Uses of Calcium Ions in the Body - Essay Example

Name : xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx Tutor :xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx Title : USES OF CALCIUM IONS IN THE BODY Institution : xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx Date :xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx @ 2012 Uses of Calcium ions in the body Introduction Calcium is one of the most important minerals in the body. Calcium ions play a very critical role in the biochemistry and physiology of the body and the cell. It is very important in the pathways of signal transduction as it acts as the second messenger, contraction of the cells in all types of muscles, inneurotransmitter release from neurons and fertilization (Senisi, Fong 2003 pp130). Calcium ions are needed by many enzymes as a cofactor especially those involved in blood clotting. Calcium therefore plays a role in blood clotting and also maintains the potential difference across cell membranes that are excited as well as in the formation of bones. Calcium ions in the construction of skeletal muscles The skeletal muscles of a human being display a huge variability in its functions like the rate of force of production, energy metabolism, and resistance to fatigue, metabolism of energy together with a big spectrum from physiology that is slow anaerobic to that which is fast anaerobic. To add to this, skeletal muscles show high plasticity that a rises from the ability of the muscle fibers to go through cytoarchitecture changes as well as change in composition of particular muscle protein isoforms. Muscle fibers have adaptive changes that take place in response to various stimuli like hormones, growth and differentiation factors, and exercise and nerve signals. Muscle fibers are organized in compartments functioning as independent subunits. Every muscle fiber makes use of calcium ions as the main signaling and regulatory molecule. Contractile properties of the muscle fibers rely on variable expressions of proteins that take part in calcium ion handling and signaling (Sun, and Irving 2009 pp. 65). Diversity in molecules of main proteins within the calcium ion signaling apparatus or calcium cycle to a large extent determines the relaxation and contraction properties of the fibers of the muscle. The calcium ions signaling apparatus includes ryanodine receptor that acts as the sarcoplasmic reticulum channel for release of calcium, the troponin protein complex mediating the calcium ion effect to myofibrillar structures causing contraction, the calcium ion pump that does the reuptake of calcium ions into the sarcoplasmic reticulum and calsequestrin which is the protein that stores calcium ions in the sarcoplasmic reticulum. To add to this there are several calcium ions binding proteins in the muscle tissues among them calmodulin, parvalbumin, annexins, S100 proteins, myosin light chains, sorcin, calpain, calcineurin, and β-actinin (Senisi, Fong 2003 pp112). These calcium ion binding proteins can either play a critical role in muscle contractions triggered by calcium ions in certain conditions or modulate the other activities of muscles like differentiation, protein metabolism and growth. Recently many calcium ion handling and signaling molecules have appeared as being altered in diseases of the muscles. Functional alterations of calcium ion handling are responsible for pathophysiological conditions that occur in dystrophinopathies malignant hyperthermia and brody’s disease. This shows how important the affected molecules are for the correct performance of the muscles (Bowen 2003 pp 99). As shown above, calcium ions are very critical in the process of muscle contraction. The process involves various steps as shown below all of which are dependent on the availability of calcium ions. Initially, an action potential with its origin in the Central Nervous System gets to an alpha motor neuron. The neuron transmits an action potential through its axon. The action potential works by through the activation of voltage gated sodium channels through the axon to the neuromuscular junction. When it gets to the junction an influx of calcium ions is forced through the voltage gated ion channels. This influx of calcium ions causes those vesicles having the neurotransmitter acetylcholine to have a fusion with the plasma membrane. This action releases acetylcholine in to the space outside the cell between the skeletal fiber neuromuscular junction and the terminal of the motor neuron (Sun, and Irving 2009 pp. 65). Acetylcholine then diffuses through the synapse then binds itself to and activates the nicotinic acetylcholine receptors found on the neuromuscular junction. When the nicotinic receptor opens the potassium/sodium intrinsic channel sodium rushes in as potassium goes out. Since the permeability of the channel to sodium is high there is a positive charge in the muscle fiber membrane that triggers an action potential. The action potential created spreads through the network of muscle fibers made of T-tubules hence causing a depolarization of the inner parts of the muscle fiber. This depolarization has the effect of activating the L-type