electroactive
neural membrane sensitive to electrical change
hydration shell
bigger molecules can pass if energetically favorable, eg. water molecules surrounding molecules such as K+, easier to pass through than Na+ since energetically favorable to do so
leak channels
persistently open
voltage gate channel
sensitive to electrical potential, depends on membrane charge
ligand-gated ion channels
iontropic receptors, open in response to ligands (neurotransmitters)
variety of channels
sensory systems, respond to unique stimuli
eg. skin, hair cells...
dynamic equilibium
constant movement of ions, no net movement of charge, balanced
Nernst Equation (simplified)
Ex = 58 log ([x]o/[x]i)
Nernst Equation
Ex = RT/zF ln([x]o/[x]i); calculates reversal potential for given ion x; assumes all channels are open
R
ideal gas constant; 8.314 J/K*mol; way to convert # of molecules and energy that molecules exert
T
temperature; ~292K
z
electrical charge; predict direction of ion movement based on ion charge; represents influence exerted by electrical gradient
Na+ and K+; z = +1
Cl- = -1
Ca2+ = +2
F
faradays constant; 96,485 coulombs/mol
Goldman-Hodgkin-Katz equation (GHK equation)
combines Nernst equation w/ 3 relevant ions (K+, Na+, Cl-)
gives value of membrane potential Vm; explains how movement of Na+ across membrane causes cell to become more positive.
p
permeability; the higher the permeability the higher the Vm is to the Ex of that ion
resting membrane potential
-70mV, dominated by
pk = 1, pcl = 0.55, pNa = 0.04
-80mV, -60mV, +55 mV
threshold
around -55 mV
action potential
short lasting change in membrane potential that travels down axon; driven by ion movement
graded potentials
subthreshold changed in Vm
depolarization
Vm becomes more positive
hyperpolarization
Vm becomes more negative
steps of the action potential
...
1. depolarization from incoming neurons
neurotransmitters from presynaptic neurons cause ion movement via postsynaptic ligand-gated ion channels. postsynaptic potentials PSPs - small deviations in membrane voltage, release of EPSPs cause small depolarizations, IPSPs cause small hyperpolarizations
spatial summation
2 EPSPs from 2 adjacent inputs
temporal summation
multiple EPSPs from same input close in time
2. opening of voltage-gated Na+ channels
depolarization past threshold opens these channels leading to the influx of Na+ into the cell leading to further depolarization with a peak of around +40 mV
3. opening of voltage-gated K+ channels
large depolarization leads to a more positive cell, this positive charge pushes K+ out of the cell; the opening of these channels leads to the Vm becoming more negative than resting potential (closer to Ek)
4. inactivation of voltage-gated Na+ channels
when cell reaches + potential, channels innactivate, prevents movement of excitatory, depolarizing Na+ ions
5. deactivation of voltage - gated K+ channels
cell becomes negative again, since K+ leaves the cell. hyperpolarization stops, membrane potential returns to equilibrium of resting potential
shapes of action potential
depolarization, repolarization, and afterhyperpolarization
1. depolarization
Vm becomes more positive due to Na+ influx
K+ channels open
2. repolarization
Na+ channels inactivate
K+ driven out of the cell
Vm becomes more negative
3. afterhyperpolarization
gradual deactivation of K+ channels
absolute refractory period
time window where 2nd action potential cnanot be fired
happens because Na+ voltage-gated channels are innactivated
relative refractory period
exists on a gradient, more difficult to fire action potential
Na+ channels reset @ inactive state
K+ channels still open, movement still happening
movement of K+ hinders depolarization
action potential is unidirectional
1. Na+ moves to lower conc. unlikely to move backward
2. previous patch is in absolute refractory period, impossible for action potential to travel backwards
myelin
layer of lipid coatory axon. increases conduction velocity, speed by which action potential travels down length of axon.
works by blocking K+ leak channels in membrane
causes + charge to be unable to exit cell
signal moves rapidly
saltatory conduction
AP jumps from node to node