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67 Cards in this Set

  • Front
  • Back

Membrane Potential Vm

electrical voltage across cell membrane


remember with a cell that has no sodium pump and is only permeable to K, K would not leak out because of electroneutrality - this is not true some DOES leak out- establishing Membrane Potential

Diffusion driven by

- Concentration Gradients


- Electrical potential differences


+ -> -


- -> +

Measure Membrane PD _____ with respect to _____

inside , outside

FORMULA Nernst Equation

z = valance charge

z = valance charge


FOR A NEGATIVE NUMBER

Membrane vs Equilibrium Potential

Membrane - true voltage PD across membrane




Equilibrium - voltage (determined by the Nernst equation) that perfectly balancesthe chemical diffusional driving force determined by a concentration difference across the cellmembrane

Typical Equilibrium Potentials

EK = - 100 mV


ENa = + 50 mV


ECl = - 70 mV

Resting Membrane Potential

ionic permeability of cell membranes is unchanging with time

Membrane Ionic Conductances (gNa, gk, gCl)

easier way to measure rmp


directly proportional to permeability




i = gV




iK = gK (Vm - Ek)


iCl = gCl (Vm - ECl)


iNa = gNa (Vm - ENa)



Vm is stable then total net current iT =

iT = 0 (t = sum of all i's)

Positive current


Negative current

Positive current (ik) = outward current, makes Vm more negative




Negative current (iCl) = inward current, makes Vm more positive

Hyper polarizing


Depolarizing

H - More negative


D - Less negative/more positive

Most cells resting potential

~ -70 mV

Vm FORMULA

Vm = gkEk + gNaENa + gClECl / gT

Motor Neuron Anatomy

Motor Neuron Anatomy

Motor neuron - innervates muscle




In Spinal Cord


Soma - cell body (nucleus, receives connections)


Dendrites - branching, receives connections




Outside Spinal Cord


nerve - bundle of axons with many neurons

Action Potential

Short in duration (3msec) - neuron impulse

Phases of AP

A - resting potential (-70 mV)
B - rapid depolarization (peak at 40 mV)
C - rapid depolarization (back to resting)
D - after hyperpolarization undershoot (-90)
A - return to resting

A - resting potential (-70 mV)


B - rapid depolarization (peak at 40 mV)


C - rapid depolarization (back to resting)


D - after hyperpolarization undershoot (-90)


A - return to resting

What causes AP?

NA and K channels

Voltage-Gated Channels of AP

Na+ Channel


- m gate (activation)


- h gate (inactivation)




K+ Channel


- n gate (activation)

AP Channels - Na+

At Rest: Na+ closed


Depolarization: activates/open rapidly - inc in GNa more depolarization, + feedback inc GNa more


Repolarization: when Vm gets more positive, channel will inactivate/close (dec GNa and iNa)

AP Channels - K+

At Rest: K+ open - causes negative rp


Depolarization: more activate/open and remain open after inactivation of Na channels


Repolarization: an inc of gK causes Vm to get more negative - produces after shoot

Ratio of Na:K channels

4:1 - reason for the depolarization

Gates + Phases
A: M + N closed, H open
B: M + H open, N closed
C: M + N open, H closed
D: M + H closed, N open

A: M + N closed, H open


B: M + H open, N closed


C: M + N open, H closed


D: M + H closed, N open

Hyperkalemia

Higher than normal extracellular K+ levels




Less negative EK




Vm becomes less negative, closure of H gates




Na+ channels won't open -> NO AP

Ionic Concentration Gradient

Even though AP result in an inc in Na in and an dec of K out, this is countered by the sodium pump -> pumps out extra Na and restores lost K

Ouabain

No immediate effect on AP, the neuron could still fire 1000s of AP before the gradient would be dissipated enough to cause an effect

Initiation of AP

Vm must be depolarized to threshold


AP are all are none - same amplitude and duration

Refractory Periods

Absolute - 2nd AP can't occur no matter what




Relative - 2nd AP can occur if stimulus is large enough, must be after relative refractory

Tetraethyl ammonium cation (TEA+)

Blocks K+ channels, doesn't prevent AP - prolongs duration and removes afterhyperpolarization

Tetrodotoxin (TTX)

Blocks Na+ irreversibly - not used clinically


Blocks AP LETHAL

Local anesthetics (lidocaine)

