TSR Med Students' Society Part III

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)

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)

Yeah that's true - so what's your question sorry?

Essentially, I am told that the parasympathetic NS secretes acetylcholine which ultimately slows the heart rate by increasing the time between successive action potentials.

However, I am also told that a positive inotropic agent (i.e. something that makes the heart contract more forcefully, as I'm sure you know) works by increasing permeability of muscle cells to Calcium.

Wikipedia tells me that increasing calcium influx causes vesicles containing ACh to fuse with the plasma membrane and secrete ACh and the effects are thus:

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.'


I.e. the ACh is causing an action potential, when I've just been told it inhibits and slows successive action potentials, but going by the paragraph above, that doesn't seem to be the case.

Hope that's clear! Thanks for any advice.

Yeah that's where you went wrong - Vagal ACh binds to MUSCARINIC (M2 if you care enough) receptors. This is G protein coupled, and the end result is to increase potassium and decrease Calcium, thus slowing the heart rate and AV conductance.

Hope that makes a bit more sense now.

Okay, thanks, so if ACh serves to slow the heart rate, what on Earth is Wikipedia referring to when it says it triggers action potentials? And do you happen to know why an influx of calcium actually causes an increased inotropic effect? Is it because of binding to tropinin? Sorry to bombard you with questions! That's for explaining that last one, it's very much appreciated.

Woody. Stop making my brain hurt.

Okay, thanks, so if ACh serves to slow the heart rate, what on Earth is Wikipedia referring to when it says it triggers action potentials? And do you happen to know why an influx of calcium actually causes an increased inotropic effect? Is it because of binding to tropinin? Sorry to bombard you with questions! That's for explaining that last one, it's very much appreciated.

Neurotransmitters functions are largely dictated by the receptor - It all depends on the exact cell, system or whatever you're talking about. It (ACh) triggers action potentials in the NMJ because the receptors are nicotinic. It hyperpolarizes the cardiac (nodal) cells because the receptors are muscarinic (M2).

hope that clears it up a bit! and off the top of my head, I think it's calcium that binds to troponin, which pulls tropomyosin off actin (allowing the myosin to work its magic)

but you'd want to check that before writing it in an exam

:/

damn, did I get it wrong somewhere?

(I should have mentioned i'm an idiot before posting)

Then I read 2nd year UCL medic and realised who it was! Long time no see/speak.

Hey Jess! Yeah it's been aaaaaages, how's it all going?

(btw, super lol at your sig)

damn, did I get it wrong somewhere?

(I should have mentioned i'm an idiot before posting)

Ditto. I'm ashamed that I supposedly have two years more medical knowledge than him and yet understood about three words of that entire conversation

I'm glad someone appreciates the sig! It's mostly going well, our formatives are on monday and to prevent another epic fail I'm trying to revise. It's going really slowly and I have two modules to complete tomorrow along with sociology and the rest of PDS. Bad times. Looking forward to intermodular week though, in a way I get double the fun as I get one next week and my second year buddies will be celebrating theirs the week after so I'm going to join the festivities on both weeks. Not particularly pertaining to a healthy liver/bank balance/academic workload but gaaah, when did I ever have a healthy any of those things?


How's it going for you? How's second year shizz?

Well actually I was only doing that because you wrote stuff I already had. But now I realise you were talking out of context too haha. The reason calcium slows the action potential won't be that.



How's second year? The really tough pre-clinical year aye.

Ah best of luck with that It'll be great after they're over! have you got a spotter? I'm not sure if they've just taken them out of mocks completely or if they just don't have any in second year =\

ah sociology.. that old beast :P I saw scambler on tcr the other day, haven't seen him at all this year I don't think! but double celebrations sounds like a good deal and hey, why do you think the liver regenerates? :P



ah right :P - I was just writing in reponse to Woody's response to your awesome explanation.. I thought he was asking how ACh can both trigger action potentials and exert negative inotropy (ie serve two different functions) and I just thought I'd emphasise the whole receptor theory thing... but reading back I don't think that was the right interpretation of his comment anyway, and I was talking about something completely different

Second year is a mixed bag - Neuro is really interesting and Endo is pretty easy, but there's just so many lectures! Have been working through the MEQ past papers preparing for the mocks, seems the best bet atm! How's fourth year? Do you spend much time at UCH?