Inwardly rectifying potassium (Kir) channels play key roles in functions, including maintaining the resting membrane potential and regulating the action potential duration in excitable cells. Using in situ whole-cell recordings, we investigated Kir currents in mouse fungiform taste bud cells (TBCs) and immunologically identified the cell types (type I-III) expressing these currents. We demonstrated that Kir currents occur in a cell-type-independent manner. The activation potentials we measured were -80 to -90 mV, and the magnitude of the currents increased as the membrane potentials decreased, irrespective of the cell types. The maximum current densities at -120 mV showed no significant differences among cell types (p>0.05, one-way ANOVA). The density of Kir currents was not correlated with the density of either transient inward currents or outwardly rectifying currents, although there was significant correlation between transient inward and outwardly rectifying current densities (p<0.05, test for no correlation). RT-PCR studies employing total RNA extracted from peeled lingual epithelia detected mRNAs for Kir1, Kir2, Kir4, Kir6, and Kir7 families. These findings indicate that TBCs express several types of Kir channels functionally, which may contribute to regulation of the resting membrane potential and signal transduction of taste.
In order to study the mechanisms of Se-mediated growth improvement as related to carbon (C) and nitrogen (N) metabolism, wheat plants were cultivated hydroponically with adequate (4 mM, Na) or low (1 mM, Nd) N supply and treated with 10 and 50 μM Na2SeO4 for six weeks. The Se supplementation enhanced plant biomass; it was significant for shoots of Na plants at 50 μM Se. Chlorophyll fluorescence parameters were significantly lowered under Nd conditions but restored completely by Se addition reaching values of those in Na plants. Net CO2 assimilation rate (PN) decreased only slightly by limited N availability, but it enhanced significantly in both Nd and Na plants equally by 10 and 50 μM Se. Effect of Se on PN in the Na plants occurred mainly due to the stomata opening, while it was related to both stomatal and nonstomatal mechanisms in the Nd plants. The Se treatment resulted in enhancement of nitrate reductase (NR) activity in both Na and Nd plants with an optimal response at 10 μM Se. Negative correlations between nitrate concentration and NR activity indicated a partial nitrate depletion in the roots following by elevated NR activity in Nd plants. In contrast, nitrite concentrations were higher in the Se treated plants. Higher amino acids and protein concentrations in the Se-treated plants might be an indication of a general upregulation of N metabolism. However, in Na plants, the stimulation of N metabolism was not observed at 50 μM Se which could not be attributed to lesser availability of C skeletons because of maintaning higher CO2 fixation under these conditions. It implies the function of some regulatory mechanisms that are responsible for coordination of C and N metabolism in whole plant., R. Hajiboland, N. Sadeghzade., and Obsahuje bibliografii
One of the significant limiting complications of paclitaxel is
painful peripheral neuropathy during its therapy for several types
of cancers. Our recent study showed that impairment of
Nrf2-antioxidant response element (Nrf2-ARE) and upregulation
of oxidative signals in the dorsal root ganglion (DRG) of rats with
treatment of paclitaxel result in neuropathic pain. The purpose of
this study was to examine the beneficial role played by
electroacupuncture (EA) in modifying neuropathic pain evoked by
paclitaxel via Nrf2-ARE and oxidative mechanisms. Behavioral
test was performed to determine mechanical and thermal
sensitivity in rats. Western Blot analysis and ELISA were used to
examine expression of Nrf2-ARE and superoxide dismutases
(SOD); and the levels of products of oxidative stress in the DRG.
Our data showed that paclitaxel increased mechanical and
thermal sensitivity and this was accompanied with impaired
Nrf2-ARE and SOD in the DRG and amplified products of
oxidative stress (i.e. 8-isoprostaglandin F2α and 8-hydroxy-2’-
deoxyguanosine). EA treatment largely restored the levels of
Nrf2-ARE/SOD and inhibited products of oxidative stress and
thereby attenuated mechanical and thermal hypersensitivity
induced by paclitaxel. In conclusion, we revealed specific
signaling pathways leading to paclitaxel-evoked neuropathic pain,
including impairment of Nrf2-ARE and heightened oxidative
signals. We further provided evidence for the role of EA in
alleviating paclitaxel-neuropathic pain via these molecular
mediators.