A technique called functional electrical stimulation (FES), in which implanted electrodes deliver electrical current to trigger muscle contractions, provides a way to reconnect this loop.
In transgenic Caenorhabditis elegans expressing this magnetoreceptor in myo-3-specific myo-3-specific myo-3-specificc neurons, application of the external muscleicellsld triggered muscle cortraction and withdrawal behavior of the worms, indicative of mec-4-specificnt applicationof muscle cells and thech rexternalneurons, respectively.
For example, CaV1.2 channels are localized close to, and efficiently activate, RyR2 channels, thereby triggering muscle contraction.
Calcium influx via voltage-gated Ca2+ channels (Cav) play vital roles in cell physiology, such as triggering muscle contraction and hormone secretion [1].
High intracellular Ca2+ levels are crucial for triggering muscle contraction, whereas low levels are critical for initiating muscle relaxation.
During every heartbeat, a pulse of calcium is released from the sarcoplasmic reticulum (SR) into the cytoplasm of cardiac muscle cells through a calcium release channel (RyR, ryanodine receptor), thus triggering muscle contraction.
Shining light on those cells triggered muscle contractions in the diaphragm.
The minimum dose of 0.2 µg of toxin triggered muscle contractions in the crab, causing paralysis within 1 minute.
Complement factors C3 and C5 are potent chemoattractants for inflammatory cells (neutrophils and eosinophils) and anaphylatoxins, which trigger smooth muscle contraction and regulate vasodilation (Bolger et al. 2007).
DOI: http://dx.doi.org/10.7554/eLife.03293.007 To test whether direct activation of PDF or HGN1 neurons could trigger gut muscle contraction, we first expressed ChR2 in the PDF neurons and use a Minos insertion line to label the hindgut.
