Membrane Potentials Polarity

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Membrane Potentials Polarity

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1. 1 Membrane Potentials (Polarity) Information found in 3 places: Chapter 3 - pp. 82-83 Chapter 9 - pp. 289-290 Chapter 11 – pp. 397- 405 and pp. 409- 413

2. 2

3. 3 Resting Membrane Potential (Vr)

4. 4 Neuromuscular Junction

5. 5 Action Potential A transient depolarization event that includes polarity reversal of a sarcolemma (or nerve cell membrane) and the propagation of an action potential along the membrane

6. 6 Neuromuscular Junction When a nerve impulse reaches the end of an axon at the neuromuscular junction: Voltage-regulated calcium channels open and allow Ca2+ to enter the axon Ca2+ inside the axon terminal causes axonal vesicles to fuse with the axonal membrane

7. 7 Neuromuscular Junction

8. 8 Neuromuscular Junction This fusion releases ACh into the synaptic cleft via exocytosis ACh diffuses across the synaptic cleft to ACh receptors on the sarcolemma Binding of ACh to its receptors initiates an action potential in the muscle (ACh – acetylcholine)

9. 9 Role of Acetylcholine (Ach) ACh binds its receptors at the motor end plate Binding opens chemically (ligand) gated channels Na+ and K+ diffuse out and the interior of the sarcolemma becomes less negative This event is called depolarization

10. 10 Depolarization Initially, this is a local electrical event called end plate potential Later, it ignites an action potential that spreads in all directions across the sarcolemma Threshold – critical level of stimulus

11. 11 The outside (extracellular) face is positive, while the inside face is negative This difference in charge is the resting membrane potential Action Potential: Electrical Conditions of a Polarized Sarcolemma

12. 12 The predominant extracellular ion is Na+ The predominant intracellular ion is K+ The sarcolemma is relatively impermeable to both ions Action Potential: Electrical Conditions of a Polarized Sarcolemma

13. 13 An axonal terminal of a motor neuron releases ACh and causes a patch of the sarcolemma to become permeable to Na+ (sodium channels open) Action Potential: Depolarization and Generation of the Action Potential

14. 14 Na+ enters the cell, and the resting potential is decreased (depolarization occurs) If the stimulus is strong enough, an action potential is initiated Action Potential: Depolarization and Generation of the Action Potential

15. 15 Polarity reversal of the initial patch of sarcolemma changes the permeability of the adjacent patch Voltage-regulated Na+ channels now open in the adjacent patch causing it to depolarize Action Potential: Propagation of the Action Potential

16. 16 Thus, the action potential travels rapidly along the sarcolemma Once initiated, the action potential is unstoppable, and ultimately results in the contraction of a muscle Action Potential: Propagation of the Action Potential

17. 17 Action Potential: Repolarization Immediately after the depolarization wave passes, the sarcolemma permeability changes Na+ channels close and K+ channels open K+ diffuses from the cell, restoring the electrical polarity of the sarcolemma

18. 18 Action Potential: Repolarization Repolarization occurs in the same direction as depolarization, and must occur before the muscle can be stimulated again (refractory period) The ionic concentration of the resting state is restored by the Na+-K+ pump

19. 19 Time from the opening of the Na+ activation gates until the closing of inactivation gates The absolute refractory period: Prevents the neuron from generating an action potential Ensures that each action potential is separate Enforces one-way transmission of nerve impulses Absolute Refractory Period

20. 20 The interval following the absolute refractory period when: Sodium gates are closed Potassium gates are open Repolarization is occurring The threshold level is elevated, allowing strong stimuli to increase the frequency of action potential events Relative Refractory Period

21. 21 Absolute Refractory Period

22. 22 Hyperpolarization Occurs when membrane potential increases Inside of membrane becomes more negative

23. 23 Absolute Refractory Period

24. 24 Used to integrate, send, and receive information Membrane potential changes are produced by: Changes in membrane permeability to ions Alterations of ion concentrations across the membrane Types of signals – graded potentials and action potentials Membrane Potentials: Signals

