BCH 420 TUTORIAL QUESTION AND ANSWER Question 1 With adequate illustration name the structural and functional types of neurons ANS Based on their roles, the neurons found in the human nervous system can be divided into three classes: sensory neurons, motor neurons, and interneurons. Sensory neurons Sensory neurons are the nerve cells that are activated by sensory input from the environment - for example, when you touch a hot surface with your fingertips, the sensory neurons will be the ones ring and sending off signals to the rest of the nervous system about the information they have received. The inputs that activate sensory neurons can be physical or chemical, corresponding to all five of our senses. Thus, a physical input can be things like sound, touch, heat, or light. A chemical input comes from taste or smell, which neurons then send to the brain. Most sensory neurons are pseudounipolar, which means they only have one axon which is split into two branches. Motor neurons Motor neurons are part of the central nervous system (CNS) and connect to muscles, glands and organs throughout the body. These neurons transmit impulses from the spinal cord to skeletal and smooth muscles (such as those in your stomach), and so directly control all of our muscle movements. There are in fact two types of motor neurons: those that travel from spinal cord to muscle are called lower motor neurons, whereas those that travel between the brain and spinal cord are called upper motor neurons. Motor neurons have the most common type of ‘body plan’ for a nerve cell - they are multipolar, each with one axon and several dendrites. Interneurons As the name suggests, interneurons are the ones in between - they connect spinal motor and sensory neurons. As well as transferring signals between sensory and motor neurons, interneurons can also communicate with each other, forming circuits of various complexity. They are multipolar, just like motor neurons. Based on their structure, the neurons found in the human nervous system can be divided into three classes Unipolar neuron A unipolar neuron is a type of neuron in which only one protoplasmic process (neurite) extends from the cellbody. Unipolar neurons are common in insects, where the cell body is often located at the periphery of the brain and is electrically inactive. These cell bodies often send a single neurite into the brain; however, this neurite may ramify into a large number of branches making a very complex set of connections with other neurites, integrations of neuropil. Bipolar neuron A bipolar neuron or bipolar cell, is a type of neuron which has two extensions (one axon and one dendrite).Bipolar cells are specialized sensory neurons for the transmission of special senses. As such, they are part of the sensory pathways for smell, sight, taste, hearing and vestibular functions. Common examples are the bipolar cell of the retina, the ganglia of the vestibulocochlear nerve, and the extensive use of bipolar cells to transmit efferent (motor) signals to control muscles. Multipolar neuron A multipolar neuron is a type of neuron that possesses a single axon and many dendrites (and dendric branches), allowing for the integration of a great deal of information from other neurons. These processes are projections from the nerve cell body. Multipolar neurons constitute the majority of neurons in the central nervous system. They include motor neurons and interneurons/relaying neurons are most commonly found in the cortex of the brain, the spinal cord, and also in the autonomic ganglia. Pseudounipolar neuron A pseudounipolar neuron has one axon with two branches: central and peripheral. These axonal branches should not neuron, in that they do not have separate dendrites and an axonal process, but rather one branched process that serves both functions. The axon has a peripheral branch (from the cell body to the periphery: skin, joint and muscle) and a central branch (from the cell body to spinal cord). Question 2 With 2 illustrative pathway discuss energy source in muscle ANS a) Short term mechanism using high energy phosphate bond E.g creatine phosphate. Muscle contraction are fuelled by ATP, the energy currency of the body. In the absence of oxygen (Anaerobic condition) the ATP needed for muscle contraction is derived from phosphocreatine or creatine phosphate. The muscle uses phosphocreatine an energy storing molecule to derive the first few minutes of muscle contraction. Phosphocreatine also known as creatine phosphate can rapidly donates it’s phosphate group to ADP & creatine under anaerobic condition. This provides immediate synthesis of ATP. ATP and creatine phosphate together are called phosphagen system and are critically important source of energy for muscle contraction especially in athletic activities that need high power for a short period of time. In the recovery phase after muscle contraction, creatine phosphate is re-synthesized from its breakdown product, creatine and inorganic phosphate at the expense of ATP. The energy (ATP) required for phosphagen replenishment comes from aerobic metabolism. b) Medium term mechanism via Anaerobic Glycolysis. As the phosphocreatine store of the muscle becomes depleted, the muscle switch to another source of energy which is glycolysis. Glycolysis is the pathway for the catabolism of glucose. It occurs in the cytosol. In the presence of O2 , pyruvate which is the end product of the pathway is converted to acetyl-coA and in the absence of O2, pyruvate is coverted to lactate. In the absence of O2, glycolysis is used