sarcoplasmic reticulum

Examples of sarcoplasmic reticulum in the following topics:

• Regulatory Proteins

  • Troponin, which regulates the tropomyosin, is activated by calcium, which is kept at extremely low concentrations in the sarcoplasm.
  • The concentration of calcium within muscle cells is controlled by the sarcoplasmic reticulum, a unique form of endoplasmic reticulum in the sarcoplasm.
  • Muscle contraction ends when calcium ions are pumped back into the sarcoplasmic reticulum, allowing the muscle cell to relax.
  • The inward flow of calcium from the L-type calcium channels activates ryanodine receptors to release calcium ions from the sarcoplasmic reticulum.
  • Calcium remains in the sarcoplasmic reticulum until released by a stimulus.

• Excitation–Contraction Coupling

  • A neural signal is the electrical trigger for calcium release from the sarcoplasmic reticulum into the sarcoplasm.
  • The action potential triggers the sarcoplasmic reticulum to release of Ca2+, which activate troponin and stimulate muscle contraction.
  • The sarcoplasmic reticulum is a specialized endoplasmic reticulum found in muscle cells.

• Skeletal Muscle Fibers

  • The sarcoplasm is rich with glycogen and myoglobin, which store the glucose and oxygen required for energy generation, and is almost completely filled with myofibrils, the long fibers composed of myofilaments that facilitate muscle contraction.
  • Each myofibril is surrounded by the sarcoplasmic reticulum, which is closely associated with the transverse tubules.
  • The sarcoplasmic reticulum acts as a sink of Ca+ ions, which are released upon signalling from the transverse tubules.
  • A skeletal muscle cell is surrounded by a plasma membrane called the sarcolemma with a cytoplasm called the sarcoplasm.

• Short-Term Chemical Control

  • When stimulated a signal transduction cascade leads to increased intracellular calcium from the sarcoplasmic reticulum through IP3 mediated calcium release, as well as enhanced calcium entry across the sarcolemma through calcium channels.
  • Once elevated, the intracellular calcium concentration is returned to its basal level through a variety of protein pumps and calcium exchangers located on the plasma membrane and sarcoplasmic reticulum.
  • This is accomplished through reuptake of ions into the sarcoplasmic reticulum via exchangers and expulsion across the plasma membrane.

• Rigor Mortis

  • ATP is no longer provided to operate the SERCA pumps in the membrane of the sarcoplasmic reticulum; these pumps move calcium ions into the terminal cisternae.
  • This release of calcium is caused by the loss of ATP-mediated function of calcium pumps of the sarcoplasmic reticulum, due to ATP depletion in the absence of cellular respiration.

• The Endoplasmic Reticulum

  • The endoplasmic reticulum is an organelle that is responsible for the synthesis of lipids and the modification of proteins.
  • The smooth endoplasmic reticulum (SER) is continuous with the RER but has few or no ribosomes on its cytoplasmic surface.
  • In muscle cells, a specialized SER called the sarcoplasmic reticulum is responsible for storage of the calcium ions that are needed to trigger the coordinated contractions of the muscle cells.
  • This transmission electron micrograph shows the rough endoplasmic reticulum and other organelles in a pancreatic cell.
  • Describe the structure of the endoplasmic reticulum and its role in synthesis and metabolism

• Creatine Supplementation

  • This is specifically caused by eccentric exercise altering muscle ultrastructure and sarcoplasmic reticulum functioning.

• Mechanism and Contraction Events of Cardiac Muscle Fibers

  • Intracellular calcium is then removed by the sarcoplasmic reticulum, dropping intracellular calcium concentration, returning the troponin complex to its inhibiting position on the active site of actin, and effectively ending contraction as the actin filaments return to their initial position, relaxing the muscle.

• Peripheral Motor Endings

  • The depolarization activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the T-tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum.

• Muscle Fatigue

  • Accumulation of metabolites from these reactions other than lactic acid, such as Mg2+ ions or reactive oxygen species, can also induce fatigue by interfering with the release of Ca+ ions from the sarcoplasmic reticulum or through reduction in the sensitivity of troponin to Ca+.