voltage dependent calcium channels otherwise called dihydropyridine receptors inside the T tubule membrane that are closely situated to channels of calcium release called ryanodine receptors within the sarcoplasmic reticulum next to them (Carmeliet et al 2010 pp. 43). Activated volate-gated calcium channels interact physically with the channels of calcium release so that they are activated and this causes the release of calcium from sarcoplasmic reticulum. The calcium gets bound to the troponin C available on the thin myofibrils that have actin. Tropomyosin is then modulated allosterically by troponin. In ordinary circumstances, tropomyosin obstructs binding sites the myosin binding sites on the thin filament. When calcium gets bound to the toponin C there is an allosteric change within the troponin protein. The binding sites are unblocked when tropoyosin is allowed by troponin T to move. Myosin that has inorganic phosphate and ADP on its nucleotide binds to the uncovered binding sites on the thin filament. Myosin is then bound to actin in a very strong state of binding (Anonymous 2010). The release of inorganic phosphate and ADP are coupled to the power stroke. The Z bands are then pulled to each other and this shortens the I band and the sarcomere. ATP is bound to myosin and this makes it release actin and therefore enter the weak binding state. When there is no ATP this step cannot occur. What results is the rigor motis state. The ATP is then hydrolyzed by myosin and the energy is used to get back to the cocked back conformation (Senisi, Fong 2003 pp 69). The above two steps are repeated but with the presence of calcium ions on the thin filament. In the process of the above steps calcium gets pumped in an active way into the sarcoplasmic reticulum. When there is no calcium on the thin filament the conformation of tropomyosin is changed back to the former state so that the binding sites can be blocked again. The myosin stops binding on the thin filament causing the contractions to stop. Calcium ions get out of the molecule of troponin so that the concentration of calcium ion is maintained in the sarcoplasm. There is a deficiency of calcium ions created in the fluid surrounding the myofibrils when the calcium ions are actively pumped into the sarcoplasmic reticulum. As a result calcium ions are removed from troponin (Anonymous 2010). Calcium ions in the Central Nervous System Calcium ions are required for homeostasis in the Central Nervous System. Intracellular homeostasis with calcium is very important for neural function and development. The influx of calcium ions through voltgate gated calcium channels (VGCC) are responsible for regulating many processes within the CNS among them the growth of neurons, excitability, motility, secretion of hormones and neurotransmitters, differentiation, neurotoxicity, synaptic plasticity, neural gene expression and neurotoxicity. Regulation of the entry of calcium via the VGCC is of critical importance in motor functions and sensory processing (Traverso 2004). Due to the important role of the calcium ions in the process of signaling, interference with their functions may result into big disturbances in the nervous system functioning and structure. Increased intracellular calcium levels take part in neurodegenerative mechanisms of the tissue of the brain and neurological disorders can result from mutations in genes that encode calcium channel subunits (Carmeliet et al 2010 pp. 34). In the calcium homeostasis in developing brains neural development of cells is normally under the control of a tightly regulated and organized sequence of activities including differentiation, cellular proliferation, maturation and migration. Calcium ion signaling plays a very important part in all of these events. VGCC are expressed highly in the process of development and their function is important for the development of neurons. In a postnatal brain development there is a transitional period for neurons that are developing where any disruptions in calcium homeostasis may cause poor results (Anonymous 2010). Neuronal gene expression Calcium channels tend to influence neural activities and many others through the signaling pathways controlling gene expression. Regulation of different transcription factors such as CREB is also involved here. Entry of calcium particularly via LTCC is critical for transcriptional responses inside the muscle, neurons, osteoblasts and pancreatic beta cells. By stimulating CREB calcium in the nucleus can modulate expression of many genes among them neurotransmitter receptors and scaffolding and transmembrane proteins (National Center for Biotechnology Information 1997). Purkinje neurons Purkinje cells are some GABAergic neurons found within the cerebellar cortex. The survival and proliferation of GABAeric neurons including the Purkinje neurons in a brain that is developing depends on a calcium influx that is highly regulated through the VGCC. Reducing or increasing the currents of calcium via these channels has been seen to cause significant effects on the existence of cell cultures (Traverso 2004). Undeveloped and Young Purkinje neurons without dendrites in culture