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Week 9
Shape of cell
• Without some sort of “skeleton” cells would have
a spherical shape - a shape of lowest energy.
• Redblood cells have a donut shape- how?
– Cell cortex provides a scaffold of spectrin molecules on
the cytosolic side of the membrane. (see Fig. 11-32)
Cell surface
• Non-cytosolic side
• find
– glycolipids
– glycoproteins
– proteoglycans
• Glycocalyx (see Fig. 11-33)
– made up of the sugar coating from the above glycomolecules.
• Important in keeping cells from sticking to themselves and
other surfaces. Acts as a lubricant, absorbs water, antigenic,
and is important for cell recognition.
Membrane
• Semi-selective barrier (see Fig. 11-20)
– Order of permeability starting with most
permeable
• small hydrophobic molecules
– CO2, O2, N2, C6H6
• small, uncharged polar molecules
– H2O, ethanol, glycerol
• large uncharged molecules
– amino acids, sugars
• ions (least permeable)
– Na+, K+, HCO3-, H+
Membrane transport
• Types of membrane transport proteins (see
Figure 12-2)
– carrier proteins
– channel proteins
Classes of membrane proteins
(see Fig. 11-21)
Types of Membrane proteins
• Membrane proteins can be classified as:
– transmembrane
• an integral protein - requires detergents to remove
from membrane
– lipid-linked
• an integral protein
– protein attached
• a peripheral protein - gentle extraction methods to
remove from membrane
• See Fig. 11-22
Transmembrane proteins
• See Fig. 11-24
• Alpha helix secondary structure spans the lipid
bilayer
– hydrophobic amino acid side chains face towards the
fatty acids
– hydrophilic peptide links face inward to form the
hydrogen bonds needed for the alpha helix structure
Transmembrane proteins
• Beta barrel
– composed of beta sheets
– form a wide pore with an aqueous channel
• Multiple alpha helices
– See Fig. 11-25
– form an aqueous channel
– vary channel width by varying the number of
alpha helices
Transmembrane proteins
• Proteins do not float freely in the sea of
phospholipids of the bilayer. They stay in
membrane domains.
• Proteins remain “fixed” in their position by:
– cell cortex proteins
– tight junctions
• see Fig. 11-37
Membrane gradients
• Concentration gradient
• electrochemical gradient (syn. Membrane
potential)
– cell’s cytosolic side of the membrane is more
negatively charged relative to the cell’s noncytosolic side of the membrane.
Magnitudes of concentration
gradients
Solute
Na
+
Cell’s Interior Cell’s Exterior
10mM
145mM
K
+
140mM
5mM
H
+
pH7.2
pH7.4
+2
-7
10 M
1-2mM
-
5-15mM
110mM
Ca
Cl
Mechanism of transport
• See Fig. 12-5
• Passive transport
– substance moves down concentration gradient
without additional energy input
• Active transport (see Fig. 12-8)
– solutes transported against concentration
gradient and therefore requires an energy
source.
Active transport
• Na+/K+ pump (an ATPase)
– see Fig. 12-11
– Oubain inhibits the pump by preventing the
binding of K+
• Moves Na+ out of the cell and K+ into the
cell coupled to the hydrolysis of ATP.
– Maintains osmotic balance in animal cells
– Maintains membrane potential across cell
membrane
Types of carrier proteins
• See Fig. 12-12
• Uniport
– transport a solute in one direction
• Symport
– transport two solutes in one direction
• Antiport
– transport two solutes in opposite directions
Glucose uptake
(see Fig. 12-14)
• Coupled transport mechanism for uptake of
glucose by intestinal epithelium cells
– Na+/glucose symport
– Na+ moves down its concentration gradient and drags
glucose along
• i.e., more sodium outside cell than inside cell
• Passive transport for transfer of glucose out of cell
– glucose uniport
Ion channels
• Rapid entry and exit of ions into and out of
cell
– 1000x faster than a carrier protein rate
• Selectivity determined by size and charge of
the pore’s inner lining
Ion Channels
• Gated
– open and closed configurations
• Types of gates (see Fig. 12-22)
– voltage gated
– ligand gated
– stress activated gated
Membrane potential
• Membrane potential governed by the membrane’s
permeability to ions, particularly to K+ (see Fig.
12-26)
• Quantitation of membrane potential
– Nernst equation
• V = 62 x log(Co/Ci)
• Co/Ci = ratio of ion (K+) concentration outside the cell to the
concentration inside the cell. Note: A higher concentration
inside causes the value V to be negative.
• When ion channels open, there is a change in the
membrane potential resulting in an electrical
impulse
Neurons
• Nerve cells
– see Fig. 12-28
– resting potential ~ -70mV
Neuron’s Action Potential
• Action potential = an electrical impulse that
moves down the neuron
• Na+ concentration greater outside neuron
than inside
• K+ concentration greater inside the neuron
than outside
Action potential mechanism
• See Fig. 12-32 and 12-33
• 1. Stimulus causes Na+ voltage gates to open
• 2. Na+ ions flow rapidly inside the neuron
depolarizing the membrane **
• 3. Na+ channels inactivated
• 4. Depolarization causes K+ voltage gates to open
• 5. K+ ions flow out of cell
• ** this stimulates additional Na+ gates to open
• 6. Na+ / K+ pump restores original cationic balance with
high concentrations of Na+ outside cell and K+ inside cell
- repolarizes the membrane
Nerve terminal
• Axon bulbs
– nerve terminal
• Ca2+ voltage gates open in response to membrane’s
depolarization
• Ca2+ rushes into cell causing neurotransmitter-carrying
vesicles to fuse with the membrane and release the
neurotransmitter into the synaptic cleft by exocytosis.
• Neurotransmitter binds to a specific ligand-gated ion
channel on the post-synaptic neuron causing it to open, a
new electrical impulse is propagated through this neuron
(see Fig. 12-35 and 12-36)
Nerve terminal cont
• The neurotransmitter must be removed from
the synaptic cleft
• Two mechanisms
– reuptake e.g., serotonin
– enzymatic breakdown e.g., acetylcholine by
acetylcholine esterase
Types of neurotransmitters
• See Fig. 12-37
• Excitatory
– cause Na+ voltage gates to open
– Include acetylcholine, glutamate, serotonin
• Inhibitory
– cause Cl- voltage gates to open
– Include gama aminobutyric acid (GABA) and
glycine
Neuro toxins
• Curare - causes paralysis by preventing the
opening of Acetylcholine ligand gates
• Strychnine - causes convulsions by acting as an
atagonist of glycine
• Botulism - causes paralysis by blocking the
release of acetylcholine
• Tetanus - causes convulsions by blocking the
release of inhibitory neurotransmitters
• Check out my BIOL1114 website under Chemical
defences