Principle of Physiology - Assignment Example

?Question a) Below is a schematic diagram of a nerve cell showing the different organs a neuron can terminate onto. Fill-in-the-blanks (spelling MUST be correct to receive full marks) (i) Skeletal muscles are all innervated by neurons from the peripheral nervous system. The neurotransmitter released from the terminal end of the neuron is acetylcholine which binds to nicotinic receptors on the muscle membrane. (ii) Communication across the synapse is one-way because only the presynaptic neuron releases neurotransmitter, and only the postsynaptic membrane reacts to the presence of neurotransmitter. (iii) An action potential is generated at the axon hillock and is propagated via saltatory conduction in a myelinated nerve. In such nerves in the peripheral nervous system the myelin sheath is produced by the Schwann cell. Question 2 (a) Below is part of a very basic diagram of a synapse. Use this diagram to explain how a nerve impulse travels across a synapse. You can add labels, symbols, and numbers that refer to point form annotation. Figure 1. Illustration of a synapse releasing chemical neurotransmitters (acetylcholine) across the synaptic cleft into the post-synaptic cell membrane. The process of synaptic transmission starts with the arrival of an action potential at the presynaptic terminal (Koeppen and Stanton, 2008). This action potential depolarizes the presynaptic membrane causing Ca++ channels to open. Calcium ions then enter the terminal and increase the intracellular Ca++ concentration, leading to the fusion of synaptic vesicles containing chemical neurotransmitter for instance, acetylcholine with the plasma membrane (Burt, 2010). After which, the chemical transmitter is released into the synaptic cleft, diffuses across it, and binds to specific receptors on the postsynaptic membrane (Ganong, 2005). The binding of transmitters to their receptors causes influx of ions into the cell or activation of secondary messengers, depending on the type of receptors (Koeppen and Stanton, 2008). This in turn causes changes in the postsynaptic membrane potential that alters the excitability of the cell (Koeppen and Stanton, 2008). (b) On your diagram shown in part (a) describe how the drug curare affects synaptic transmission. You can add labels, symbols, and numbers that refer to point form annotation. Figure 2. Schematic diagram of a synapse showing disruption of chemical transmission due to binding of curare, an acetylcholine antagonist to nicotinic receptors. Curare is a neuromuscular blocking drug that is similar in structure to acetylcholine and thus, exerts its action by virtue of competitive binding to nicotinic acetylcholine receptors in the postsynaptic membrane (Mycek et al., 2000). Once the action potential has opened the calcium channels and allow Ca ions to fuse the synaptic vesicles with the presynaptic plasma membrane, acetylcholine molecules are extruded into the synaptic cleft. However, curare competes with acetylcholine molecules for binding on the alpha subunit of the nicotinic receptors( Mycek et al., 2000). In large doses, curare could also enter the pore of the ion channels and blocks the entrance. In both instances, ions could not pass through the ion channels, preventing depolarization of the muscle cell membrane (Mycek et al., 2000). (c) In the presence of the toxin curare an action potential can be elicited in a nerve axon. Curare if given to a living organism causes paralysis. Explain why? An action potential (AP) is a signal carrying property of the nervous system characterized by an all-or-none change in membrane potential followed by a return to the resting membrane potential (Koeppen and Stanton, 2008). The generation and propagation of action potentials throughout the axonal length is mediated by voltage-gated channels. Hence, action potentials can still be demonstrated even in the presence of curare. Curare, as mentioned above binds to acetylcholine receptors and not on voltage-gated channels, so APs are not affected. Rather, the effect of curare is seen as blockade of cholinergic transmission between the motor end plate and postsynaptic nicotinic receptors (Mycek et al., 2000). Blocking the interaction of acetylcholine molecules with their receptors prevents the influx of ions into the muscle cells (the post-synaptic cell in this particular case). Without these ions, no membrane excitability on the muscle fiber is generated and so no signal for muscle contraction is perceived. No muscle contraction can occur, hence the paralysis (Mycek et al., 2000). Question 3 - Describe two evolutionary advantages achieved by the myelination of nerves? Myelin sheath produced by the Schwann cells is a good insulator that decreases flow of ions through the membrane about 5000 times (Guyton and Hall, 2006). Even so, ions are still able to pass through the membrane in unmyelinated areas called nodes of Ranvier. Hence, action potentials only occur from one node to another in a process known as salutatory conduction. With this is mind, it can be inferred that myelination of nerve is of value for two reasons. First, by allowing the depolarization of membrane to occur from node to node, the velocity of impulses throughout the length of a myelinated axon is increased by as much as 5-50 times (Guyton and Hall, 2006). Second, myelination conserves energy. Remember that depolarization only occurs in the nodes. This results in less loss of ions since ion flow takes place only in a limited area and hence, would require little energy expenditure to re-establish the ion gradients across the membranes (Guyton and Hall, 2006) References: Burt, A. 2010. Synaptic Transmission. Accessed at: http://www.biologyreference.com Date accessed: April 10, 2012. Ganong, W. 2005. Review of Medical Physiology, Twenty-Second Edition. Guyton, A., and Hall, J. 2006. Textbook of Medical Physiology. 11th edition. Elsevier Inc., Philadelphia, Pennsyllvania. pp 67-69 Koeppen, B and Stanton, B. 2008. Berne and Levy Physiology. 6th edition. Elsevier Inc., Philadelphia, Pennsyllvania. pp 67-69; 82-103 Mycek, M., Harvey, R., and Champe, P. 2000. Lippincott’s Illustrated Reviews-Pharmacology. 2nd edition. Lippincott Williams and Wilkins, 530 Walnut St. Pennsylvania. pp. 50-53 Read More