The whole cell patch clamp method was used to measure Ca current through L-type Ca channels in enzymatically isolated ventricular myocytes of crucian carp (Carassius carassius L.) heart. Fish were acclimated to 22 degrees C for more than 4 wk, and properties of Ca current were measured at room temperature (21 +/- 1 degrees C). Depolarizing voltage steps from -50 mV evoked rapidly activating Ca currents, which exhibited a bell-shaped voltage dependence with peak amplitude at 0 mV. The currents were suppressed by nifedipine (5 microM), verapamil (2.5 microM), and Cd2+ (175 microM). The current amplitude was increased by 67.5 +/- 17.2% (n = 5) in the presence of 1 microM isoproterenol. Steady-state inactivation and activation curves showed half-maximal inactivation at -31.3 +/- 0.95 mV, with a slope factor of 5.88 +/- 0.51, and half-maximal activation at -10.6 +/- 1.65 mV, with a slope factor of 7.84 +/- 0.54 (n = 9). The overlap of inactivation and activation curves suggests the presence of a small window current, which is maximally 4% of the peak current at -27 mV. The density of L-type Ca current was 6.95 +/- 0.79 pA/pF at 0 mV (n = 35). A total increment in cellular Ca contributed by L-type Ca current during a 500-ms voltage clamp pulse was calculated from the integral of Ca current and cell volume. The charge transfer through L-type Ca current was 0.325 +/- 0.023 pC/pF, and the mean cell volume was 1,377 +/- 44 microns3. The increment in total cellular Ca by Ca influx through L-type Ca channels was calculated to be 39.3 +/- 2.8 microM. These findings imply that Ca influx through L-type Ca channels can contribute significantly to the activation of contraction in the ventricular myocytes of fish heart.

Crucian carp Carassius carassius show great phenotypic plasticity in individual morphology and physiology, and strong variation in population density in different fish communities. Small fish with shallow bodies and large heads are typical in overcrowded monospecific fish communities in small ponds, whereas deep-bodied, large fish are found in larger, multispecies lakes. Crucian carp are especially vulnerable to predation by piscivorous fish and their greater relative body depth in multispecies fish communities has been proposed to be an induced defence against size-limited predation, and hence to be an adaptive feature. Data are presented here on the two divergent body forms in field populations in eastern Finland, together with results of laboratory experiments on predator effects on morphology and physiology (growth, respiration, heart rate). The deep body can be achieved in a few months by introducing a low population density of shallow-bodied fish into a food-rich environment with no piscivores. In the laboratory, both the presence of piscivores (chemical cues) and enhanced food availability increased the relative depth of crucian carp, but only to a modest extent when compared to natural variation. It is concluded that the deep-body form of crucian carp in the low density populations of multispecies fish communities is the normal condition. Reproduction in monospecific ponds results in high intraspecific competition, low growth rate and a stunted morphology. According to pilot tests, the mechanism behind the predator effect in the laboratory might be a behavioural reaction to chemical cues (alarm substances/predator odour) causing changes in energy allocation: predator-exposed crucian carp adopt a ' hiding ' mode with decreased activity (less swimming, lower respiration and heart rate) and with higher overall growth. Whether, and to what extent, this predator-induced mechanism works in nature is unclear.1997 The Fisheries Society of the British Isles

phenotype of trout heart was induced by 4-wk acclimation at 4°C and was characterized by 32.7% increase in relative heart mass and 49.8% increase in ventricular myocyte size compared with warm-acclimated (WA; 18°C) fish (P Ͻ 0.001). Effect of temperature acclimation on transcriptome of the rainbow trout heart was examined using speciesspecific microarray chips containing 1,380 genes. After 4 wk of temperature acclimation, 8.8% (122) of the genes were differently expressed in CA and WA hearts, and most of them (82%) were upregulated in the cold (P Ͻ 0.01). Transcripts of genes engaged in protein synthesis and intermediary metabolism were most strongly upregulated, whereas genes contributing to the connective tissue matrix were clearly repressed. Extensive upregulation of the genes coding for ribosomal proteins and translation elongation and initiation factors suggest that the protein synthesis machinery of the trout heart is enhanced in the cold and is an essential part of the compensatory mechanism causing and maintaining the hypertrophy of cardiac myocytes. The prominent depression of collagen genes may be indicative of a reduced contribution of extracellular matrix to the remodeling of the CA fish heart. Temperature-related changes in transcripts of metabolic enzymes suggest that at mRNA level, glycolytic energy production from carbohydrates is compensated in the heart of CA rainbow trout, while metabolic compensation is absent in mitochondria. In addition, the analysis revealed three candidate genes: muscle LIM protein, atrial natriuretic peptide B, and myosin light chain 2, which might be central for induction and maintenance of the hypertrophic phenotype of the CA trout heart. These findings indicate that extensive modification of gene expression is needed to maintain the temperature-specific phenotype of the fish heart. gene expression; fish heart; temperature-induced hypertrophy PHYSIOLOGICAL PLASTICITY is needed to adapt body functions to changing environmental conditions and involves activation of proper genetic programs. Ectothermic animals of north-temperate latitudes experience large seasonal changes in temperature, which strongly affect the rate of body functions. To compensate for the effects of temperature changes, ectotherms can respond to chronic temperature changes by increasing the quantity of tissue or enzyme needed for different physiological tasks, or by expressing proteins isoforms that are more appropriate for the new thermal conditions (16,19,21). On the other hand, proteins which are needed in lesser amounts in the new thermal regime could be depressed or downregulated. Although expression of proteins can be changed by multiple mechanisms during synthesis and degradation, temperaturedependent changes in transcription of genes are one of the key events in modifying the proteome of the tissues (16, 37).Circulatory system integrates different body functions through the transport of material and humoral messages and serves the well being of all body cells by providing oxygen and fuels for e...

