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Temperature, the abiotic master
environmental factor, has a profound effect on the abundance and distribution
of animals on the earth, in particular ecotherms. Ectothermic animals (fishes,
frogs, reptiles, and invertebrate animals), cannot physiologically regulate
their body temperature, and are therefore especially vulnerable to temperature
changes to which they are not adapted but to which they might be exposed on the
warming earth. Indeed, understanding how climate change will affect animal life
is one of the greatest challenges of the current biological research. Climate
warming is considered to be the most critical environmental threat, in
particular for aquatic ecosystems and their biodiversity. According to the
current scenarios, the annual mean temperature in Finland is projected to rise
by 2-5°C and 2-7°C by the 2050s and 2080s, respectively. The duration of ice
cover in lakes will become shorter, winters will be milder and extreme
temperature peaks are likely to be higher and occur more often which inturn
will affect fish populations in Finland. Predicted increases in ambient
temperature will acts as a leading factor which control the boundary of
habitats, locomotion, reproduction, development, immune defense and general
performance level of fishes and other ectotherms, and thereby will impact the
distribution and abundance of animal species and possibly distort the precise balance
of the ecosystems to which they belong.

represent the most variable and largest group among vertebrates. Acute and
chronic temperature changes will be reflected on the cardiac function which
considers as a key physiological variable in environmental adaptation and
acclimation of aquatic vertebrates via delivery oxygen and nutrients to different
tissues and providing homeostatic balance between body parts. In northern
latitudes, All fishes have to tolerate large seasonal temperature changes:
their hearts have to function close to zero in winter, while summer
temperatures may be 20-30 degrees higher. Heart muscle is electrically
excitable, i.e. a small voltage change of plasma membrane (cardiac action
potential, AP) sets the rate and rhythm of the heart, initiates contraction and
regulates force production of cardiac myocytes. Cardiac AP is generated by a complex
interaction between several ion channels in the cell membrane. Hence, small
disturbances in ion channel function may generate cardiac arrhythmias, conduction
failure and compromise force of cardiac contraction. Moreover,  thermal plasticity of fish heart is substantial
to maintain contractility and to avoid disturbances in the electrical
excitability that should be sensitive and stable to temperature changes to
produce temperature-dependent acceleration and deceleration of heart rate (fH)
and parallel changes in the rate of impulse conduction (action potential; AP)
over the heart. Strongly response of fishes to the warming makes them as
indicator for detecting and documenting climate-induced modifications on aquatic
ecosystems. To this end, effects of seasonal acclimatzation on the electrical
excitbility of roach (Rutilus rutilus) heart, one of the most abundant
fish species in Finnish lakes and coastal waters, is examined. Also, the hypothesis
of temperature-dependent depression of electrical excitation (TDEE) is recently
suggested by Vornanen (2016), the mismatch between the temperature-dependent of
outward K+ and inward Na+ may cause compromise in the
electrical excitability, is examined in roach cardiomyocytes. Responses of roach
heart to temperature changes are determined at different levels of biological
organization starting from in vivo recordings of heart function in
living animals down to organ, cell and molecule level of in vitro

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The present
study revealed that seasonal acclimatization of electrical excitation is crucial
for proper function of roach heart under widely range of water temperatures in
winter and summer seasons. Seasonal thermal acclimation of electrical
excitability increases pumping capacity of the roach heart by increasing fH
in both seasons to the maximum without compromising the stability of cardiac
excitatability. Sensitivity to thermal disturbances increases with increasing
complexity of biological organization, i.e., molecular functions being
generally the the most temperature sensitive and the intact organism is the
most temperature resistant. The upper thermal tolerance of fH
is higher in summer- than in winter-acclimatized roach. Evidence of cardiac
arrhythmias clearly appeared with rising temperature around and above the break
point temperature (TBP), the temperature after which steady
increase/decrease of the variables in response to temperature changes reversed
into continuous decrease/increase, respectively, initially as missing QRS
complexes to complete cessation of contractility (asystole) in both seasonal acclimatized
groups. Interestingly, Action potential (AP) of atrial myocytes in summer roach
recorded by microelectrode technique were characterized by a rapid initial
repolarization where the striking shortening in atrial AP duration at 10% (APD10)
and 20% (APD20) repolarization levels in comparison to atrial
myocytes of winter roach. Among ion currents of roach heart, the inward
rectifier K+ current (IK1) has the highest thermal
tolerance, while sodium current (INa) is the lowest one in both
seasonal groups. in winter acclimatized roach, the lower thermal tolerance of INa
is consistent with the lower thermal tolerance of in vivo fH,
while the matching between INa and fH is not ideal
in summer- as winter-acclimatized roach, thus other factors beside INa
may be included. In both seasonal acclimatized groups, molecular composition of
ion channels regulates ion currents in temperature-dependend manner and
consistent with the electrophysiological data.

capture and handling stress can cause remarkable changes in the metabolite and
ion composition of the extracellular fluid and elevate extracellular K+
concentration (K+o) which may cause a significant
post-stress mortality of fishes. In the present study, The combined effects of high
temperature and high K+o on the electrical excitability
of winter-acclimatized roach ventricular myocytes was examined. Surprisingly,
some myocytes completely failed to elicit all-or-none AP in 8 mM K+o
at 24°C with reduction in AP amplitude and overshoot by elevation of K+o.
Effects of high K+o antagonizes the negative effects of
high temperature on excitation threshold, the steepy depression of the rate of
AP upstroke (Vmax) and complete loss of excitability in some
myocytes suggest that the combination of high temperature and high K+o
will severely impair ventricular excitability in roach.

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