The isolated chick biventer-cervicis muscle- The mechanism of action of depolarising and non depolarising blockers

This experiment was an investigation into the mechanism by which depolarising and non depolarising blockers have their effect on the nicotinic receptors of the neuromuscular junction. The nicotinic receptor of the neuromuscular junction is an ionotropic, ligand gated receptor which when stimulated by acetylcholine (or another agonist e.g. Nicotine) opens and allows the passage of sodium ions through the channel into the intracellular environment whilst potassium ions are simultaneously passing through the channel to the extracellular environment. This causes a depolarisation leading to an action potential. This via the influx of calcium from voltage gated calcium channels causes muscle contraction.

This experiment is concerned with the blocking of the nicotinic receptor, and therefore decreasing muscle contractility, by the mechanisms of depolarising and non depolarising blockers and investigating the results to allow us to distinguish between these two kinds of blockers.

The basic action of these (without going into too much deta

The next step of the experiment once the preparation had recovered was to add 0.2ml of 1*10-7M Succinylcholine and the effects of the drug allowed to reach equilibrium at which point the drug was washed out. The application of Succinylcholine was repeated, however this time at the peak response Tubocurarine was added (same concentration as used before) and the effects noted.

1- From the experiments that were performed it can be said for certain that Tubocurarine is acting postjunctionally. The reason for this conclusion is as follows;

1- There is a large difference in the effects of Succinylcholine and Tubocurarine. Succinylcholine’s effect on the readings from the muscle fibre is to first increase the baseline of the response which rises until there is a maximum peak response. From this point there is a sharp decrease in response which drops rapidly to a point to where the twitches provoke no response at all. It is at this point that the Succinylcholine block has now been set up. These results are the hallmark of a depolarising blocker, as the increase of the baseline response is due to the Succinylcholine causing a huge release of Acetylcholine, i.e. in its initial stages it has the appearance of a powerful Nicotinic agonist. However the ionotropic Nicotinic receptor is only designed to be open for short periods of time. The effect of the prolonged depolarization is to desensitise the Nicotinic receptor and inactivate the voltage gated sodium channels which results in less receptors for transmitter to target and therefore a decrease in muscle contraction. Tubocurarine is a competitive non-de

Some topics in this essay:
, Tubocurarine Succinylcholine’s, Acetylcholine Tubocurarine, Succinylcholine Tubocurarine, nicotinic receptor, organ bath, depolarising blockers, tubocurarine added, depolarising depolarising blockers, organ bath washed, muscle contractility, peak response, receptor sites, depolarising depolarising, twitches switched, baseline response, increase baseline response, allowed reach equilibrium, equilibrium edrophonium added,