BIO 122 LECTURE 2: MEMBRANE PHYSIOLOGY

J4R4FFE

CELL MEMBRANE STRUCTURE

1.
2.
3.
4.

Cell-surface markers glycoproteins that identify cell

type
Receptor proteins recognize and bind to substances
outside the cell
Enzymes assist chemical reactions inside the cell
Transport proteins help substances move across the cell
membrane

Amphipathic
phospholipid heads = hydrophilic
phospholipid tails = hydrophobic
Fluid Mosaic Model (Singer & Nicolson)
fluid = lipid bilayer
mosaic = integrated proteins and other molecules

MEMBRANE LIPIDS
1.

Phospholipids

Phosphatidylethanolamine (PE)

Phosphatidylcholine (PC)

second most abundant

most abundant

key component of membrane

bilayers
derived from glycerol

key component of membrane

bilayers
derived from glycerol
precursor of sphingomyelin and
PS

phospholipids of CNS

membrane fusion, fission;

modulates membrane curvature;
stabilizes membrane protein
conformations

2.
-

primary phosphate circulating the

plasma; integral component of
lipoproteins
transporters of chol:
HDL = good lipids; promotes
uptake in storage sites; tanggal
chol from blood
LDL = bad chol; transport chol
to diff. cells

Cholesterol
steroid rings
interact with and partly immobilize the upper regions of the
HC chains less deformable, less fluid, less permeable to
water-soluble molecules
interferes with close packing/solidification of fatty acid
tails (lower regions)

Phosphatidylserine (PS)
most abundant negatively charged
phospholipid in eukaryotic
membrane

derived from glycerol

Glycolipids
asymmetrically distributed in CM
derived from sphingosine
cell-surface markers = for cell-to-cell recognition; e.g.
blood types and recognition of foreign bodies

most abundant sphingolipid

important component of myelin
sheath
derived from sphingosine

precursor for other phospholipids

maintained by flippase at inner
side of CM

with long and saturated

hydrocarbon tails = closely packed
+ more compact lipid rafts

blood coagulation, regulation of

apoptosis

associated with lipid rafts involved

in membrane sorting and
trafficking, signal transduction and
cell polarization

MEMBRANE PROTEINS
1.

2.
3.
-

Shingomyelin (SM)

3.

Integral Proteins
functional on both sides of bilayer
for transport of molecules
transmembrane proteins: channels, carriers (undergo
conformational change), receptors
Peripheral Proteins
attached to the surface membrane
enzymes
Glycoproteins
protein-(covalent bond)-CHO

MEMBRANE FUNCTONS
MEMBRANE FLUIDITY
1.
2.
3.

Mobility
a. Lateral Mobility
b. Flip Flop
Saturation
a. Unsaturated HC chains with cis-double bonds
b. Saturated HC chains
Presence of cholesterol within membrane

1.
2.
3.
4.
5.
6.

barrier and selection

controlled transport
signal transduction
enzymatic reactions
cell-to-cell communication
cytoskeleton anchor

MEMBRANE TRANSPORT
1.

2.

Passive Transport
a. Simple Diffusion
i.
through lipid bilayer
lipid-soluble (O2, CO2, N2, alcohol)
high lipid solubility, fastest diffusion
ii.
through protein pore channels
lipid-insoluble (water, ions)
o Semi-permeable
size of channel
electrical charge of channel
o Gated

Voltage-gating
Na+ gate closed = (-); open = less (-)
K+ gate closed = less (+); open = more (+)

Chemical-gating
opens when a ligand binds with the protein
Ach channel, nerve-to-nerve, nerve-to-muscle
b. Facilitated Diffusion
carrier-mediated diffusion
glucose, amino acids

Active Transport
movement of molecules against a concentration
gradient
energy-requiring
a.

Primary Active Transport

makes use of energy derived from breakdown
of ATP
requires carrier proteins that impart energy to
bounded molecule
i.

Na+-K+-ATPase
phosphorylation of the carrier
protein by splitting action of
ATPase = ATP ADP + P
Na+-K+ pump is electrogenic
for every 3 Na+ out, 2 K+ in = net of
1 positive charge in ECF
basis for reestablishing Na-K
gradients after action potential in
nerves

ii.

o
o

Rate factors
lipid solubility
molecular size
cell membrane thickness
concentration gradient
membrane surface area
composition of lipid layer
Gibbs-Donnan Equilibrium
equilibrium where permeating charged ions are
asymmetrically distributed across the membrane due to
the presence of charged nonpermeating solutes
uneven electric charge
Osmosis
net movement of water caused by difference in
concentration of water
permeating water, nonpermeating NaCl, selectively
permeable membrane
Osmotic pressure
difference in hydraulic pressures of a solution and water
which must be overcome to prevent entry of water into
the solution across the membrane
Osmolarity
osmoles per liter (particles/L of solution)
total concentration of solute particles in a solution
regardless of their chemical composition
determining factor for the diffusional movement of
water
molarity (mol/L) x no. of particles in a solution
Osmolality
osmoles per kg of water (particles/kg of water)
Osmoticity

Isoosmotic 300 mOsM/L of solute

Hyperosmotic > 300 mOsM/L of solute

Hypoosmotic < 300 mOsM/L of solute

*300 mOsM = normal osmolarity of the human body
Tonicity
describes solutions that tell what would happen to cell
size/volume changes when placed in the solution
depends on nature of solutes (not just osmolarity = vs.
osmoticity) and permeability of membrane

Isotonic 300 mOsM of nonpenetrating solutes

Hypertonic > 300 mOsM of nonpenetrating solutes

Hypoosmotic < 300 mOsM of nonpenetrating solutes

b.

