The temperature dependence of electrical excitability in fish hearts

Vornanen, Matti

doi:10.1242/jeb.128439

Cited by 81 publications

(76 citation statements)

References 115 publications

(140 reference statements)

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“…Several seasonal differences were evident in transcript expression of K + channel subunits. A major change occurred in genes (kcnh2, kcnh6) coding for the rapid component of the delayed rectifier K + current, I Kr , the major repolarising current of the fish hearts (Vornanen, 2016). kcnh6 was strongly up-regulated in winter, consistent with earlier findings showing that I Kr is up-regulated under cold acclimation in practically all fish species that have been studied Hassinen et al, 2008a;Galli et al, 2009;Haverinen and Vornanen, 2009b;Abramochkin and Vornanen, 2015).…”

Section: Discussionsupporting

confidence: 87%

Effects of prolonged anoxia on electrical activity of the heart in Crucian carp (Carassius carassius)

Tikkanen

Haverinen

Egginton

et al. 2016

Journal of Experimental Biology

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The effects of sustained anoxia on cardiac electrical excitability were examined in the anoxia-tolerant crucian carp (Carassius carassius). The electrocardiogram (ECG) and expression of excitationcontraction coupling genes were studied in fish acclimatised to normoxia in summer (+18°C) or winter (+2°C), and in winter fish after 1, 3 and 6 weeks of anoxia. Anoxia induced a sustained bradycardia from a heart rate of 10.3±0.77 beats min −1 to 4.1±0.29 beats min −1 (P<0.05) after 5 weeks, and heart rate slowly recovered to control levels when oxygen was restored. Heart rate variability greatly increased under anoxia, and completely recovered under reoxygenation. The RT interval increased from 2.8±0.34 s in normoxia to 5.8±0.44 s under anoxia (P<0.05), which reflects a doubling of the ventricular action potential (AP) duration. Acclimatisation to winter induced extensive changes in gene expression relative to summer-acclimatised fish, including depression in those genes coding for the sarcoplasmic reticulum calcium pump (Serca2a_q2) and ATP-sensitive K + channels (Kir6.2) (P<0.05). Genes of delayed rectifier K + (kcnh6) and Ca 2+ channels (cacna1c) were up-regulated in winter fish (P<0.05). In contrast, the additional challenge of anoxia caused only minor changes in gene expression, e.g. depressed expression of Kir2.2b K + channel gene (kcnj12b), whereas expression of Ca 2+ (cacna1a, cacna1c and cacna1g) and Na + channel genes (scn4a and scn5a) was not affected. These data suggest that low temperature pre-conditions the crucian carp heart for winter anoxia, whereas sustained anoxic bradycardia and prolongation of AP duration are directly induced by oxygen shortage without major changes in gene expression.

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Section: Discussionsupporting

confidence: 87%

Effects of prolonged anoxia on electrical activity of the heart in Crucian carp (Carassius carassius)

Tikkanen

Haverinen

Egginton

et al. 2016

Journal of Experimental Biology

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“…The physiological basis of cardiac arrhythmias is being explored (Badr et al, 2016;Vornanen, 2016), but more important to present concerns, they are observed with acute warming of perfused working heart preparations (A. Badr and M. Vornanen, pers.…”

Section: Discussionmentioning

confidence: 99%

Acclimation potential of Arctic cod (Boreogadus saida Lepechin) from the rapidly warming Arctic Ocean

Drost

Carmack

et al. 2016

Journal of Experimental Biology

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As a consequence of the growing concern about warming of the Arctic Ocean, this study quantified the thermal acclimation responses of Boreogadus saida, a key Arctic food web fish. Physiological rates for cardio-respiratory functions as well as critical maximum temperature (T c,max ) for loss of equilibrium (LOE) were measured. The transition temperatures for these events (LOE, the rate of oxygen uptake and maximum heart rate) during acute warming were used to gauge phenotypic plasticity after thermal acclimation from 0.5°C up to 6.5°C for 1 month (respiratory and T c,max measurements) and 6 months (cardiac measurements). T c,max increased significantly by 2.3°C from 14.9°C to 17.1°C with thermal acclimation, while the optimum temperature for absolute aerobic scope increased by 4.5°C over the same range of thermal acclimation. Warm acclimation reset the maximum heart rate to a statistically lower rate, but the first Arrhenius breakpoint temperature during acute warming was unchanged. The hierarchy of transition temperatures was quantified at three acclimation temperatures and was fitted inside a Fry temperature tolerance polygon to better define ecologically relevant thermal limits to performance of B. saida. We conclude that B. saida can acclimate to 6.5°C water temperatures in the laboratory. However, at this acclimation temperature 50% of the fish were unable to recover from maximum swimming at the 8.5°C test temperature and their cardio-respiratory performance started to decline at water temperatures greater than 5.4°C. Such costs in performance may limit the ecological significance of B. saida acclimation potential.

