Biological Membranes

Chapter 8: Biological Membranes

5 min read Updated Apr 18, 2026
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1. (8.1) The fluid mosaic model describes the cell membrane as:
C. Singer-Nicolson model: phospholipid bilayer behaves like a 2D liquid (lateral diffusion is fast, transverse "flip-flop" is slow), with integral and peripheral proteins embedded or attached, and cholesterol modulating fluidity.
2. (8.1) Cholesterol's effect on membrane fluidity:
A. Cholesterol's rigid ring system packs between phospholipid tails. In hot, fluid membranes it reduces excess motion. In cold, rigid membranes it prevents the tails from crystallizing. Net effect: smaller swing in fluidity across temperature changes.
3. (8.2) Integral (transmembrane) proteins typically:
D. Transmembrane segments are usually alpha helices of ~20 hydrophobic residues, long enough to span the bilayer. Multi-pass proteins (like GPCRs) weave through the membrane multiple times.
4. (8.2) Peripheral membrane proteins:
B. Peripheral proteins bind to integral proteins or to membrane lipids via weak interactions. Removed without disrupting the bilayer. Integral proteins require detergents to extract (because they are embedded in the hydrophobic core).
5. (8.3) Passive diffusion moves solutes:
A. Passive = "no energy input." Small, uncharged or nonpolar molecules (O2, CO2, small alcohols, steroid hormones) dissolve in the lipid bilayer and diffuse across down their gradient. No transporter, no ATP.
6. (8.3) Facilitated diffusion differs from simple passive diffusion in that it:
C. "Facilitated" = assisted by a protein. Still passive (no ATP), still down-gradient. Examples: GLUT glucose transporters, ion channels, aquaporins (water). Saturable kinetics because the transporter can be maxed out.
7. (8.4) The Na+/K+-ATPase pumps:
D. Net +1 charge exported per cycle contributes slightly to the negative resting potential. Na+/K+-ATPase is ~13\frac{1}{3} of a neuron's ATP budget. Ouabain inhibits it (and, via raised intracellular Na, indirectly raises Ca2+ in cardiac myocytes - the mechanism of digoxin).
8. (8.4) Secondary active transport:
B. The primary pump (Na/K-ATPase) spends ATP to set up a Na+ gradient. Secondary transporters (SGLT glucose symporter, Na+/Ca2+ antiporter) couple Na+ flowing down to a second solute being pushed uphill - ATP is used indirectly.
9. (8.5) A cell placed in a hypotonic solution will:
A. Hypotonic = lower solute than the cell → water flows IN → cell swells. Hypertonic = higher solute outside → water flows OUT → cell shrinks. Isotonic = balanced.
10. (8.5) Osmotic pressure is:
C. Osmotic pressure scales with total particle concentration (van't Hoff: π = iMRT). That's why NaCl (i = 2 after dissociation) exerts ~twice the osmotic pressure of an equivalent concentration of glucose (i = 1).
11. (8.6) Phagocytosis is a form of endocytosis that:
B. "Cell eating." Macrophages, neutrophils, and dendritic cells use phagocytosis to engulf pathogens. Pinocytosis = "cell drinking" (small volumes). Receptor-mediated endocytosis = selective uptake via clathrin-coated pits.
12. (8.6) Exocytosis releases molecules from the cell by:
D. SNARE proteins mediate vesicle-plasma-membrane fusion. Ca2+-triggered exocytosis is how neurons release neurotransmitters at synapses and how pancreatic beta-cells release insulin.
13. (8.7) The resting membrane potential of a typical neuron is:
A. Created mostly by K+ leak channels (the membrane is most permeable to K+ at rest) and maintained by the Na/K-ATPase. The Nernst equation predicts the equilibrium potential for each ion; the Goldman equation weights contributions from all ions.
14. (8.7) The Nernst equation calculates:
C. Nernst: EionE_{\text{ion}} = (RT/zF) ln([out]/[in]). At 37°C for a monovalent cation: ≈ 61.5 log([out]/[in]) mV. Gives the voltage at which the electrical force balances the concentration force for that ion.
15. (8.8) Ligand-gated ion channels:
B. Ligand-gated channels are ionotropic receptors. Acetylcholine at the nicotinic ACh receptor opens a cation channel. GABA-A receptors are chloride channels. Fast (ms) responses vs. slower GPCR-mediated metabotropic signaling.
16. (8.8) Nuclear hormone receptors (e.g., the estrogen receptor) act by:
D. Steroid and thyroid hormones cross membranes directly (lipid-soluble) and bind intracellular receptors that function as ligand-activated transcription factors. Slower onset (minutes to hours) but longer-lasting effects than membrane-receptor signaling.
17. (8.9) Which molecule is a common second messenger produced by adenylyl cyclase?
A. Activated Gαs stimulates adenylyl cyclase to make cAMP from ATP. cAMP activates PKA, which phosphorylates downstream targets. Gαi inhibits the same enzyme. Other major second messengers: DAG + IP3 (PLC pathway), Ca2+, NO, cGMP.
18. (8.9) IP3 (inositol trisphosphate) acts as a second messenger by:
C. PLC cleaves membrane PIP2 into DAG (membrane-bound, activates PKC) and IP3 (cytosolic, triggers ER Ca2+ release). Raised cytoplasmic Ca2+ activates many targets via calmodulin. This is the Gαq pathway.

Every cell is a membrane-bound volume of cytoplasm. The plasma membrane separates what is inside from what is outside, controls which molecules cross, and relays signals from the environment to the cell interior. Every MCAT Bio/Biochem exam has multiple questions about membranes.

The Membrane is a Swimming Pool

The fluid mosaic model is the mental image to carry through this chapter. The phospholipid bilayer is a pool of water. Proteins are floating objects: some sit on the surface (peripheral), some are partly submerged (integral), some span the full depth (transmembrane). Cholesterol is dissolved between the tails. Glycans on the outer surface are pool floats sticking up above the water. Everything is fluid - the matrix flows, proteins drift.

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