Transmembrane Ca²⁺ influx through voltage-dependent Ca²⁺ channels (VDCC) triggers Ca²⁺ release from the sarcoplasmatic reticulum (SR) in the adult heart; this is named Ca²⁺ induced Ca²⁺ release (CICR). To investigate the role of CICR in the embryonic heart, single mouse cardiomyocytes of early (EDS, E9.5) and late embryonic stages (LDS, E16.5) were loaded with Fura2AM, field stimulated and characterized by fast Ca²⁺ imaging (80Hz). No significant differences in mean diastolic [Ca²⁺]_i (EDS: 60.8±9.9nM, n=10 vs LDS: 74.5±11.9nM, n=13) and in amplitude of Ca²⁺ transients ([Delta][Ca²⁺]_i EDS: 157.1±29.0nM vs LDS: 174.5±17.7nM) were detected. To estimate the contribution of the SR, its function was abolished by caffeine (10mM) under field stimulation. In contrast to adult cardiomyocytes, embryonic cardiomyocytes still displayed Ca²⁺ transients with [Delta][Ca²⁺]_i reduced by 42.6±3.8% in EDS and by 43.7±3.2% in LDS indicating a lower contribution of the SR to D[Ca²⁺]_i at the embryonic stage. The initial rate of Ca²⁺ release (R1), which is known to be CICR related was faster in LDS (3.51±0.59mM/s) compared to EDS (1.74±0.54mM/s, P<0.05). In the presence of caffeine this age-related difference in R1 disappeared (reduction by 49.2±5.4% to 0.67±0.09mM/s for EDS and by 75.5±5.2% to 0.64±0.06mM/s for LDS). Similar findings were obtained in the presence of thapsigargin (2mM). Thus, in the embryonic heart Ca²⁺ release from the SR contributes less than in the adult.