TSR Med Students' Society Part III

Right, thanks for the clarification! So there are ionotropic receptors and metabotropic receptors (the main divisions?) )

dependents what you mean by main divisions, there are lots of receptors that aren't GPCRs/ionotropic (tyrosine kinases, guanylyl cyclase linked, serine-threonine kinases... etc etc)

This is obviously an issue without a "right" or "wrong" answer.

It's going to be down to opinion.

But mine would be is, whilst your considered such that you shouldn't partake in normal society, nor should you have any bearing on the daily running of the country.

Again it's subjective and there are arguments on both sides.

Maybe you're just ahead of your time

Legal human rights aren't a matter of opinion - there are definate rights and wrongs.

For instance, we don't ritually beat prisoners, no matter how many people have the opinion that such a thing is a good idea for those who break the law.

Lesson learnt. Never miss sportsnight for anything PDS related

I just get a nice lie-in on thursdays. It'd be rude NOT to go to sportsnight. It's quite bad that one of my biggest achievements of this year is my 100% sportsnight attendance record. Something to say when I run for captain at the AGM.

Is it bad that I always thought Onychophagia was a girl?

A 100% record is definitely something to be proud of. I was part of that elite group up until Wednesday; I can't believe I gave it up.



Yes.

Being mistaken for a girl on an online forum = -1000 lad points

Legal human rights or legal British rights?

Hey guys

Word up. Long time no see.

Hey guys

Yes.

Being mistaken for a girl on an online forum = -1000 lad points

Long time never seen

Just you wait.

Sorry to ask yet more science-y questions but I've yet again managed to confuse myself. Acetylcholine is released by the parasympathetic NS to slow heart rate, right? By increasing permeability of the nodal cells to potassium. I've just been reading that drugs that cause a positive inotropic effect on the heart must increase intracellular stores of calcium in the muscle cells to achieve this increased contraction. I wondered why increasing calcium increased contractility and came upon this in Wikipedia:

'The Ca2+ influx causes vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine out into the extracellular space between the motor neuron terminal and the motor end plate of the skeletal muscle fiber.

The acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the motor end plate of the muscle cell. Activation of the nicotinic receptor opens its intrinsic sodium/potassium channel, causing sodium to rush in and potassium to trickle out. Because the channel is more permeable to sodium, the muscle fiber membrane becomes more positively charged, triggering an action potential.'

As you can see, this is almost the opposite of what it's saying in my book, could anyone offer any explanation?

You are confusingtransmission at the neuromuscular junction with parasympathetic function generally. I could be wrong, but I'm not convinced that there is significant vagal innervation of the heart - particularly not the SA node, this is part of the reason the Resus Council in 2010 changed some of the guidelines for PEA/Asystole so that Atropine is no longer given - because vagal tone is not considered a major factor in cardiac function.

Hmm, I'm sure you could be right but Pocock is telling me that there is parasympathetic innervation to the SAN (as that's what tonically affects our heart rate) but not in the ventricles (where there is only sympathetic innervation). As for atropine, I've only read that it's an inhibitor of the muscarining ACh receptors, and can be used to show that the heart is under vagal tone (as inhibition raises heart rate)