4. action potentials and conductance

leak channels

specific; always open for K and Na in resting cell so responsibe for resting potential

gated channels

open or closed

two types:

• voltage gated

• ligand gated: open when ligand/chem substance binds

the action potential

stimulating of a resting neuron creates disruption in the membrane that results n the opening of voltage-gated channels for Na

depolarization

any change that moves the membrane closer to zero

what threshold voltage generates an action potential?

-50-55 mV

stimuli

make Na channels open; at peak/channels K channels open

what causes action potential?

rapid inward influx of Na through voltage gated channels

• depolarizes membrane to 0

  • first Na neutralize the K on the resting membrane and then established a (+) charge on interior membrane called the overshoot (peaks at +30-50 mV)

hyperpolarized

• inward Na influx stops as Na vg channels close

• outward influx of K starts as K vg open

but bc not all the K voltage channels close in time, the potential becomes hyper-polarized briefly

the dip is physically farther away from the threshold value

kinetics of Na or K is slower?

K

are Na and K vg channels stimulated by the same stimuli?

yes

three characteristics of action potentials:

1. all or none: reach the threshold its gunna happen

2. absolute refractory period: impossible to generate second action potential

3. relative refractory potential: possible to generate second action potential but require stronger stimulus to reach threshold

mechanism of absolute refractory period

sodium channel inactivation

*closed state can be reopened by stimulus but inactivated cannot; ball = inactivated

IFM

string of aas that block the channel

explain blockage of action potentials with local anesthetics

hydrophobic mines like lidocaine enter cell and move in and binds ball and chain to inhibit its release; keeps it closed

describe conduction

cell depolarized in segments; regenerate action potential as it continues each axon segment

green is refractory but action potentials cannot go back!

action potential Na (in or out) v refractory period K (in or out) to go back to (blank)

in

out

resting potential (first hyper polarization)

regenerative current

new action potential generated each segment of the axon

cable conduction

passive depolarization; not segments but a flow

electrical can conduct through myelin sheath

false; at nodes of ranvier you can conduct current (only nodes depolarize)

saltatory conduction

a rapid mode of signal transmission along myelinated neurons, where the electrical impulse jumps from one node of Ranvier to the next; depolarize axon in segments not entire axon like other conductions

faster 120m/s VS 0.5m/s

the leakier the cel, the spread of potential becomes

limited

Na can leak out membrane

length constant λ

distance that a graded electrical potential can travel passively down an axon before it decays to ~37% of its original amplitude

=√r_m/r_i

r_m

resistance to ion current through membrane

high means membrane not leaky to Na; more chance for potential as charge (Na) stays inside

r_i

resistance to ion flow in axoplasm (movement of things down axon); viz axial resistance = increase in conduction velocity

the lower the resistance, the easier it is for ions to move across the cell membrane

T or F: low r_i and high r_m means greater λ

true! means axon will depolarize to threshold further down from where injection occurs

length constant is a function of

• axon diameter

• myelination

T or F: larger axons have higher axial resistance

false they have lower axial resistance (r_i)

T or F: myelin sheaths raise the r_m

true

fastest neurons vs slowest diameter and myelination

• fast: large diameter myelinated

• slow: small diameter, non-myelinated

multiple sclerosis

myelin sheaths sleuth off

Na come at node but no normal channels so leaks!

• exposes axon membrane which lacks Na channels but has K channels; nodes have Na channels

• inward Na current dissipated in demyelinated region by outward K current which prevents depolarization from reaching Na channel in subsequent node

• demyelination promotes conduction failure

sodium channels become abnormally distributed along demyelinated axons, moving away from the nodes of Ranvier where they are normally concentrated, which disrupts proper signal transmission. excessive sodium influx into axons, which in turn triggers a reverse sodium-calcium exchanger, causing a harmful buildup of calcium within the axon and contributing to axonal degeneration