The zebrafish (Danio rerio) has become a popular model for human cardiac diseases and pharmacology including cardiac arrhythmias and its electrophysiological basis. Notably, the phenotype of zebrafish cardiac action potential is similar to the human cardiac action potential in that both have a long plateau phase. Also the major inward and outward current systems are qualitatively similar in zebrafish and human hearts. However, there are also significant differences in ionic current composition between human and zebrafish hearts, and the molecular basis and pharmacological properties of human and zebrafish cardiac ionic currents differ in several ways. Cardiac ionic currents may be produced by non-orthologous genes in zebrafish and humans, and paralogous gene products of some ion channels are expressed in the zebrafish heart. More research on molecular basis of cardiac ion channels, and regulation and drug sensitivity of the cardiac ionic currents are needed to enable rational use of the zebrafish heart as an electrophysiological model for the human heart.

Electrical activity of the heart is assumed to be one of the key factors that set thermal tolerance limits for ectothermic vertebrates. Therefore, we hypothesized that in thermal acclimation--the duration of cardiac action potential and the repolarizing K+ currents that regulate action potential duration (APD)--the rapid component of the delayed rectifier K+ current (I(Kr)) and the inward rectifier K+ current (I(K1)) are more plastic in eurythermal than in stenothermal fish species. The hypothesis was tested in six freshwater teleosts representing four different fish orders (Cadiformes, Cypriniformes, Perciformes, Salmoniformes) acclimated at +4 degrees C (cold acclimation) or +18 degrees C (warm acclimation). In cold acclimation, a compensatory shortening of APD occurred in all species regardless of thermal tolerances, life styles, or phylogenies of the fish, suggesting that this response is a common characteristic of the teleost heart. The strength of the response did not, however, obey simple eurythermy-stenothermy gradation but differed among the phylogenetic groups. Salmoniformes fish showed the greatest acclimation capacity of cardiac electrical activity, whereas the weakest response appeared in the perch (Perciformes) heart. The underlying ionic mechanisms were also partly phylogeny dependent. Modification of the I(Kr) current was al- most ubiquitously involved in acclimation response of fish cardiac myocytes to temperature, while the ability to change the I(K1) current under chronic thermal stress was absent or showed inverse compensation in Salmoniformes species. Thus, in Salmoniformes fish, the thermal plasticity of APD is strongly based on I(Kr), while other fish groups rely on both I(Kr) and I(K1).

No abstract

Temperature has a strong influence on the excitability and the contractility of the ectothermic heart that can be alleviated in some species by temperature acclimation. The molecular mechanisms involved in the temperature-induced improvement of cardiac contractility and excitability are, however, still poorly known. The present study examines the role of sarcolemmal K(+) currents from rainbow trout (Oncorhynchus mykiss) cardiac myocytes after thermal acclimation. The two major K(+) conductances of the rainbow trout cardiac myocytes were identified as the Ba(2+)-sensitive background inward rectifier current (I(K1)) and the E-4031-sensitive delayed rectifier current (I(Kr)). In atrial cells, the density of I(K1) is very low and the density of I(Kr) is remarkably high. The opposite is true for ventricular cells. Acclimation to cold (4 degrees C) modified the two K(+) currents in opposite ways. Acclimation to cold increases the density of I(Kr) and depresses the density of I(K1). These changes in repolarizing K(+) currents alter the shape of the action potential, which is much shorter in cold-acclimated than warm-acclimated (17 degrees C) trout. These results provide the first concrete evidence that K(+) channels of trout cardiac myocytes are adaptable units that provide means to regulate cardiac excitability and contractility as a function of temperature.

Rainbow trout (Oncorhynchus mykiss, Walbaum) were acclimated to 4 degrees C and 17 degrees C for more than 4 weeks and heart rate was determined in the absence and presence of adrenaline to see how thermal adaptation influences basal heart rate and its beta-adrenergic control in a eurythermal fish species. The basal heart rate in vitro was higher in cold-acclimated than warm-acclimated rainbow trout at temperatures below 17 degrees C. On the other hand, adaptation to cold decreased thermal tolerance of heart rate so that the maximal heart rates were achieved at 17 degrees C (75 +/- 4 bpm) and 24 degrees C (88 +/- 2 bpm) in cold-acclimated and warm-acclimated trout, respectively. Beta-adrenergic response of the heart was enhanced by cold-adaptation, since adrenaline (100 nmol l(-1)) caused stronger stimulation of heart rate in cold-acclimated (29 +/- 14%) than in warm-acclimated fish (10 +/- 1%; P = 0.03). Furthermore, adrenaline strongly opposed the temperature-dependent deterioration of force production in cold-acclimated trout but not in warm-acclimated trout. The results indicate that adaptation to cold increases basal heart rate but decreases its thermal tolerance in rainbow trout. Cold acclimation up-regulates the beta-adrenergic system, and beta-adrenoceptor activation seems to provide cardioprotection against high temperatures in the cold-adapted rainbow trout.