to meet short term demand of energy by the muscle. This involve the incomplete breakdown of carbohydrate to lactic acid. It is involved in muscular activities that last for a short period of time (few minutes). The glycolytic process is sustained in the muscle due to recycling of NAD and NADH. The continuance of the glycolytic process in the muscle in the absence of O2,,leads to the accumulation of lactate which lead to muscle fatigue or tissue damage. Question 3 Calcium is a necessary factor in muscle contractibility, explain. ANS. Events that stimulates muscular activities begins with the excitation of the neuromuscular junction. An action potential reaches the axon of the motor neuron, this action potential activates voltage gated calcium ion channel on the axon and calcium rushes in. the calcium causes acetylcholine vesicles in the axon to fuse with membrane releasing the acetylcholine into the cleft. The muscular fibre is excited as the acetylcholine diffuses across the cleft and binds to nicotin receptors on the motor end plate. This result in the opening of channels in the membrane for sodium and potassium. Sodium rushes in and potassium rushes out. However because sodium is more permeable, the muscle fibre becomes more positive generating an action potential. The action potential on the muscle fibre causes the sarcoplasmic reticulum to release calcium ion. This calcium binds to troponin present on the filaments of myofibrils. The tropini then allosterically modulates the tropomyosin. Normally the tropomyosin physically obstruct binding sites for cross bidge. Once calcium binds to troponin, the troponin forces the tropomyosin to move out of the way unblocking the binding site in actin. This allows the myosin head to then form a corss bridge with the actin filament known as actin-myosin complex. The formation of the actin-myosin complex involves the hydrolysis of an ATP molecule to ADP and Pi. As long as a calcium ions remain in the sarcoplasmic to bind troponin and as long as ATP is available, the contraction process will continue and the muscle fibre will shorten. Question 4 Muscle movement involves conversion of chemical to mechanical energy , explain using myosin. ANS ATP is critical for muscle contractions because it breaks the myosin-actin crossbridge, freeing the myosin for the next contraction. ATP first binds to myosin, moving it to a high-energy state. The ATP is hydrolysed into ADP and inorganic phosphate (Pi ) by the enzyme ATPase. The energy released during ATP hydrolysis changes the angle of the myosin head into a “cocked” position, ready to bind to actin if the sites are available. ADP and Pi remain attached; myosin is in its high energy configuration The muscle contraction cycle is triggered by calcium ions binding to the protein complex troponin, exposing the active binding sites on the actin. As soon as the actin-binding sites are uncovered, the high-energy myosin head bridges the gap, forming a cross-bridge. Once myosin binds to the actin, the Pi is released, and the myosin undergoes a conformational change to a lower energy state. As myosin expends the energy, it moves through the “power stroke,” pulling the actin filament toward the M-line. When the actin is pulled approximately 10 nm toward the M-line, the sarcomere shortens and the muscle contracts. At the end of the power stroke, the myosin is in a low-energy position. After the power stroke, ADP is released, but the cross-bridge formed is still in place. ATP then binds to myosin, moving the myosin to its high-energy state, releasing the myosin head from the actin active site. ATP can then attach to myosin, which allows the cross-bridge cycle to start again; further muscle contraction can occur. Therefore, without ATP, muscles would remain in their contracted state, rather than their relaxed state. Question 5 Explain how calcium concentration is regulated in the body ANS High plasma level When the concentration rises the parafollicular cells of the thyroid gland increase their secretion of calcitonin (a proteinaceous hormone) into the blood. At the same _me the parathyroid glands reduce their rate of parathyroid hormone (or PTH, also a proteinaceous hormone) secre_on into the blood. The resulting high levels of calcitonin in the blood stimulate the skeleton to remove calcium from the blood plasma, and deposit it as bone. The reduced levels of PTH inhibit removal of calcium from the skeleton. The low levels of PTH have several other effects: they increase the loss of calcium in the urine, but more importantly inhibit the loss of phosphate ions via that route. Phosphate ions will therefore be retained in the plasma where they form insoluble salts with calcium ions, thereby removing them from the ionized calcium pool in the blood. The low levels of PTH also inhibit the formation of calcitriol (not to be confused with calcitonin) from cholecalciferol (vitamin D3) by the kidneys. The reduction in the blood calcitriol concentration acts (comparatively slowly) on the epithelial cells (enterocytes) of the duodenum inhibiting their ability to absorb calcium from the intestinal contents. The low calcitriol levels also act on bone causing the osteoclasts to release fewer calcium ions into the blood plasma. Low plasma level When the plasma ionized calcium level is low or falls the opposite happens. Calcitonin secretion is inhibited and PTH secretion is stimulated, resulting in calcium being removed from bone to rapidly correct the plasma calcium level. The high plasma PTH levels inhibit calcium loss via the urine while