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 glyco-

molecules. • 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 non-cytosolic side of the membrane.

Magnitudes of concentration gradients

Solute Cell’s Interior Cell’s Exterior

Na+ 10mM 145mM

K+ 140mM 5mM

H+ pH7.2 pH7.4

Ca+2 10-7 M 1-2mM

Cl- 5-15mM 110mM

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

Other types of pumps(see Table 12-2)

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