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ELECTRICAL SIGNALS Electrical communication will be the topic of the next few sections as we cover the Nervous System. The Nervous System is specialized for rapid communication of signals throughout the body, and is composed of two primary cell types: neurons and glial cells. Neurons are responsible for producing and transmitting electrical and chemical signals to cells throughout the body, whereas glial cells are the support cells for the system. We will focus our attention on neurons, which have three basic parts: the cell body, the axon, and the dendrites. As you have learned, electrical signaling along the neuron is due to ion movement across its membrane. Different portions of the neuron conduct electrical signals differently. The conduction of action potentials occurs only on the axon. The cell body and dendrites lack the fast Na+ channels necessary for the initiation of an action potential, and instead exhibit smaller electrical changes called graded potentials. Graded potentials are summed, and if they surpass the threshold for the membrane, an action potential is created. Action potentials cannot be summed, and are called “all or none” phenomena. I assume you know basic neuronal anatomy! ELECTRICAL SIGNALS IN NEURONS 1. Neurons and muscle cells are called excitable tissues because they do what? (p. 236) ______________________________________________________ 2. What two factors influence membrane potential? (p. 236) ______________________________________________________ ______________________________________________________ 3. _________ is the major ion contributing to the resting membrane potential. 4. Which ion is more concentrated in the ECF: Na+ or K+ ? Which is more concentrated in the ICF? ______________________________________________________ ______________________________________________________ 5. If the cell membrane is made suddenly permeable to Na+, in which direction will it move? What is causing this movement? (p. 238) ______________________________________________________ 1 6. When the membrane potential moves from –70 mV to +10 mV, what happens to the existing concentration differences across the membrane? (p. 238) ______________________________________________________ 7. If the cell membrane suddenly becomes more permeable to K+, what happens to the state of the membrane? Why? ______________________________________________________ ______________________________________________________ 8. How do cells alter their permeability to ions? (p. 238-39) ______________________________________________________ 9. How are ion channels classified? Describe each type briefly (p. 239) ______________________________________________________ ______________________________________________________ ______________________________________________________ 10. What is a graded potential? (p. 240) ______________________________________________________ ______________________________________________________ 11. How are action potentials different from graded potentials? ______________________________________________________ ______________________________________________________ 12. Where on the neuron do graded potentials occur? Action potentials? (p. 240-41) ______________________________________________________ ______________________________________________________ ______________________________________________________ 13. What determines the magnitude of the graded potential? (p. 240) ______________________________________________________ 14. Describe two ways in which ion movement can hyperpolarize a cell. ______________________________________________________ ______________________________________________________ 2 15. Where is the trigger zone? (p. 241) ________________________________________ 16. If a graded potential reaches threshold at the trigger zone, what happens? (p. 241-42) ______________________________________________________ ________________________________________________________________ 17. If several graded potentials reach the trigger zone at the same time, what do you think will happen? Explain. ______________________________________________________ ______________________________________________________ 18. Define an action potential. (p. 242) ______________________________________________________ ______________________________________________________ 19. What does “all-or-none” mean when referring to action potentials? (p. 242) ______________________________________________________ ______________________________________________________ 20. Action potentials specifically involve the movements of what two ions? In which direction are they moving? (p. 243) ______________________________________________________ ________________________________________________________________ 21. For each phase of the action potential listed below, indicate what is happening to ion permeability, which ions are moving, and in what direction (in or out of cell). Rising phase: Peak: Falling phase: After-hyperpolarization: 22. Name the two gates of the voltage-gated Na+ channels. (p. 245) ______________________________________________________ 23. In the resting neuron, which of these gates are closed and which are open? ______________________________________________________ 3 24. Depolarization opens the _____________________________ gate. 25. When do inactivation gates close? Why do they close? (p. 245) ______________________________________________________ ________________________________________________________________ 26. What must happen to the gates before the next action potential can take place? ______________________________________________________ 27. Define refractory period. (p. 245-46) ______________________________________________________ ______________________________________________________ 28. How do the absolute & relative refractory periods differ? ______________________________________________________ ______________________________________________________ ______________________________________________________ 29. Why might the absolute refractory period be a “good thing”? (p. 246) ______________________________________________________ ______________________________________________________ 30. Describe the role of the Na+/K+ ATPase pump in the action potential. (p. 246) ______________________________________________________ ______________________________________________________ ______________________________________________________ 31. What is meant by the conduction of action potentials? (p. 246) ______________________________________________________ 32. When Na+ channels in the middle of an axon open, depolarizing current flow will spread in both directions along the axon. Why then don’t action potentials ever reverse and move back toward the cell body? ______________________________________________________ 4 ______________________________________________________ 33. List two factors that affect the speed of action potential conduction. (p. 247-49) ______________________________________________________ 34. Explain saltatory conduction. (p. 249) ______________________________________________________ ______________________________________________________ 35. What happens to conduction through axons that