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“…Ultimately, acute warming may lead to cardiac arrhythmia or cardiac collapse (Anttila et al ., ; Eliason et al ., ; Farrell et al ., ; Verhille et al ., ; Vornanen et al ., ). With temperature acclimation, many fishes, but not all, can reset f H and hence their cardiac response to acute warming (Drost et al ., ; Ferreira et al ., ; Klaiman et al ., ; Vornanen, ). For example, cold‐acclimation of cold‐active fish like the rainbow trout Oncorhynchus mykiss (Walbaum 1792) results in a compensatory elevation in f H , which helps maintain heart and whole organismal activity despite the direct effects of being colder (Aho & Vornanen, , ).…”

Section: Introductionmentioning

confidence: 99%

“…The sarcoplasmic reticulum Ca 2+ ‐ATPase (SERCA) pump then restores SR calcium (Monfredi et al . ; Vornanen, ). In contrast, the membrane clock mechanism involves a funny current ( I f ) via an inward hyperpolarisation‐activated mixed Na + and K + channel (HCN), which produces a spontaneous depolarisation of the pacemaker cell that triggers an action potential (Brown et al ., ).…”

Section: Introductionmentioning

confidence: 99%

“…Continued SR calcium release increases intra-cytosolic concentrations of calcium to a crescendo triggering the emptying of SR calcium stores, initiating an action potential. The sarcoplasmic reticulum Ca 2+ -ATPase (SERCA) pump then restores SR calcium (Monfredi et al 2013;Vornanen, 2016). In contrast, the membrane clock mechanism involves a funny current (I f ) via an inward hyperpolarisation-activated mixed Na + and K + channel (HCN), which produces a spontaneous depolarisation of the pacemaker cell that triggers an action potential (Brown et al, 1979).…”

Section: Introductionmentioning

confidence: 99%

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Membrane and calcium clock mechanisms contribute variably as a function of temperature to setting cardiac pacemaker rate in zebrafish Danio rerio

Marchant

Farrell

2019

Journal of Fish Biology

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Here, we show that heart rate in zebrafish Danio rerio is dependent upon two pacemaking mechanisms and it possesses a limited ability to reset the cardiac pacemaker with temperature acclimation. Electrocardiogram recordings, taken from individual, anaesthetised zebrafish that had been acclimated to 18, 23 or 28°C were used to follow the response of maximum heart rate (fHmax) to acute warming from 18°C until signs of cardiac failure appeared (up to c. 40°C). Because fHmax was similar across the acclimation groups at almost all equivalent test temperatures, warm acclimation was limited to one significant effect, the 23°C acclimated zebrafish had a significantly higher (21%) peak fHmax and reached a higher (3°C) test temperature than the 18°C acclimated zebrafish. Using zatebradine to block the membrane hyperpolarisation‐activated cyclic nucleotide–gated channels (HCN) and examine the contribution of the membrane clock mechanisms to cardiac pacemaking, f Hmax was significantly reduced (by at least 40%) at all acute test temperatures and significantly more so at most test temperatures for zebrafish acclimated to 28°C vs. 23°C. Thus, HCN channels and the membrane clock were not only important, but could be modified by thermal acclimation. Using a combination of ryanodine (to block sarcoplasmic calcium release) and thapsigargin (to block sarcoplasmic calcium reuptake) to examine the contribution of sarcoplasmic reticular handling of calcium and the calcium clock, f Hmax was again consistently reduced independent of the test temperature and acclimation temperature, but to a significantly lesser degree than zatebradine for zebrafish acclimated to both 28 and 18°C. Thus, the calcium clock mechanism plays an additional role in setting pacemaker activity that was independent of temperature. In conclusion, the zebrafish cardiac pacemaker has a limited temperature acclimation ability compared with known effects for other fishes and involves two pacemaking mechanisms, one of which was independent of temperature.

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The temperature dependence of electrical excitability in fish hearts

Cited by 81 publications

References 115 publications

Effects of prolonged anoxia on electrical activity of the heart in Crucian carp (Carassius carassius)

Effects of prolonged anoxia on electrical activity of the heart in Crucian carp (Carassius carassius)

Acclimation potential of Arctic cod (Boreogadus saida Lepechin) from the rapidly warming Arctic Ocean

Membrane and calcium clock mechanisms contribute variably as a function of temperature to setting cardiac pacemaker rate in zebrafish Danio rerio

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