25. 25 Short-lived, local changes in membrane potential Decrease in intensity with distance Their magnitude varies directly with the strength of the stimulus Sufficiently strong graded potentials can initiate action potentials Graded Potentials

26. 26 Graded Potentials

27. 27 A brief reversal of membrane potential with a total amplitude of 100 mV Action potentials are only generated by muscle cells and neurons They do not decrease in strength over distance They are the principal means of neural communication An action potential in the axon of a neuron is a nerve impulse Action Potentials (APs)

28. 28 Na+ and K+ channels are closed Leakage accounts for small movements of Na+ and K+ Each Na+ channel has two voltage-regulated gates Activation gates – closed in the resting state Inactivation gates – open in the resting state Action Potential: Resting State

29. 29 Na+ permeability increases; membrane potential reverses Na+ gates are opened; K+ gates are closed Threshold – a critical level of depolarization (-55 to -50 mV) At threshold, depolarization becomes self-generating Action Potential: Depolarization Phase

30. 30 Sodium inactivation gates close Membrane permeability to Na+ declines to resting levels As sodium gates close, voltage-sensitive K+ gates open K+ exits the cell and internal negativity of the resting neuron is restored Action Potential: Repolarization Phase

31. 31 Action Potential: Hyperpolarization Potassium gates remain open, causing an excessive efflux of K+ This efflux causes hyperpolarization of the membrane (undershoot) The neuron is insensitive to stimulus and depolarization during this time

32. 32 Repolarization Restores the resting electrical conditions of the neuron Does not restore the resting ionic conditions Ionic redistribution back to resting conditions is restored by the sodium-potassium pump Action Potential: Role of the Sodium-Potassium Pump

33. 33 Phases of the Action Potential 1 – resting state 2 – depolarization phase 3 – repolarization phase 4 – hyperpolarization

34. 34 What if ……..? The amount of extracellular K+ were below normal? The release of the NT from the synaptic knob were prevented? Receptor sites for the NT were blocked? The number of NT receptor sites were reduced? Opening of the voltage-gated sodium channels were prevented? You grab a live 120V electric wire?

35. 35 What if the amount of extracellular K+ were below normal? Hypokalemia (hi-po-KAY-lemia) E.g. due to loss of K+ through diuretics or diarrhea Stronger tendency of K+ to diffuse out Results in hyperpolarization of RMP Therefore more difficult to reach threshold and action potential Signs and symptoms = muscle weakness, sluggish reflexes, cardiac dysrhythmias

36. 36 What if release of NT were prevented? e.g. botulism: a rare but deadly form of food poisoning Bacteria from improperly canned foods produce botulinus toxin 0.0001mg is lethal. 500 lbs could kill the entire human population

37. 37 What if receptor sites for the NT were blocked? E.g. curare binds to but not does not activate the Ach receptors No Na+ entry…no depolarization …no contraction Results in Flaccid Paralysis

38. 38 What if amount of extracellular Ca++ were below normal Need to know: When ECF concentrations of Ca++ are appropriate Ca++ binds to receptors on voltage gated Na+ channels keeping them closed. e. g. Hypocalcaemia ( due to lack of dietary calcium, , lack of Vit. D, lack parathyroid hormone) Some of the Na= channels which are normally closed will remain open Results in Hyperpolarized RMP and therefore easier to reach threshold and action potential Signs and Symptoms – nervousness, muscle spasms tetany.

39. 39 The # of NT receptor sites reduced E.g. Myasthenia Gravis: an autoimmune disorder where antibodies bind to and destroy some of the ligand-gated receptors More difficult to reach threshold and action potential Muscles feel week and easily fatigued due to smaller % of muscle fibers working)

40. 40 Opening of the voltage-gated sodium channels were prevented e.g. local anesthetics such as Xylocaine (lidocaine) prevent action potentials from traveling to brain = no pain Commonly used for dental work

41. 41 You grab a live 120V electric wire ???????????????????

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