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