Seebohm G, Sanguinetti MC & Pusch M (2003). Tight coupling of rubidium conductance and inactivation in human KCNQ1 potassium channels. J Physiol552, 369–378.
On page 371, Equation 2 should have appeared as:
 |
(2) |
Pollok B, Gross J, Dirks M, Timmermann L & Schnitzler A (2004). The cerebral oscillatory network of voluntary tremor. J Physiol 554, 871–878.
On page 874, it was stated in the second paragraph that the distribution of phase differences between S1/M1 and EMG showed peaks at certain points. These stated values should have read −170 ± 7.5 deg, −78.2 ± 5.4 deg, 69.5 ± 4.2 deg and 159.1 ± 6.5 deg (mean ±s.e.m.)
Lyall V, Alam RI, Malik SA, Phan T-HT, Vinnikova AK, Heck GL & DeSimone JA (2004). Basolateral Na+-H+ echanger-1 in rat taste receptor cells is involved in neural adaptation to acidic stimuli. J Physiol556, 159–173.
On page 169, part of the third paragraph was obscured by Fig. 12. The text should have read:
In polarized TRCs, stimulating the apical membrane with acidic stimuli induced sustained decreases in pHi (Lyall et al. 2001, 2002a,b). Thus both strong acids and weak organic acids gain entry into TRCs across the apical cell membrane and induce a decrease in pHi. Weak organic acids permeate the apical membrane as neutral molecules, and strong acids via an H+ entry pathway that is both amiloride- and Ca2+-insensitive, but is activated by cAMP (Lyall et al. 2001, 2002a,b; DeSimone et al. 2001b). During acid stimulation, a decrease in TRC pHi, rather than a decrease in pHo, is the stimulus intensity variable that correlates specifically with increased CT taste nerve activity. Since inhibiting acid-induced TRC acidification also inhibits the acid-evoked CT response (Lyall et al. 2001, 2002b), it indicates that a decrease in TRC pHi is the proximate stimulus for sour taste.
Martinez V, Wang L, Rivier J, Grigoriadis D & Taché Y (2004). Central CRF, urocortins and stress increase colonic transit via CRF1 receptors while activation of CRF2 receptors delays gastric transit in mice. J Physiol556, 221–234.
On page 228, part of the second paragraph was obscured by Fig. 3. The text should have read:
Effects of i.c.v. CRF receptor antagonists on restraint stress-induced defecation.
In mice maintained in non-stressful conditions, pellet output was low (2.0 ± 0.7 pellets h−1, n= 7). Restraint stress for 1 h increased defecation to 10.4 ± 1.3 pellets h−1 (n= 10, P < 0.05; Fig. 6A). The peak defecatory response occurred during the first 15 min of stress (5.7 ± 0.6 pellets h−1P < 0.05 versus non-stress: 0.3 ± 0.2 pellets h−1), thereafter values decreased, although at 30 min, values were still significantly elevated (Fig. 6B). NBI-35965 at 50 or 100 µg reduced stress-induced defecation to 4.8 ± 1.0 and 4.0 ± 1.5 pellets h−1, respectively (n= 9 and 5; both P < 0.05 versus vehicle + stress; F4,33= 10.025, P < 0.001) while astressin2-B (10 µg, i.c.v.), did not modify the colonic motor response to restraint stress (10.0 ± 0.7 pellets h−1,n= 5; Fig. 6). None of the CRF receptor antagonists tested by themselves (NBI-35965, n= 7; astressin2-B, n= 4), had a significant effect on pellet output in non-stressed mice.
Eskurza I, Monahan KD, Robinson JA & Seals DR (2004). Effect of acute and chronic ascorbic acid on flow-mediated dilatation with sedentary and physically active human ageing. J Physiol556, 315–324.
On page, 319, Table 2 should have appeared as follows:
Table 2.
Brachial artery parameters and hyperaemic flow
| Parameter | BA diameter (mm) | FMD (Δmm) | FMD (%) | HF (% increase) | EID (%) | |
|---|---|---|---|---|---|---|
| Young sedentary | Baseline | 4.1 ± 0.1 | 0.33 ± 0.02 | 8.1 ± 0.5 | 314 ± 21 | 20.7 ± 0.9 |
| Acute | 4.1 ± 0.1 | 0.34 ± 0.02 | 8.2 ± 0.6 | 302 ± 26 | 20.8 ± 1.0 | |
| Chronic | 4.1 ± 0.1 | 0.31 ± 0.02 | 7.8 ± 0.3 | 330 ± 26 | 21.3 ± 1.0 | |
| Older sedentary | Baseline | 4.3 ± 0.1 | 0.20 ± 0.01* | 4.6 ± 0.2* | 324 ± 31 | 20.8 ± 0.8 |
| Acute | 4.3 ± 0.1 | 0.29 ± 0.02‡ | 6.7 ± 0.3*‡ | 291 ± 24 | 20.6 ± 0.8 | |
| Chronic | 4.3 ± 0.1 | 0.22 ± 0.03* | 5.4 ± 0.4* | 325 ± 18 | 18.8 ± 1.1 | |
| Older trained | Baseline | 4.0 ± 0.1 | 0.28 ± 0.02† | 7.0 ± 0.6† | 273 ± 17 | 21.7 ± 2.2 |
| Acute | 4.1 ± 0.1 | 0.30 ± 0.01 | 7.3 ± 0.3 | 306 ± 23 | 21.4 ± 1.7 | |
| Chronic | 4.0 ± 0.1 | 0.28 ± 0.01† | 7.0 ± 0.4† | 305 ± 38 | 22.5 ± 1.9 |
Data are means ±s.e.m. Acute = post-infusion; Chronic = end of oral supplementation. BA = brachial artery; FMD = flow-mediated dilatation; HF = hyperaemic flow; EID = endothelium-independent dilatation.
P< 0.05 versus young sedentary;
P < 0.05 versus older sedentary;
P < 0.05 versus baseline.