Fig 2: Distances between antibody-labeled (TOMM20) mitochondria and TASK-potassium channels in rat Carotid Body Type I cells were measured using confocal microscopy. Distribution of software-measured distances showed approximately 72% of TASK-1 and approximately 79% of TASK-3 total measurements were =0.5 µm.

Fig 3: Videomorphometric analysis of the hypoxic response of intra- (A) and pre-acinar (B) arteries of WT and TASK-1 KO mice.The luminal area of vessels before exposure to hypoxia was set as 100%, and changes in the luminal areas are presented as relative values. Hypoxia-induced constriction of intra-acinar arteries was comparable in both mouse strains, whereas in KO pre-acinar arteries, it started to fade earlier as compared to WT. Data are presented as mean ± SEM. n is number of vessels/number of animals. Tests of significance were done at the time points indicated by arrows. *, #, §, $ P= 0.05 and **, ## P= 0.01 (Mann–Whitney U-test).

Fig 4: Age-related changes in the expression of select K+ channels the rostral medullary raphe. (A) Kcnj10, Kcnj16, Kcnk3, Kcnk9, and Kcna2 gene expression patterns across age (P0, 7, 19, and adult) within the rostral raphe (*P < 0.05 vs. P0 by one-Way ANOVA). Western blots from raphe tissues collected from different ages showed increases in both a high molecular weight band (~250 kDa) Kir4.1HMW and expected (42.5 kDa) Kir4.1 bands (B), Kir5.1HMW (~250 kDa) and expected (48 kDa) Kir5.1 bands (C), and TASK-1 (45–65 kDa) and TASK-3 (45 kDa) (D) with respective quantification normalized to ß-actin (E; *P < 0.05 vs. P0 by one-way ANOVA). Note that the quantification for Kir5.1 protein in (E) was from two blots from P0 (n = 3), P7 (n = 4), P18 (n = 6), and adult (n = 3), but only one is shown in (C).

Fig 5: Neuroprotective effects of the Sp1-interfering agent Mit-A in the SOD1-G93A mouse model of ALS. a mRNA (left) and protein (right) levels for Sp1 in the spinal cord of SOD1-G93A mice and their Non-Tg littermates at the indicated ages. b Confocal images showing Sp1-immunolabeled nuclei of SMI32-positive lumbar MNs from 3-month-old Non-Tg and SOD1-G93A mice. Boxed areas in low magnification images for the Non-Tg condition are displayed at higher magnification together with similar areas obtained from transgenic mice. Box plot represents the mean intensity of nuclear Sp1-labeling of Non-Tg or SOD1-G93A MNs. c Mechanism of action by which Mit-A might protect neurons against excitotoxic degeneration. d Daily administration of Mit-A (30 µg kg-1 day-1) in the drinking water, beginning at P30, dysregulated mRNA (left) and protein (right) levels of p11 and TASK1, in the lumbar spinal cord of SOD1-G93A mice at P120. e Number of SMI32-positive MNs (left), in the L3–L5 spinal cord segment of SOD1-G93A mice and their Non-Tg littermates, treated with Mit-A or vehicle. Scale bars, 50 µm. f–h Cumulative probability curves of symptoms onset f and survival h, and time course of body weight g, against the age of SOD1-G93A mice receiving the indicated treatments. Mit-A treatment as in d. i–k Representative electromyographic recordings from the gastronecmius muscle of Non-Tg and SOD1-G93A mice at weeks 13 i, j and 15 k. Transgenic mice received treatments as in f–h. In i, fibrillation potentials (dots) were recorded by needle electromyography from a 13-week-old transgenic mouse. These spontaneous muscle discharges were absent in Non-Tg mice j. l, m Maximal (l) and mean (m) frequency of fibrillations in SOD1-G93A animals at the indicated weeks treated with vehicle or Mit-A. Number of independent samples is in parentheses. Error bars, SEM. *p < 0.05, **p < 0.01, ***p < 0.001; n.s., not significant; by Student's t-test a, b, d, e, l, m or two-way ANOVA with post hoc Holm–Sidak method g. Statistic outputs determined by Log-Rank test, Kaplan–Meier analysis f, h or two-way ANOVA g between treatments are stated on plots. Source data are provided as a Source Data file