes less than 1,000 nm when in contact with groundwater. The bentonite colloids easily form pseudo-colloid with the released nuclides and migrate through the water-conducting rock to the biosphere. Therefore, understanding the generation and migration of bentonite colloids is crucial in assessing the safety of the HLW repository. In this study, an artificial fracture system was prepared to investigate colloid release from compacted bentonite. A 250 mm diameter acrylic artificial fracture system was used, with 30 mm of compacted calcium bentonite installed. Artificial groundwater flow was injected into the system at a flow rate of 250 μL/h, and every 6 mL of leachate was collected by a fraction collector. A film-type pressure sensor was equipped to monitor the swelling pressure, and the swelling was observed using a digital microscope. The results indicate that the compacted bentonite formed a mineral ring originating from the swelling of the bentonite, and the end of the ring generated colloid particles due to chemical erosion. Although the release rate of colloids increased with increasing flow rate, the colloid ratio depended on the low ionic strength of the injected artificial groundwater. This work contributes to the understanding of the chemical erosion and colloid release mechanism of compacted bentonite.

Nitric Oxide (NO) is an important signaling molecule in the nociceptive process. Our previous study suggested that high concentrations of sodium nitroprusside (SNP), a NO donor, induce a membrane hyperpolarization and outward current through large conductances calcium-activated potassium (BKca) channels in substantia gelatinosa (SG) neurons. In this study, patch clamp recording in spinal slices was used to investigate the sources of Ca²+ that induces Ca²+-activated potassium currents. Application of SNP induced a membrane hyperpolarization, which was significantly inhibited by hemoglobin and 2-(4-carboxyphenyl) -4,4,5,5- tetramethylimidazoline-1-oxyl-3-oxide potassium salt (c-PTIO), NO scavengers. SNP-induced hyperpolarization was decreased in the presence of charybdotoxin, a selective BKCa channel blocker. In addition, SNP-induced response was significantly blocked by pretreatment of thapsigargin which can remove Ca²+ in endoplasmic reticulum, and decreased by pretreatment of dentrolene, a ryanodine receptors (RyR) blocker. These data suggested that NO induces a membrane hyperpolarization through BKca channels, which are activated by intracellular Ca²+ increase via activation of RyR of Ca²+ stores.