have lost their myelin? (p. 249) ______________________________________________________ THINGS TO TRY: 1. Lidocaine inactivates voltage-gated Na+ channels on the neuronal membrane. If lidocaine is placed on the axon of a nerve that normally transmits signals from a pain receptor to the brain (to be interpreted by the brain as “pain”), the pain is not “felt” by the individual. Explain why. 2. Draw/label a neuron. Indicate on your picture exactly where graded potentials would be generated and where action potentials would be generated 3. Drug Z prevents sodium inactivation (“h”) gates from moving from their resting position (“resting” refers to their position when the membrane is at its RMP). How would administration of Drug Z affect the function of a neuron? SYNAPSES READING: p. 253- An action potential can travel down the length of the neuronal membrane and communicate the electrical information to another cell. This transmission occurs via a synapse. A synapse is a junction between a neuron and a target cell, which could be another neuron, a muscle cell, or a gland. At a synapse, the axon of the presynaptic neuron passes information to receptors on the dendrites or cell body of the postsynaptic target cell(s). Most synapses are chemical junctions, and involve the release of neurotransmitter from the presynaptic neuron onto the postsynaptic cell. Neurotransmitters are manufactured in the cell bodies of neurons (where the organelles are located) and travel down to the axon terminal where they are housed in vesicles until signaled for release. When the appropriate signal (action potential) arrives, neurotransmitter is released via exocytosis. The neurotransmitter then travels by diffusion to the postsynaptic membrane where it opens ion channels, resulting in some type of electrical potential change. Because this electrical change occurs on the dendrites or cell body, it is a graded potential. The overall postsynaptic potential change will determine whether or not an action potential will be fired. 5 Synaptic transmissions that bring the postsynaptic membrane closer to threshold are called excitatory postsynaptic potentials, or EPSPs. Inhibitory postsynaptic potentials, or IPSPs, take the membrane further from threshold. As mentioned, it is the overall postsynaptic potential that will determine if an action potential is fired on the postsynaptic cell. 1. Name the seven classes of neurotransmitters. (p. 254-57) ______________________________________________________ ______________________________________________________ ______________________________________________________ *Note: we will spend a lot of time in class on specific NT’s, so just read over the info on pg. 255 to get familiar with them. 2. What are the possible places for neurotransmitter synthesis? Where is it stored? (p. 257) ______________________________________________________ ______________________________________________________ 3. At a chemical synapse, describe the sequence of events that leads to neurotransmitter release, beginning with an action potential traveling along the presynaptic membrane. (p. 258) ______________________________________________________ ______________________________________________________ ______________________________________________________ ______________________________________________________ 4. What is the chemical trigger for neurotransmitter release? ______________________________________________________ 5. How does the new “kiss and run” pathway compare to regular exocytosis? (p. 258) ______________________________________________________ 6. What happens to Ach after it is released into the synaptic cleft? (Fig. 8-19, p. 259) ______________________________________________________ 7. How, using the same neurotransmitter, might an olfactory neuron alert you to a stronger smell? (p. 260) ______________________________________________________ 8. Draw a picture of neurons converging and another of neurons diverging. (p. 262) 6 9. Name one advantage of convergence. (Fig. 8-22, p. 262) ______________________________________________________ ______________________________________________________ 10. A slow synaptic potential would likely cause what type of effect? (Fig 8-23, p. 263) ______________________________________________________ 11. What is spatial summation of graded potentials? (p. 264-65) ______________________________________________________ ______________________________________________________ ______________________________________________________ 12. Describe postsynaptic inhibition (p. 266) ______________________________________________________ ______________________________________________________ 13. Describe temporal summation (Fig. 8-24, p. 264) ______________________________________________________ ______________________________________________________ 14. Define long-term potentiation (p. 267) ______________________________________________________ ______________________________________________________ 15. When might long-term potentiation be useful? ______________________________________________________ ______________________________________________________ ______________________________________________________ 7 16. List some pharmacological agents that can alter synaptic transmission. (p. 268) ______________________________________________________ ______________________________________________________ 17. Neuron A, Neuron B and Neuron C are all presynaptic to Neuron F. If A and B fire, F fires. If A and C fire, nothing happens. Draw this scenario below. What can you conclude about the synapse between C and F? Between A and F? What other information might you need? ______________________________________________________ ______________________________________________________ 18. Neuron J, Neuron K, and Neuron L are all presynaptic to Neuron T. J and K are both excitatory to T, whereas L is inhibitory to T. Assume that T needs a net input of +2 (one EPSP is +1; one IPSP is -1) to fire an action potential. Describe how temporal summation could result in an action potential on T. Describe how spatial summation could result in an action potential on T. ______________________________________________________ ______________________________________________________ ______________________________________________________ THINGS TO TRY: 1. Neuron A, Neuron B and Neuron C are presynaptic to Neuron D. When A fires an action potential, D fires an action potential. When A and B fire simultaneously, D does not fire. When A, B, and C fire simultaneously, D fires. This is an example of... A. inhibition by D and temporal summation by A and B. 8 B. inhibition by B and temporal summation by A and C. C. inhibition by B and spatial summation by A and C. D. inhibition by B and spatial summation by A and D. E. inhibition by A and spatial summation by B and C. Defend your choice. 2. Black widow venom causes an explosive release in acetylcholine from the axon terminals of neurons leading to skeletal muscle. Discuss why this might be problematic to the victim. 3. Botulism toxin blocks the release of acetylcholine from these same neurons. How would the effects of this toxin compare to black widow venom? Can you explain why the victim would experience respiratory distress in both cases? 9