only display the calcium current with high threshold which is increased roughly by half in amplitude in the process of development. This indicates that conductance of calcium is very important in the maturation and development of Purkinje neurons. One important function of entry of calcium through LTCC in the neurons is that the signaling pathway seems to be conveying developmental cues to the nucleus directly and through this it activates factors of gene transcription such as CREB and the expression of proteins of the cell. This effect gets increased by the release of more calcium from stores within the cell (Norris 2007 pp. 98). Structural organization, branching, neuronal differentiation, growth and migration Signaling of calcium regulates the dendritic and axonal branching in many types of neurons that are still developing among them Purkinje neurons. This effect causes mechanisms such as CREB activation which is dependent on calcium (Bobick, Balaban 2008 pp. 68). Calcium regulates the growth of neurons and the motility of growth cones and this process depends on the activation of G-proteins. Optimum calcium influx levels enhance normal axonal and dendritic elongation and growth cone activities involved in path finding of neural direction and recognition of targets. These activities are very crucial for the assembly of circuits that are functional in the developing nervous system as well as for regeneration after damage. The alterations in the amounts of calcium inside the cells and the way it enters the cells can cause major effects on the function and structure of the networks of neurons. Calcium transients do the regulation of growth cone advance through direct effects on the growth cone (Carmeliet et al 2010 pp. 134). Suggestions have been made to the effect that calcium signals via LTCC affect differentiation of the neural stem or progenitor cells (NSC). A study done on the NSC of the brain cortex after birth showed that their differentiation has a strong relationship with LTCC expression and that calcium ion influx via these channels plays a very important role in the promotion of differentiation in neurons. Calcium transients have been found to play an important role in the organization and migration control of neuronal and non neuronal cells in CNS that is still developing. In vitro migration of neurons is associated with non neuronal cells with cellular aggregates being formed. Chan such cell complexes for cultured embryonic chick ciliary ganglion were observed as a result of treatment that lowered or increased the concentration of calcium within the cell (Body and Bouillon 2003 pp. 123). Calcium homoestasis in neuroglia Changes in the levels of intracellular calcium are critical signals for the communication between neurons and glial cells. Recent evidence shows that voltage gated calcium channels tend to regulate the process. Microglia has a crucial role to play in the Central Nervous System inflammatory responses as well as its secretory and migratory responses may be modulated through the increased calcium through LTCC. Many lipopolysaccharides can exert this kind of influence directly or by activating chemokine receptors. Such mechanisms of rise in the level of calcium after activation of chemokine receptors have been seen in oligodendrocytes that have a major function of myelinating axons (Bowen 2003 pp 87). Conclusion In conclusion, the role of calcium ions in the body cannot be overemphasized. Calcium ions are very crucial in many of the functions of the body. They are involved in processes such as bone and teeth formation, CNS, muscle contraction among other things. In this paper the focus has been on two major roles of calcium in the body. The role of calcium in the CNS and muscle contraction has been discussed. It is important to note that without the presence of calcium ions muscle contraction is impossible. These ions play very important roles in this process. Calcium is also very important in the Central nervous system since it takes part in its formation and development as well as its day to day functions. Bibliography Anonymous (2010) Calcium homeostasis in the Central Nervous System – implications for brain development and autism (Online) Available at: Viewed 19 April 2012. Bobick, Balaban (2008) The Handy Anatomy Answer Book Visible Ink Press Body J. and Bouillon R. (2003) Reviews in Endocrine and Metabolic disorders. Emergencies of calcium Homeostasis Sage Bowen R. (2003) Calcium Homeostasis; Colorado State University Biomedica HyperTexts Carmeliet G. et al (2010); Clinical Endocrinology and Metabolism, Disorders of calcium Homeostasis. National Center for Biotechnology Information, U.S. National Library of Medicine, (1997) The importance of calcium ions in the body. (Online) Available at: . Norris D. (2007) Vertebrate endocrinology Elsevier. Amazon publishers. New York city. Senisi S., Fong (2003) Body structures and Functions; Cengage learning Sun, Y and Irving, M; (2009). The molecular basis of the steep force-calcium relation in heart muscle, Journal of Molecular and Cellular Cardiology Traverso M. (2004) Chemistry 154, Washington University (Online) Available at: . Read More