What is the role of calcium ions in muscle contraction

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Structural analysis for a ryanodine receptor 1 gain insight into calcium release during muscle contraction

Muscle contraction is known to be regulated by calcium. An action potential generated by a motor neuron propagates on the muscle cell surface, activates voltage-gated calcium channels and allows calcium flow into the muscle cell. This calcium activates another ion channel called ryanodine receptor (RyR1 in muscle cells) which releases even more calcium stored inside the sarcoplasmic reticulum to the cytoplasm of the cell. Calcium diffusing in the cytoplasm between myosin and actin filaments of the muscle fibrils causes the filaments to slide into each other, triggering the contraction of the entire muscle fiber. As the action potential decays, the calcium ions are actively pumped back into the sarcoplasmic reticulum with the SERCAs pump (Sarcoplasmic/endoplasmic reticulum calcium ATPase).

In the current research the vesicles of sarcoplasmic reticulum were purified, imaged by cryo-electron tomography and the structure was solved by averaging to a resolution of 12.6 Å. The presence of native context showed several features which have not been observed previously; helix-like electron densities crossing the bilayer about 5 nm from the RyR1 transmembrane domain can be seen, as well as sarcoplasmic extensions connecting RyR1 with a putative calsequestrin network. The primary conformation of RyR1 in native membranes and its structural variants are documented. Surprisingly, the activation of RyR1 is associated with changes in membrane curvature and movement in the sarcoplasmic extensions.

These structures provide an insight into the mechanism of RyR1 in its natural environment.

From The School of Biomedical Sciences Wiki

Ca2+ ions play an important role in muscle contraction by creating interactions between the proteins, myosin and actin. The Ca2+ ions bind to the C component of the actin filament, which exposes the binding site for the myosin head to bind to in order to stimulate a muscle contraction[1].

Bone Mineralization

Bone rigidity is partially due to a salt in its osteoid matrix which consists of calcium and phosphate ions. If the ion concentrations are above the threshold value then bone mineralization will occur. In order to maintain the ion concentrations:

If there is a calcium deficiency in the blood, mineralization does not complete causing a disease called osteomalacia. This causes the bone to soften and become more vulnerable to damage leading to rickets or other bone deformities[2].

Parathyroid Hormone

Parathyroid glands, located in the region of the neck, release the hormone parathormone which maintains the calcium concentration in the blood. In order to increase the concentration it mobilizes the calcium stored in mineralized bone[3] by stimulating osteoclastic activity[4]. This works by reducing the loss of calcium ions in the kidney and by increasing the reabsorption of the ion into the small intestine.

When calcium ions levels are persistently low the constant activity of parathyroid glands cause them to swell. This swelling is called parathyroid hyperplasia. Additionally, an over-secretion of parathormone brings about excessive damage to the bone and a surplus of calcium in the blood.

Synaptic Transmission

As an action potential reaches the presynaptic membrane of a neurone, voltage-gated calcium channels open, allowing calcium ions to diffuse in down their concentration gradient[5]. The increase in concentration of calcium in the presynaptic neurone causes microtubules to physically dock synaptic vesicles into active zones of the presynaptic membrane[6]. SNARE proteins on the membrane of the synaptic vesicles and in the presynaptic membrane then interact, allowing exocytosis of neurotransmitters contained within the synaptic vesicles[7]. The release of neurotransmitters into the synaptic cleft carries the signal that there has been an action potential in the previous neurone. This subsequently induces depolarisations or hyperpolarisations of the postsynaptic membrane, and therefore allows the transmission of action potentials between neurones.

Muscle Contraction

Skeletal Muscle Cells

During muscle contraction, high concentrations of calcium are required to displace troponin and reveal the active site at which myosin binds to for the power stroke. Calcium is released from the sarcoplasmic reticulum through calcium ion channels when the membrane of the T-tubular system is excited. It binds to Troponin C causing it to conform, hence permitting the myosin head to latch onto the actin filament, onsetting muscle contraction[8].

Cardiac Muscle

Similarly to skeletal muscles, the contraction of cardiac muscles is regulated by the concentration of calcium ions. However, some main differences in contraction mechanisms are that:

The T-tubular system in cardiac muscles has much greater invaginations on the cell surface.
The sarcoplasmic reticulum is much less complex in comparison to that in the skeletal muscle[9].

References

↑ https://teaching.ncl.ac.uk/bms/wiki/index.php/Ca2%2B_ions
↑ Lowe, J. and Stevens, A. (2005:256) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
↑ Lowe, J. and Stevens, A. (2005:279) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
↑ Lowe, J. and Stevens, A. (2005:261) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
↑ Khan Academy. The Synapse. Date Unknown [cited 06/12/2017]. Available from: https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/the-synapse
↑ Author Unknown. Synaptic Activity. February 2010 [cited 06/12/2017]. Available from: http://www.albany.edu/faculty/cafrye/apsy601/Ch.04feb10,psychopharmacology.html
↑ Ribchester RR. The Neuromuscular Junction: Structure and Function. 2013 [cited 06/12/2017]. Available from: http://www.dns.ed.ac.uk/rrrweb/nwplecture3nmjphysiolmorphol13.pdf
↑ Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.
↑ Lowe, J. and Stevens, A. (2005:75) Human Histology, 3rd edition, Maryland: Elsevier Mosby.

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