myoplasm

myoplasm

 [mi´o-plazm]
the contractile part of the muscle cell.

my·o·plasm

(mī'ō-plazm),
The contractile portion of the muscle cell, as distinguished from the sarcoplasm.
[myo- + G. plasma, a thing formed]

my·o·plasm

(mī'ō-plazm)
The contractile portion of the muscle cell, as distinguished from the sarcoplasm.
[myo- + G. plasma, a thing formed]

myoplasm

the cytoplasmic SOL content of a muscle cell.
References in periodicals archive ?
At that state the excess amount of [Ca.sup.2+] entering the cytoplasm is not able to be withdrawn from myoplasm and, subsequently, damages cellular structures.
Type I ryanodine receptors are located in the sarcoplasmic reticulum in close proximity to the L-type channels [13] and physical coupling between the type I ryanodine receptors and the L-type calcium channels (they either directly or through accessory proteins cause the ryanodine receptors to undergo a conformational change and open releasing calcium into the myoplasm) [14].
The inorganic phosphate enters the myoplasm before moving into the SR, where the [P.sub.i] combines with [Ca.sup.++] to form calcium phosphate (Ca[P.sub.i]).
When the input resistance is measured by double-barreled microelectrode, current [I.sub.o] flows through resistance of the myoplasm [r.sub.pl], resistance of intercellular contacts [r.sub.k] and resistance of the electrogenic membrane [r.sub.m] (electric diagram in Fig.
The mechanisms leading to the PSS-susceptibility crisis involve a high concentration of free calcium in the myoplasm released by a faulty membrane system in calcium storing organelles including sarcoplasmic reticulum (14).
Changes in both voluntary and electrically evoked muscle performance during the SSE are likely not to be attributed to an increase in the myoplasm of metabolites, like phosphate and hydrogen ions, since the duration of the jump (0.5-0.55 s) was too small for ATP and PCr to be decreased significantly while the resting period of 30 s was sufficient for ATP and PCr to be restored.
The discovery of an animal model for malignant hyperthermia, a certain breed of pigs, led to the realisation that the essential biochemistry of malignant hyperthermia was increased calcium in the myoplasm. In the early 1970s, Kalow and Britt (9,10) showed that muscle samples from affected individuals contracted to a greater extent than normal when exposed to caffeine in vitro.
However, this approach provides direct information only about the small amount of [Ca.sup.2+] that is actually free in the myoplasm. The total movements of [Ca.sup.2+] can only be estimated by modelling the large quantities of other [Ca.sup.2+] buffers in the cell (e.g., parvalbumin and troponin; 4), but the amounts and the kinetics of these calcium buffers are not always known in detail.
Most muscle cells contain a salt solution, called the myoplasm, and a storage compartment for calcium, called the sarcoplasmic reticulum.
The B-line presumptive muscle cells of ascidian embryos have extensive potential for self-differentiation dependent on determinants prelocalized in the myoplasm of fertilized eggs (2).
Normal distributions of myoplasm were altered in ascidian embryos by using a microcompression technique (Whittaker, 1980).
occulta may be due to the absence of a protein that is recognized by a vertebrate intermediate filament antibody (NN18) localized in the myoplasm of M.