Calcium-Hydrogen-ATPase

Calcium pump
maintains Ca2+ ICF << Ca2+ ECF
plasma membrane calcium pump =
cell signaling
sarcoplasmic reticulum calcium
pump = muscle contraction

Hydrogen pump
gastric glands of stomach =
hydrochloric acid secretions in
stomach
distal tubules and collecting ducts of
kidneys = H+ ions secreted into
urine
Secondary Active Transport
makes use of stored energy from Primary AT in
form of ionic concentration differences between
two sides of membrane
requires carrier proteins that impart energy to
bounded molecule
i.

ii.

3.

Co-transport
makes use of stored energy gradient
Na+ concentration gradient: high at
ECF
symport
Na+-glucose co-transport (2:1)
Na+-amino acid co-transport

Countertransport
makes use of stored energy gradient
Na+ concentration gradient: high at
ECF
antiport
Na+-Ca2+ countertransport
Na+-H+ countertransport
Vesicular/Vacuolar Transport
transport of large particles is across but not through
the lipid bilayer
accomplished through vesicle formation
vesicle membrane = plasma membrane
a. Endocytosis
entry into the cell
phagocytosis, pinocytosis, receptor-mediated
b. Exocytosis
exit from the cell

*Protein-mediated transport
faster than non-mediated passive transport
displays saturation kinetics
displays specificity
similar chemical classes exhibit competitiveness
prevented by inhibitors
MEMBRANE POTENTIAL

B.

Potential ~ Voltage
force resulting from the tendency of oppositely charged
ions to move toward one another
fundamental property of cells resulting from an excess of
negative charges on one side of the PM and an excess of
positive charges on the other
unequal distribution of ions across the membrane
used to transmit signal among electrically excitable cells,
nerves and muscles
A.

Resting Membrane Potential (RMP)

potential difference (voltage) across cell membrane at
rest
experimentally measured as:

neurons = -75 mV

skeletal muscles = -90 mV

smooth muscles = -60 mV

attributed to unequal ion distribution; e.g. Na+, K+ Clmore negative inside since large anions cannot pass
through cell membrane
at rest, K+ ions leak through the channels
DIFFUSION POTENTIAL
*EQUILIBRIUM POTENTIAL of an ion: ions are
at equilibrium across the membrane; no net
movement of ions; opposes the diffusion of ion down
their conc. gradient (diffusion potential)

considers distribution and permeability of

several ions simultaneously
RMP is therefore the result of the nature of all
ions along the membrane
RMP resulting primarily from diffusion
potential (of largly K+ ions) and active transport
(Na-K pump)

Action Potential
transient and rapid changes in membrane polarity of
nerves and muscles
negative MP (rest) positive MP (action)
initiates at axon hillock
synapse
nerve impulse

down the length of axons in velocities of 2.5

m/s (small nonmyelinated axons) to 120 m/s (in
myelinated axons)

axon hillock axon terminals

voltage-dependent

Conduction velocity of AP is affected by:

1.

Myelination
axon covered with Schwann cells (PNS) or
oligodendroglia (CNS)
node is the only region of ion permeability and
current flow
saltatory conduction

2.

Axon diameter
diameter, resistance, conduction velocity
giant axons = axons larger than other axons within
the same animal

What generates an action potential?

Nernst equation

used to predict the EP of a specific ion

1.
2.

stimuli from the environment

impulse from a preceding neuron

Goldman-Hodgkin-Katz/Goldman equation

derived Nernst eqn

used to predict the EP of several permeating

ions depending on their

permability

concentration

electric charge

a MP that is 15-30 mV above the RMP (action potential

threshold = threshold of excitation)
all or none
threshold Na+ influx depolarization (+ feedback
goes back to Na+ influx) peak voltage of +60 mV = EP
of Na+ repolarization = closing of Na+ channels; slowly
closing of K+ channels; K+ still exit neuron goes back to
threshold

Mechanisms of Action Potential

(1)
resting potential:
K+-Na+ leak
channels
(K+ channels more
permeable)

(2)
depolarization:
voltage-gated Na+ channels
open

(3)
depolarization:
voltage-gated K+ channels
open

(4)
voltage-gated K+
channels remain open
(lag)

increase in Na+ permeability

K+ channels open more

slowly than Na+ channels
increase in K+ permeability

hyperpolarization:
K+ efflux from cell is
greater than resting
state as voltage-gated
K+ channels remain
open

less Na+ influx and more K+

efflux repolarization
restore RMP

more negative than

RMP

Na enters cell down is

electrochemical gradient

refractory:
Na+ channels can be:
a. closed and ready
b. open
c. closed and not ready
PNa PNa >> PK PNa

PK >> PNa

PK >> PNa

Summary:
1.
2.
3.
4.
5.

Threshold all or none response

Depolarization less negative membrane potential; due to
Na influx
Repolarization more negative membrane potential (=
RMP); due to K efflux
Hyperpolarization membrane potential more negative
than RMP
Refractory Period absolute vs. relative

Hodgkin Cycle
positive feedback relationship between depolarization and
corresponding increase in Na+ current flow across the cell
membrane
membrane depolarization increase in PNa Na+ influx
back to membrane depolarization

(5)
refractory period:
recovery time for the membrane
before another AP can be
elicited
Absolute RP

Relative RP

no membrane
depolarization

occurring
depolarizations
will not reach
threshold
levels
caused by
opening of K+
channels

caused by
residual
inactivation
of Na+
channels