In the name of God

Session 3 1-Resting Membrane Potentials 2-Action potential M.Bayat PhD

Electrochemical gradient

Equilibrium potential Nernst Potential. in Out Electro motive force

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. 0. -60

if RMP = -90 Cin K =140 Cout =14 -60 log 140/14= -60 Inward or outward current? if RPM= -60 Cin K= 100 Cout= 1 -60 log 100/1= -120

if RMP = -90 Cin Na =14 Cout =140 -60 log 14/140= +60 Inward or outward current? if RMP = +60 Cin Na =10 Cout =100 -60 log 10/100= +60

Inward or outward current? if RMP = +85 Cin Na =14 Cout =140 -60 log 14/140= +60 Inward or outward current? if RMP = +60 Cin Cl =14 Cout =140 +60 log 14/140= -60 if RMP = -100 Cin Cl=14 Cout =140 +60 log 14/140= -60 Inward or outward current?

What is resting membrane potential (RMP)?

Resting membrane potential

excitable cells (regenerative AP) RMP= -60,-90 mv Every cell has resting membrane potential 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

What is the origin of RMP?

1 100

Goldman equation

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

Hyperkalemia Hypokalemia In Out

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

What is difference between following RM?

Generation and Conduction of Action Potentials

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

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),

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

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,

Local anesthetic drugs : Novacain, Lidocaine 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. 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 .

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.

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

Saltatory conduction of AP

Saltatory conduction is of value for two reasons 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.

ELECTROTONIC CONDUCTION in internodes and dendrite Dendritic Cable Properties ELECTROTONIC CONDUCTION in internodes and dendrite -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.

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 ri.

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,

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. 

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

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