Background: It is generally accepted that skeletal muscle contraction is triggered by nerve impulse and intracellular Ca²⁺([Ca²⁺]_i) released from intracellular Ca²⁺ stores such as sarcoplasmic reticulum (SR). Specifically, this process, called excitation-contraction (E-C) coupling, takes place at intracellular junctions between the plasma membrane, the transverse (T) tubule L-type Ca²⁺ channel (dihydropyridine-sensitive L-type Ca²⁺ channel, DHPR, also called tetrads), and the SR Ca²⁺ release channel (ryanodine-sensitive Ca²⁺ release channel, RyR, also called feet) of internal Ca²⁺ stores in skeletal muscle cells. Furthermore, it has been reported that the Ca^2+- dependent and -independent contraction determine the expression of skeletal muscle genes, thus providing a mechanism for tightly coupling the extent of muscle contraction to regulation of muscle plasticity-related excitation-transcription (E-T) coupling. Purpose: Expression and activity of plasticity-associated enzymes in gastrocnemius muscle strips have not been well studied, however. Methods: Therefore, in this study the expression and phosphorylation of E-C and E-T coupling-related mediators such as protein kinases, ROS(reactive oxygen species)- and apoptosis-related substances, and others in gastrocnemius muscles from rats was examined. Results: I found that expression and activity of MAPKs (mitogen-activated protein kinases, ERK1/2, p38MAPK, and SAPK/JNK), apoptotic proteins (cleaved caspase-3, cytochrome c, Ref-l, Bad), small GTP-binding proteins (RhoA and Cdc42), actin-binding protein (cofilin), PKC (protein kinase C) and Ca²⁺ channel (transient receptor potential channel 6, TRPC6) was observed in rat gastrocnemius muscle strips. Conclusion: These results suggest that MAPKs, ROS- and apoptosis-related enzymes, cytoskeleton-regulated proteins, and Ca²⁺ channel may in part functionally import in E-C and E-T coupling from rat skeletal muscles. (J Kor Soc Phys Ther 2007:19(4):1-14)