1. Week 9

2. 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)Fig. 11-32

4. Cell surface Non-cytosolic side find –glycolipids –glycoproteins –proteoglycans Glycocalyx (see Fig. 11-33)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.

6. Membrane Semi-selective barrier (see Fig. 11-20)Fig. 11-20 –Order of permeability starting with most permeable small hydrophobic molecules –CO 2, O 2, N 2, C 6 H 6 small, uncharged polar molecules –H2O, ethanol, glycerol large uncharged molecules –amino acids, sugars ions (least permeable) –Na +, K +, HCO 3 -, H +

8. Membrane transport Types of membrane transport proteins (see Figure 12-2) Figure 12-2 –carrier proteins –channel proteins

10. Classes of membrane proteins (see Fig. 11-21)Fig. 11-21

12. 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. 11-22Fig. 11-22

14. Transmembrane proteins See Fig. 11-24Fig. 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

16. Transmembrane proteins Beta barrel –composed of beta sheets –form a wide pore with an aqueous channel Multiple alpha helices –See Fig. 11-25Fig. 11-25 –form an aqueous channel –vary channel width by varying the number of alpha helices

18. 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. 11-37Fig. 11-37

20. 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.

21. Magnitudes of concentration gradients

22. Mechanism of transport See Fig. 12-5Fig. 12-5 Passive transport –substance moves down concentration gradient without additional energy input Active transport (see Fig. 12-8)Fig. 12-8 –solutes transported against concentration gradient and therefore requires an energy source.

25. Active transport Na + /K + pump (an ATPase) –see Fig. 12-11Fig. 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

27. Types of carrier proteins See Fig. 12-12Fig. 12-12 Uniport –transport a solute in one direction Symport –transport two solutes in one direction Antiport –transport two solutes in opposite directions

29. Glucose uptake (see Fig. 12-14)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

31. Other types of pumps (see Table 12-2)Table 12-2

33. 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

34. Ion Channels Gated –open and closed configurations Types of gates (see Fig. 12-22)Fig. 12-22 –voltage gated –ligand gated –stress activated gated

36. Membrane potential Membrane potential governed by the membrane’s permeability to ions, particularly to K + (see Fig. 12-26)Fig. 12-26 Quantitation of membrane potential –Nernst equation V = 62 x log(C o /C i ) C o /C i = 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

38. Neurons Nerve cells –see Fig. 12-28Fig. 12-28 –resting potential ~ -70mV

40. 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

41. Action potential mechanism See Fig. 12-32 and 12-33Fig. 12-32 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

45. Nerve terminal Axon bulbs –nerve terminal Ca 2+ voltage gates open in response to membrane’s depolarization Ca 2+ 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)Fig. 12-3512-36

46. 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

49. Types of neurotransmitters See Fig. 12-37Fig. 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

51. 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