Temperature, Hence, a small disturbance in ions distribution

Temperature, the abiotic master
environmental factor, has a profound effect on the abundance and distribution
of ectothermal animals on the earth which cannot physiologically regulate their
body temperature. Predicted increases in ambient water 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. In northern latitudes, All fishes have to accommodate
large range of temperature changes between winter and summer. Fish heart is
electrically excitable muscle, i.e. a small voltage change of plasma membrane (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 harmonious
co-operation between several ion channels in the cell membrane. Hence, a small
disturbance in ions distribution could cause cardiac arrhythmias, conduction
failure and compromise force of cardiac contraction. Electrical excitability of
fish heart 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 over the heart. Recently,
Vornanen (2016) suggests that the mismatch between the temperature-dependent of
outward K+ and inward Na+ may cause compromise in the
electrical excitability which termed as hypothesis of temperature-dependent
depression of electrical excitation (TDEE). Strongly response of fishes to the
warming makes them as indicator for reporting climate-induced modifications on aquatic
ecosystems. To this end, the thermal plasticity of electrical excitability in
fish heart and the TDEE hypotesis were tested by using seasonally acclimatized roach
(Rutilus rutilus) as an experimental animal. 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
experiments.

Generally, thermal
tolerance increases with increasing complexity of biological organization, i.e.,
molecular functions have the highest thermal tolerance while the intact fish has
the lowest one. Seasonal acclimatization increases heart rate (fH)
of roach heart in both seasons to the maximum without compromising the
stability of cardiac electrical-excitatability. The upper thermal tolerance of ECG
and AP variables are higher in summer than in winter roach. Evidence of cardiac
arrhythmias clearly appeared with rising temperature around and above the break
point temperature (TBP) in both seasonal groups. 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 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 roach, thus other factors beside INa
may be included. Collectively, INa is clearly the most
heat-sensitive ion current, and considering the weakest link which probably
limiting the upper thermal tolerance of electrical excitation in roach
cardiomyocytes. Current findings are consistent with the hypothesis of the TDEE
which provides a mechanistic explanation for high temperature-induced
arrhythmias and bradycardia and post-exercise depression of fH
in fish heart in vivo at cellular and molecular level, and therefore
poor survival of fishes exposed to thermal, exercise and handling stresses.

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