Nitric Oxide Blocks Blue Light-Induced K^+ Influx by Elevating the Cytosolic Ca^(2+) Concentration in Vicia faba L. Guard Cells

Ca2＋ plays a pivotal role in nitric oxide （NO）-promoted stomatal closure. However, the function of Ca2＋ in NO inhibition of blue light （BL）-induced stomatal opening remains largely unknown. Here, we analyzed the role of Ca2＋ in the crosstalk between BL and NO signaling in Vicia faba L. guard cells. Extracellular Ca2＋ modulated the BL-induced stomatal opening in a dose-dependent manner, and an application of 5 μM Ca2＋ in the pipette solution significantly inhibited BL-activated K＋ influx. Sodium nitroprusside （SNP）, a NO donor, showed little effect on BL-induced K＋ influx and stomatal opening response in the absence of extracellular Ca2＋ , but K＋ influx and stomatal opening were inhibited by SNP when Ca2＋ was added to the bath solution. Interestingly, although both SNP and BL could activate the plasma membrane Ca2＋ channels and induce the rise of cytosolic Ca2＋ , the change in levels of Ca2＋ channel activity and cytosolic Ca2＋ concentration were different between SNP and BL treatments. SNP at 100 μM obviously activated the plasma membrane Ca2＋ channels and induced cytosolic Ca2＋ rise by 102.4%. In contrast, a BL pulse （100 μmol/m 2 per s for 30 s） slightly activated the Ca2＋ channels and resulted in a Ca2＋ rise of only 20.8%. Consistently, cytosolic Ca2＋ promoted K＋ influx at 0.5 μM or below, and significantly inhibited K＋ influx at 5 μM or above. Taken together, our findings indicate that Ca2＋ plays dual and distinctive roles in the crosstalk between BL and NO signaling in guard cells, mediating both the BL-induced K＋ influx as an activator at a lower concentration and the NO-blocked K＋ influx as an inhibitor at a higher concentration.

Regulatory mechanisms and therapeutic potential of microglial inhibitors in neuropathic pain and morphine tolerance

Microglia are important cells involved in the regulation of neuropathic pain(NPP)and morphine tolerance.Information on their plasticity and polarity has been elucidated after determining their physiological structure,but there is still much to learn about the role of this type of cell in NPP and morphine tolerance.Microglia mediate multiple functions in health and disease by controlling damage in the central nervous system(CNS)and endogenous immune responses to disease.Microglial activation can result in altered opioid system activity,and NPP is characterized by resistance to morphine.Here we investigate the regulatory mechanisms of microglia and review the potential of microglial inhibitors for modulating NPP and morphine tolerance.Targeted inhibition of glial activation is a clinically promising approach to the treatment of NPP and the prevention of morphine tolerance.Finally,we suggest directions for future research on microglial inhibitors.