C2.1 Chemical signalling. Practice questions with markscheme.

• increase = 38 − 15 = 23 (mV);
• 23 ÷ 15 × 100 = 153 (%);

Accept 153 to 153.3 %. Award [1] for a correct difference with an incorrect or missing final step. ECF from an incorrect difference.

• depolarization increases as acetylcholine concentration increases / positive relationship;
• the increase is large between 0.1 and 100 µmol dm⁻³ (4 mV to 52 mV), OWTTE;
• there is a plateau / little further increase above 100 µmol dm⁻³ (52 mV to 54 mV);

Accept 'each tenfold increase in concentration gives a smaller increase in depolarization' for the third point.

• not significant / the two concentrations cannot be said to produce different depolarizations;
• the ranges of mean ± SD overlap (47.9 to 56.1 mV and 49.6 to 58.4 mV) / the difference between the means (2 mV) is smaller than either standard deviation, OWTTE;

The reason must refer to overlap of the standard deviations or error bars; do not award the second mark for 'the values are close'.

• (nearly) all receptors have acetylcholine bound / receptors are saturated, so all the ion channels are already open and adding more acetylcholine has no further effect;
• OR the membrane potential approaches the value at which there is no further net entry of positive ions, OWTTE;

Accept either reason.

• the toxin binds to the acetylcholine receptor at or near the binding site for acetylcholine;
• acetylcholine can no longer bind (to the occupied receptors) / the toxin is an antagonist, OWTTE;
• the ion channel in the receptor stays closed, so positively charged ions cannot diffuse into the fibre;
• so depolarization is greatly reduced (3 mV compared with 38 mV in untreated fibres at the same concentration);

Accept 'the toxin changes the shape of the receptor so the channel cannot open' as an alternative for the first two points. Do not accept 'the toxin breaks down acetylcholine'.

• acetylcholine still binds and opens the ion channel in the receptor, but there are (almost) no sodium ions outside the fibre to diffuse in;
• the large organic cation cannot pass through the channel, so there is little entry of positive charge and little depolarization (6 mV compared with 38 mV);
• (this shows that) the depolarization caused by acetylcholine is due mainly to the entry of sodium ions, OWTTE;

Accept 'the small remaining depolarization is due to other ions / residual sodium ions' as an additional point.

• the signalling chemical / ligand binds to a specific binding site on the outer part of the receptor and does not enter the cell;
• binding changes the shape of the receptor, including the part inside the cell, OWTTE;
• this sets off a sequence of responses inside the cell / a cascade of reactions, e.g. activation of a G protein, production of a second messenger such as cAMP or phosphorylation of proteins by a kinase;
• the sequence amplifies the signal, so one ligand molecule can cause a large response;
• the pathway ends in a cellular response such as activation of enzymes, opening of ion channels or a change in gene expression;

Award marks for any valid pathway; the acetylcholine receptor itself may be used as the example.

• phosphorylation increases as insulin concentration increases;
• a steep rise between 0 and 10 nmol dm⁻³ then a plateau / little further increase between 10 and 100 nmol dm⁻³, OWTTE;

• 79 % (accept 78–79 %);

• the insulin receptor is a transmembrane receptor with tyrosine kinase activity: insulin binding causes (dimerization and) phosphorylation of tyrosine residues on the receptor;
• the blocker prevents this phosphorylation (9 rather than 96 units), so the signal transduction pathway / cascade inside the cell is not initiated;
• (so) enzymes for glycogen synthesis are not activated and glycogen synthesis stays near the level with no insulin, OWTTE;

• (nearly) all receptor binding sites are occupied / receptors saturated, so adding more insulin has little further effect;

• insulin is a (hydrophilic) polypeptide that cannot pass through the (hydrophobic core of the) phospholipid bilayer, so it must bind at the cell surface;