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What is an action potential?
Rapid and reversible change in the membrane potential of an excitable cell
Put in order of faster AP to slowest AP: skeletal muscles, cardiac ventricle cell and motor neuron
Motor neuron (2msec), skeletal muscle (5 msec), cardiac ventricular cell (200 msec -- 100x longer than motor neuron)
What happens to Na permeability during an AP?
Increases rapidly and coincides with peak of AP and then is inactivated
How is resting membrane potential established?
Diffusion potentials of ions (each ion tries to attempt to drive the membrane potential toward its own equilibrium)
Why is the resting membrane potential close to the equilibrium potentials for K and Cl?
High permeability of the cell membrane to those ions at rest
At rest, the membrane has high permeability to which ions and low permeability to which ions?
High - K and Cl (lots of influence on membrane potential -> drives membrane towards its equilibrium point); low - Na and Ca (little influence on membrane potential)
How many Na and K does the Na/K ATPase pump in/out?
3 Na out, 2 K in (creates and maintains K concentration gradient to keep resting potential low)
How are Na and K permeabilities related?
Na's is fast in the upstroke, K's is slow in the repolarizing phase
How does tetrodotoxin affect the cell?
Blocks voltage-gated Na channels so only get a hyperpolarization response
Describe an AP.
1-at resting membrane potential (high K conductance, low Na conductance); 2-upstroke of AP (inward current spreads from neighboring APs and causes a depolarization of the cell to threshold -> voltage-gated Na channels open [activation gates] and Na conductance increases = inward Na current and more Na permeability so membrane potential gets near Na equilibrium); 3-repolarization (depolarization causes Na inactivation gates to close slowly and terminate the upstroke, depolarization causes K channels to open and increases K conductance = outward K current and repolarization); 4-hyperpolarizing undershoot (K conductance is higher than at rest so membrane potential approaches K equilibrium more so than at rest but then K conductance returns to normal level and cell goes back to resting potential)
What is responsible for the upstroke of the AP in nerve and skeletal muscle?
Voltage-gated Na channels
Why are refractory periods important?
Prevent the AP from going backwards up the axon; protects cells from overstimuation
What is the mechanism of relative refractory periods?
High K permeability makes it difficult to depolarize and elicit another AP (keeps the membrane close to hyperpolarization so need a supramaximal stimulation to generate another AP); Na inactivation gates are open so another AP can be generated
What is the mechanism of absolute refractory periods?
No AP is possible due to the closing of Na inactivation gates (type of conduction block)
When do the Na activation and inactivation gates open/close?
Activation gates are voltage-dependent so open when membrane reaches threshold; inactivation gates open at peak of AP since are activated by depolarization too but are slower so take longer to respond to depolarization
How do members of the -caine family (lidocaine, etc) work as a local anesthetic?
Plugs Na+ pore so ion can't flux in
Explain how local anesthetics get into the cell.
Most are in an unionized form to get across the membrane then gain a proton and become active and unable to get out of membrane; goes to block Na pore then (these drugs are pH dependent and the pH determines whether will get a proton or not)
What are properties of a block due to a local anesthetic?
1-AP amplitude decreases; 2-conduction slows; 3-voltage-dependent (during AP, inside becomes more + so membrane wants to push out molecules with a + charge [the -caine molecule stuck in the pore] but since the drug is there it's stuck and no Na+ can get in the cell); 4-use-dependent (during AP, cell pushes out drug more but it blocked -- injured cells send out more APs but are blocked); 5-pH-dependent (that's how drug can gain/not gain a proton); 6-reversible
What is electrotonic conduction?
Limited conduction over a short distance; DECREMENTAL (not propagated) so it will decrease with distance/decay; slow rate of rise; summation; no Na voltage-gated channels so can't propagate
What is AP conduction?
Long distance conduction of electrical signals; PROPAGATE in a non-decremental fashion due to voltage-gated Na channels that open with threshold depolarization; ALL OR NONE; region of depolarization moves down axon and resting potential is re-established behind it by Na/K pump
Does depolarization spread both ways or only 1 way in an axon?
Will spread both ways but can't go backwards due to absolute and relative refractory periods but THE AP GOES ONLY ONE WAY
What is a capacitor and why do we care?
Capacitory - two conducting plates separated by an insulator; plates = intracellular and extracellular fluid, insulator = axon membrane and myelin sheaths
How does myelin affect capacitance of the axon?
Decreases capacitance = increase AP velocity because less charges leak out during saltatory conduction
How does increased diameter affect capacitance and velocity?
Decreases capacitance and increases velocity
How does increased diameter affect axial resistance and velocity?
Decreases resistance and increases velocity
How does myelin help out the axon?
Increases its metabolic efficiency - fewer ions enter/leave axon so the Na/K pumps have less work to do
How does hyperkalemia affect nerve firing?
Increase in extracellular K causes depolarization of resting membrane and this SUSTAINED depolarization closes the inactivation gates of the Na channels
How does diameter relate to AP conduction velocity?
They are proportional (greater diameter = faster conduction)
Describe the nodal environment (Na and K channels, etc.).
High density Na channels, low density K channels, no myelin = high capacitance = slower velocity
Describe the myelinated environment (Na and K channels, etc.).
Low density Na channels, high density K channels, myelinated = low capacitance = high velocity
Does incoming dendritic information degrade?
Yes - incoming signals are decremental and must summate to raise voltage to threshold to trigger an AP
Are C fibers myelinated?
No - and are very slow because of it (need a high stimulus current to fire)
What do C fibers do?
Dorsal root - pain, temp, some mechanoreceptors, reflex responses; sympathetic - postganglionic sympathetics
What type of neurons are more vulnerable to damage and why?
Long sensory and motor neurons are more vulnerable to damage since they have to travel so far before synapsing (polyneuropathy is common)
Do axons have ribosomes? What is a consequence of this?
No, do not have ribosomes; must synthesize proteins, NTs and mitochondria in the soma then transport to the axons
How does leprosy affect axons?
Bacterial invasion of Schwann cells that dedifferentiate and unwrap myelin
How does polyneuropathy of long axons present?
Symmetric, distal sensory disturbances (feet first then hands) in a glove and stocking distribution (no dermatomal pattern); pain, numbness, tingling more prominent than weakness (more weakness in distal muscles than proximal); loss of distal DTRs prior to proximal ones
How does demyelination affect nerve function?
Increases capacitance so decreases conduction velocity, more K conductance = loss of current
How does remyelination in PNS occur?
2 Schwann cells wrap around 1 axon (instead of 1:1) in relapsing, remitting neuropathies (MS)
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