Abstract
The process by which muscle fiber electrical depolarization is linked to activation of muscle contraction is known as excitation-contraction coupling (ECC). Our understanding of ECC has increased enormously since the early scientific descriptions of the phenomenon of electrical activation of muscle contraction by Galvani that date back to the end of the eighteenth century. Major advances in electrical and optical measurements, including muscle fiber voltage clamp to reveal membrane electrical properties, in conjunction with the development of electron microscopy to unveil structural details provided an elegant view of ECC in skeletal muscle during the last century. This surge of knowledge on structural and biophysical aspects of the skeletal muscle was followed by breakthroughs in biochemistry and molecular biology, which allowed for the isolation, purification, and DNA sequencing of the muscle fiber membrane calcium channel/transverse tubule (TT) membrane voltage sensor (Cav1.1) for ECC and of the muscle ryanodine receptor/sarcoplasmic reticulum Ca2+ release channel (RyR1), two essential players of ECC in skeletal muscle. In regard to the process of voltage sensing for controlling calcium release, numerous studies support the concept that the TT Cav1.1 channel is the voltage sensor for ECC, as well as also being a Ca2+ channel in the TT membrane. In this review, we present early and recent findings that support and define the role of Cav1.1 as a voltage sensor for ECC.
Highlights
In skeletal muscle, electrical impulses carried by the axons of motoneurons travel to the nerve endings at the muscle endplate, where these electrical signals are converted into chemical signals that produce depolarizing postsynaptic potentials at the neuromuscular junction sarcolemma of the muscle fiber [1, 2]
The Cav1.1 channels serve as the voltage sensing machinery for the process of transverse tubular (TT) depolarization-induced calcium release from the sarcoplasmic reticulum [9] via intracellular sarcoplasmic reticulum (SR) calcium release channels, the type 1 ryanodine receptors (RyR1) [10]
The linear relationship had a small positive charge value for the extrapolation to zero peak rate of release (x intercept), indicating a small amount of pre-activating charge that was not moved during the subthreshold prepulse, but was instead moved during each test pulse, presumably the initial charge moved during the test pulse. These results demonstrated a close relationship between the extent of activation of SR Ca2+ release by a pulse and the amount of activating charge that moved during the same pulse [50]
Summary
Electrical impulses carried by the axons of motoneurons travel to the nerve endings at the muscle endplate (the muscle synapse), where these electrical signals are converted into chemical signals that produce depolarizing postsynaptic potentials at the neuromuscular junction sarcolemma of the muscle fiber [1, 2]. Voltage sensor charge moved predicts pulse durations needed to give detectable contraction An immediate question that arose after the first detection of charge movement currents was whether the voltage sensor currents detected in muscle fibers were the control system for depolarization-induced contractile activation.
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