Excitable Cells and AP Flashcards
resting membrane potential
negative value
excess of negative charges inside compared to outside
how does the electical gradient arise?
- large gradients of Na+ and K+
- relative permeability of the membrane to those ions
Nernst Equation
-60 x log [Xi/Xo]
what happens if increase extracellular K?
equilibrium potential will become less negative/depolarize
what happens if you increase intracellular K
eq potential will increase/become more negative
hyperpolarize
K equilibrium potential
-88 mV
more on inside than outside
equilibrium potential of Na
+60 mV
more on outside than inside
if suddenly very permeale to Na (AP) it moves very positive very fast
permeability to a given ion
depends n number of channels and conductance of channels
GHK equation
Goldman-Hodgkin-Katz
used to determine the potential across a cell’s membrane taking into acct all of the ions that are permeant
start w Nernst and add permeability factor for K
what happens when increase K permeability at rest
hyper polarizes
drives membrane potential closer to Keq (-88)
Na/K ATPase
ubiquitously expressed in cell membranes
maintains gradient of Na and K
3 Na out for 2 K in
energy consuming
Na/Ca exchanger
in muscle cells
3 Na in and 1 Ca out down electrochemical gradients
reversible dep on voltage
maintains low intracellular Ca2+ levels
Ca2+ pump
expressed in muscle cells
pumps Ca2+ out with ATP
maintains low intracelular Ca2+ levels
passive membrane resistors
ion channels
resist flow but allows it to move
passive membrane capacitor
stores charge
2 conductors sep by insulatior
con = ECF, ICF
ions = cell membrane
charge builds up and can store it
passive membrane as circuit
- current charges capacitor (+ to mem and displaces + on the other side
- current moves through both capacitor and ion channel (new SS - charges begin to leave through resistor)
- at SS, current moves only through channel (resisotor)
voltage change is linear and can be predicted by Ohm’s law
ionic basis of action potential
increase Na+ perm - rushes in, increase voltage to positive
incrase K+ perm - brings gradually back to negative
K channel is delayed rectifier - voltage gated!
depolarization
when sodium channels open
outward current (bc Na+ in)
hyperpolarization
when K channels open
inward current repolarizes the membrane
VG - Na channels
closed - open (Na in) - inactivated (stuck and can’t activate - have to repolarize to open) - closed
VG - K channels
delayed rectifiers
single gate - open and closed
open SLOWER
activated at more depolarized P
stays open until back to resting membrane potential
rising phages
FEED FORWARD
stim –> depol membrane –> Na channels open –> inward current –> depol mem further
falling phase
depol membrnae –> open VG K+ channels –> repolarize membrane –> return to Vrest
overshoot
voltage about 0 mV
amplitude
voltage from V rest to peak
threshold potential
voltage you begin to activate Na+ channels
absolute refractory period
if deliver 2nd stim - get NOTHING
Na+ channels are inactivated - can’t be opened, no response until “closed”
relative refractory period
get response but it’s blunted
cell has increased K+ permeability compared to rest - if fire Na+ channels, response will be smaller
action potential conduction
length constant
proportional to rm/ri
resistance - how currnet will spread and voltage will change
higher length constant - current can spread farther
time constant
time at which voltage is 63% of max
increase membrane capacitance or resitance –> increased time constant
inactive membrane
Na channels closed
electrotonic spread
spread of electrotonic current to inactive membrnae brings inactive membrane to AP threshold
r (i)
internal resistance - affects length constant (and therefore conduction velocity)
r(m)
membrane resistances - affects length const and therefore conduction velocity
factiors that influence conduction velocity
length const
time const
available Na current
diameter of axon
increased diameter = really fast
decrease r(i) –> longer length constant
