Zebrafish embryos are suitable to use as a model system to perform chemical biology experiments effectively in educational sites. In this experiment, we studied the effect of caffeine on heartbeat rate and other phenotypes of zebrafish embryos using visual microscopy and simple imaging. A small drop for concentrations of caffeine in embryo medium caused an amount-dependent decrease in heartbeat rate in 2-3-day-old zebrafish embryos, finally resulting in complete heartbeat stop. We observed the decrease pattern in heartbeat rate for an initial acute drop in heartbeat and a period of stabilization followed as 15 seconds and 60 seconds by complete cessation. The causes known to be antagonistic to caffeine when the effects of caffeine were not
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These effects include significant acute heartbeat lowering and eventual complete heart cessation. In our experiment, we focused on the use of zebrafish embryos as an “in vivo” model system for studying the effects of caffeine on the rate of zebrafish heartbeat. We measured heartbeat rate of embryos under different caffeine concentrations which is 1% and 2% of coffee in the millimolar range (1–25 mM). We found that the heartbeat rate drop immediately in present of caffeine and followed by a period of relative stability, finally resulting in complete cessation of the heart. The characteristic pattern of decrease suggested that a response in the embryos is depends on the heartbeat level following caffeine induced acute drop in heartbeat. Hypothesis make approved when the rate of heartbeat in zebrafish embryo slow down as a present of caffeine at their surround. In addition, caffeine is also known to inhibit phosphodiesterases which it caused an increase in cAMP. With a drop of caffeine and ryanodine-induced intracellular calcium release by ruthenium red did not reverse caffeine-induced effects, suggesting that changes in intracellular calcium is not the mechanism by which caffeine exerts its heartbeat effects on zebrafish …show more content…
However, available literature does allow us to suggest that ruthenium red may not influence caffeine’s overall effect on HR in zebrafish embryos, and that the mode of caffeine action may not involve intracellular calcium release. We observed other phenotypic effects of caffeine, such as cardiac arrhythmia and trunk=tail kinking, which were not seen in all the other small molecule treatments we carried out. A detailed analysis of the effects of various small molecules on all the above phenotypes can form the basis of future studies. We can expectant to study and identify all observable defects while performing experiments with high concentrations of caffeine. For this experiment, we got two distinct results between less concentration of caffeine and more concentration of caffeine. It presented that the higher concentration of caffeine as 2% used caused a lower rate of heartbeat of zebrafish embryo compare to the lower caffeine concentration with 1% that caused the accounting of heartbeat slow than original liquid medium and faster than the medium with more caffeine concentration. The experiment provides a suitable way to study the chemical biology of caffeine and related small molecules in zebrafish. Using this method, we have been able to generate the potentially innovative actions of caffeine on zebrafish embryos and provide an illustrative example of
These effects include significant acute heartbeat lowering and eventual complete heart cessation. In our experiment, we focused on the use of zebrafish embryos as an “in vivo” model system for studying the effects of caffeine on the rate of zebrafish heartbeat. We measured heartbeat rate of embryos under different caffeine concentrations which is 1% and 2% of coffee in the millimolar range (1–25 mM). We found that the heartbeat rate drop immediately in present of caffeine and followed by a period of relative stability, finally resulting in complete cessation of the heart. The characteristic pattern of decrease suggested that a response in the embryos is depends on the heartbeat level following caffeine induced acute drop in heartbeat. Hypothesis make approved when the rate of heartbeat in zebrafish embryo slow down as a present of caffeine at their surround. In addition, caffeine is also known to inhibit phosphodiesterases which it caused an increase in cAMP. With a drop of caffeine and ryanodine-induced intracellular calcium release by ruthenium red did not reverse caffeine-induced effects, suggesting that changes in intracellular calcium is not the mechanism by which caffeine exerts its heartbeat effects on zebrafish …show more content…
However, available literature does allow us to suggest that ruthenium red may not influence caffeine’s overall effect on HR in zebrafish embryos, and that the mode of caffeine action may not involve intracellular calcium release. We observed other phenotypic effects of caffeine, such as cardiac arrhythmia and trunk=tail kinking, which were not seen in all the other small molecule treatments we carried out. A detailed analysis of the effects of various small molecules on all the above phenotypes can form the basis of future studies. We can expectant to study and identify all observable defects while performing experiments with high concentrations of caffeine. For this experiment, we got two distinct results between less concentration of caffeine and more concentration of caffeine. It presented that the higher concentration of caffeine as 2% used caused a lower rate of heartbeat of zebrafish embryo compare to the lower caffeine concentration with 1% that caused the accounting of heartbeat slow than original liquid medium and faster than the medium with more caffeine concentration. The experiment provides a suitable way to study the chemical biology of caffeine and related small molecules in zebrafish. Using this method, we have been able to generate the potentially innovative actions of caffeine on zebrafish embryos and provide an illustrative example of