1. 1 In the name of God

2. 2 1-Resting Membrane Potentials 2-Action potential M.Bayat PhD Session 2

3. Electrochemical gradient 3

4. Equilibrium potential 4 Nernst Potential. Electro motive force in Out

5. Examples of the uses of the Nernst equation If K + is 10 times more concentrated on side A (0.1) than on side B(0.01), calculate the electrical potential difference that must exist between the chambers for K + to be in equilibrium across the membrane. -60

6. What is resting membrane potential (RMP)? 6

7. Resting membrane potential 7

8. excitable cells (regenerative AP) RMP= -60,-90 mv neurons- nerve fiber- cardiac cell- skeletal muscle Nonexcitable cells RMP=-20,-40 blood cells-endothelial cell- epithelial – fibroblast- adipocyte Every cell has resting membrane potential

9. What is the origin of RMP? 9

10. 10 1001

11. 11

13. Goldman equation

14. The chord conductance equation describes the contributions of permeant ions to the resting membrane potential

15. 15 Hyperkalemia Hypokalemia In Out

16. Resting Membrane potential will change if: The extracellular K concentration changes The Sodium- potassium pump activity changes Change in ionic conductance 16

17. What is difference between following RM? 17

18. Generation and Conduction of Action Potentials 18

19. http://highered.mcgraw- hill.com/sites/0072943696/student_view0/ chapter8/animation__voltage- gated_channels_and_the_action_potential __quiz_1_.html http://highered.mcgraw- hill.com/sites/0072943696/student_view0/ chapter8/animation__voltage- gated_channels_and_the_action_potential __quiz_1_.html 19

20. 20 The Passive Response or electrotonic conduction,Local (Subthreshold) The active response or SUPRATHRESHOLD or THE ACTION POTENTIAL

22. Threshold and All-or-None Property all-or-none APs are all very similar toeach other (in shape, duration, amplitude, rate of rise, and propagation velocity),

23. Refractory period, the refractory periods are proportional to the AP duration. absolute refractory period relative refractory period functional (effective) refractory period, which is defined by the highest frequency of APs that the excitable cell (e.g., neuron) can propagate impulses up to 1000/s, then the functional refractory period is 1.0 ms

24. Plateau in Some Action Potentials: First, in heart muscle, two types of channels: (1) the usual voltage-activated sodium channels, called fast channels, and (2) voltage-activated calcium-sodium channels, which are slow to open and therefore are called slow channels. A second factor that may be partly responsible for the plateau is that the voltage-gated potassium channels are slower than usual to open, 24

25. 25 Local anesthetic drugs act mainly by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane, in particular the so-called voltage-gated sodium channels. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited.sodiumion channelsneuronalcell membraneaction potential The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Local anesthetic drugs bind more readily to sodium channels in an activated or inactivated state, thus onset of neuronal blockade is faster in neurons that are rapidly firing. This is referred to as state dependent blockade. Increase in extracellular Ca does as a relative antagonist for action of local anesthetics. The calcium ion seat down on the voltage gated Na channel and inhibits the channel activation as a result prolongs channel resting state and decrease affinity for local anesthetic drugs. Increase in potassium ion in extracellular is caused membrane depolarization and increase active and inactive state of the Na channel as a result increase affinity for local anesthetic drugs. Local anesthetic drugs : Novacain, Lidocaine

26. S o d i u m a n d S o d i u m C h a n n e l s Tetrodotoxin blocks action potentials in nerves by binding to the voltage-gated, fast sodium channels in nerve cell membranes, essentially preventing any affected nerve cells from firing by blocking the channels used in the process. [5] The binding site of this toxin is located at the pore opening of the voltage-gated Na + channel.action potentialsvoltage-gatedsodium channelsnerve cellmembranes [5]binding site

27. 27 http://highered.mcgraw- hill.com/sites/9834092339/student_vie w0/chapter44/action_potential_propaga tion_in_myelinated_neurons.html http://highered.mcgraw- hill.com/sites/9834092339/student_vie w0/chapter44/action_potential_propaga tion_in_unmyelinated_neurons.html

28. Propagation of the Action Potential Direction of Propagation. All-or-Nothing Principle. 28

29. 29 Saltatory conduction of AP

30. Saltatory conduction is of value for two reasons. First, by causing the depolarization process to jump long intervals along the axis of the nerve fiber, this mechanism increases the velocity of nerve transmission in myelinated fibers as much as 5- to 50-fold. Second, saltatory conduction conserves energy for the axon because only the nodes depolarize, allowing perhaps 100 times less loss of ions than would otherwise be necessary, and therefore requiring little metabolism for reestablishing the sodium and potassium concentration differences across the membrane after a series of nerve impulses. 50- fold decrease in membrane capacitance allow repolarization to occur with very little transfer of ions.

31. Dendritic Cable Properties -Triggering of an action potential depends on how far the synapse is from the spike initiation zone and the properties of the dendrite (ie. Internal and membrane resistance.) -Some dendrites have voltage gated channels that can help amplify signals along dendrites. ELECTROTONIC CONDUCTION in internodes and dendrite

32. 32 Length constant ثابت مکانی The membrane resistance is a function of the number of open ion channels, and the axial resistance is generally a function of the diameter of the axon. The greater the diameter of the axon, the lower the r i. ion channels diameter axon

33. Saltatory Conduction(Latin saltare, to jump), energy cost of signaling is greatly decreased, increasing the effective R m by about one-hundred-fold decreasing the effective C m by about one-hundred-fold increases the length constant,

34. if you think of myelin as effectively increasing the thickness of the cell membrane, you would expect this to decrease its capacitance (thicker insulating layer). However, myelination also increases the membrane resistance, so overall the time constant (= RC) might not actually change much. Myelination increases conduction velocity mainly because the increased membrane resistance increases the length constant, λ.

35. Conduction Velocity Radius fiber Membrane Capacitance Myelin coating Length constant Time constant Resting membrane, AP amplitude temperature 35

36. membrane excitability will be increased by the greatest amount by : Increasing extracellular Na Increasing extracellular K Decreasing extracellular Cl Decreasing extracellular Ca Decreasing extracellular H 36