stimulating the excretion of phosphate ions via that route. They also stimulate the kidneys to manufacture calcitriol (a steroid hormone), which enhances the ability of the cells lining the gut to absorb calcium from the intestinal contents into the blood, by stimulating the production of calbindin in these cells. The PTH stimulated production of calcitriol also causes calcium to be released from bone into the blood, by the release of RANKL (a cytokine, or local hormone) from the osteoblasts which increases the bone resorptive activity by the osteoclasts. These are, however, relatively slow processes. Thus fast short term regulation of the plasma ionized calcium level primarily involves rapid movements of calcium into or out of the skeleton. Longer term regulation is achieved by regulating the amount of calcium absorbed from the gut or lost via the feces. Question 6 Enumerate six causes of increase urinary excretion of phosphorus ANS Chronic kidney disease Chronic kidney disease is a slow and progressive loss of kidney function over a period of several years. Eventually, a person will develop permanent kidney failure. Chronic kidney disease, also known as chronic renal failure, chronic renal disease, or chronic kidney failure, is much more widespread than people realize; it often goes undetected and undiagnosed until the disease is well advanced. Uncontrolled diabetes This causes high levels of blood sugar that can lead to serious medical problems, such as organ damage. Diabetic ketoacidosis A complication of diabetes that can happen if the body begins to run out of insulin. Harmful ketones build up in the body and blood sugar levels rise. Hypoparathyroidism A rare hormone disorder in which the body does not produce enough parathyroid hormone (PTH). PTH helps control the levels of phosphorus in the blood and bones. Hypocalcemia Low levels of calcium in the blood. Dietary source Constant and increased intake of foods high in phosphorus content Question 7. Enumerate 4 difference in myelination in PNS and CNS ANS Myelin is formed by Schwann cells in the peripheral nervous system (PNS) and oligodendrocytes in the central nervous system (CNS). Question 8 Using a named fatty acyl coa as an example discuss energy production in muscle. ANS In the first stage which is beta oxidation-the fatty acids undergo oxidative removal of successive two-carbon units in the form of acetyl-CoA, starting from the carboxyl end of the fatty acyl chain. For example, the 16-carbon fatty acid palmitic acid (palmitate at pH 7) undergoes seven passes through this oxidative sequence, in each pass losing two carbons as acetyl-CoA. At the end of seven cycles the last two carbons of palmitate (originally C-15 and C-16) are left as acetyl-CoA. The overall result is the conversion of the 16-carbon chain of palmitate to eight two-carbon acetyl-CoA molecules. The overall equation is Palmitoyl-CoA + 7CoA + 7FAD + 7NAD+ + 7H2O 8 acetyl-CoA + 7FADH2 + 7NADH + 7H+ In the second stage of fatty acid oxidation the acetyl residues of acetyl-CoA are oxidized to CO2 via the citric acid cycle, which also takes place in the mitochondrial matrix. The Overall equation for the oxidation of the 8 acetyl coa in TCA cycle is 8 Acetyl-CoA + 16O2 + 96Pi + 96ADP 8CoA + 96ATP + 104H2O + 16CO2 The first two stages of fatty acid oxidation produce the reduced electron carriers NADH and FADH2, which in the third stage donate electrons to the mitochondrial respiratory chain, through which the electrons are carried to oxygen and Coupled to this flow of electrons is the phosphorylation of ADP to ATP. the overall equation for the complete oxidation of palmitoyl-CoA to carbon dioxide and water: Palmitoyl-CoA + 23O2 + 131Pi + 13lADP CoA + 13lATP + l6CO2 + 146H2O Question 9 Name 3 means by which ATP can be resynthesized in active muscle cell ANS I. II. III. Short term mechanism using high energy phosphate bound e.g. creatine phosphate. Medium term mechanism via anaerobic glycolsis Long term mechanism via oxidative phosphorylation. Question 10 Discuss the significances of calcium ions in muscular activities ANS 1. Expose myosin-binding sites on actin filament by displacing the tropomyosin present on actin filament. Explanation: Calcium ions released by the sarcoplasmic reticulum play a vital role in contraction of muscles. From sarcoplasmic reticulum these ions(Ca2+) released into the cytoplasm of the muscle cell, specifically called as sarcoplasm. In sarcoplasm, Ca2+ ions attach to one of the three molecules of troponin. This causes the tropomyosin to displace slightly from the actin filaments. This displacement expose the binding sites on the actin filament. Thus myosin heads get instantly attached to the binding sites on actin filament and contraction of muscles occurs. 2. Regulation of Troponin and Tropomyosin Regulation of Troponin and Tropomyosin 3. Explanation. To enable muscle contraction, tropomyosin must change conformation and uncover the myosin-binding site on an actin molecule, thereby allowing cross-bridge formation. Troponin, which regulates the tropomyosin, is activated by calcium, which is kept at extremely low concentrations in the sarcoplasm. If present, calcium ions bind to troponin, causing conformational changes in troponin that allow tropomyosin to move away from the myosin-binding sites on actin. Once the tropomyosin is removed, a cross-bridge can form between actin and myosin, triggering contraction. Crossbridge cycling continues until Ca2+ ions and ATP are no longer available; tropomyosin again covers the binding sites on actin.