Blocks Na+ reversibly, used clinically

Action Potential Propagation

Action potentials travel along neurons axon


AP occurs at distance (x) = 0

λ

Length constant -> each λ traveled = decrease in potential by 63%

AP conduction




Antidromic


Orthodromic

Can conduct in 2 directions - rarely happens



Anti - abnormal direction of conduction


Ortho - normal conduction

λ FORMULA

rm = membrane resistance (1/gT)
ri = intracellular resistance 

rm = membrane resistance (1/gT)


ri = intracellular resistance

rm and ri



Myelin

Evolutionary advantage - packing of millions of high speed axons - increases λ by increasing rm




Current must flow axially down the axon to find gaps (nodes of Ranvier) - also where the Na channels are solely located - nerve conduction jumps from node to node (saltatory conduction) - highest conduction in alpha motor neurons

Multiple Sclerosis (MS)

caused by demyelination, decreases λ

Unmeylinated vs myelinated axon

Unmeylinated: grey, velocity proportional to square root of diameter, can be fast at very small diameters




Myelinated: white, long axons rapidly conducting

Local potentials

- Initiate AP


- Graded potentials


- result from ion-permeable channels


- amplitude and duration vary


- can sum in time (temporal) and distance (spatial)

Three types of local potentials

- Synaptic potentials


- Endplate potentials


- Generator potentials

Synaptic potentials

2 types of postsynaptic potentials


- EPSP - elicit AP - depolarize


- IPSP - inhibit AP - hyper polarize




Typically small events, just one can't affect AP - can be summed

EPSP

- equally permeable to Na and K


- inc gK normally hyperpolarizes, but with gNa inc depolarizes

IPSP

- permeable to K or Cl


- inc in gK hyper polarizes, gCl no change


- cancels effects of EPSP


- typically hyperpolarizing, but can also be depolarizing if ECl is less negative than Vrest

Summation of EPSP / IPSP

Can occur, because there is no rapidly activating Na channel - can't fire AP, summation leads to AP at hillock




Does NOT sum algebraically

Silent IPSP

No change in Vm but can still counter EPSP

Neural inhibition

Half of all neural synapses are inhibitory


by increasing IPSP, dec activity of postsynaptic neurons

ADHD

Inc brain activity, (normal function is to inhibits brain centers) this decreased hyperkinesis

Tetanus

causes from injection via puncture wound


blocks inhibitory synapses - loss of inhibition, muscle contraction - asphyxiation and death

End Plate Potential EPP

Endplate is in the skeletal muscle - motor neuron innervates NMJ


- inc gNa and gK


- Depolarizing, always elicits AP in muscle fiber (because much larger area)


- no inhibitor EPPS



Generator / Receptor Potentials

- detection of physical stimuli - sensory receptors


- touch/pressure receptor


- carries info to CNS


- frequency of AP varies with pressure

Pacinian corpuscle

touch receptor in palms, fingers


2 regions


- depressed naked region - Ap propagates along axon, can elicit AP


- unmyelinated - fast acting Na channels, non excitable no AP

Thin Filament is made up of

Actin - troponin 3 subunits
G-actin - globular 
tropomyosin - thin lines 

Actin - troponin 3 subunits


G-actin - globular


tropomyosin - thin lines

Thick Filament is made up of

myosin, heads line up head to head - bare zone in the middle

myosin, heads line up head to head - bare zone in the middle

Which band remains constant?

A BAND

Sliding Filament theory

1. Rigor state - tight binding 45 angle, NO ATP


2. ATP binds, myosin can dissociate from actin


3. ATPase activity of myosin hydrolyzes ATP, have ADP and Pi bound to myosin


4. REGULATED STEP Myosin head swings and wings to a new actin - 90 degree


5. Pi released POWER STROKE, actin pushed


6. ADP released back to rigor

3 Subunits of Troponin

TnC - Ca++ binding site


TnT - bound to tropomyosin


TnI - glue, holds it all together

What covers the myosin binding sites on actin

Tropomyosin, ca++ causes a conformational change of troponin-tropomyosin

Ca++ comes from?

SR through EC coupling

EC Coupling Process

AP - DHP opens ryanodine receptor (plug + cork)

Termination of contraction caused by?

Lower levels of Ca++ - calsequestrin

Isometric

Same length, doesn't shorten but generates force

Isotonic

same tension, muscle shortens, shortens more with lighter loads

Single twitch


Summation


Summation -> unfused tetanus


Summation -> complete tetanus


- muscle relates after stimuli


- muscle can't relax fully b/w 2 stimuli


- multiple stimuli far enough allow muscle to relax slightly


- muscle reaches steady tension - stops with fatigue

Why is tetanus tension 3-5x more than twitch?

because of the time needed to stretch

Length tension relationship



Strenuous vs. endurance exercise

- sprinting - high energy expenditure, long lag recovery




- long distance - lower energy expenditure, maintained longer