PHYS20008 membrane potential question

[neatfeet]

Can anyone help explain something to me?

So far I've been imagining all neurons how motoneurons look, with the cell body at one end, then the axon, and the terminals at the other end.  Heaps of other terminals synapsing onto that cell body, triggering graded potentials.  But I've just been revising a bit and have started thinking about neurons where the cell body is in the middle of the length of the neuron, like in sensory neurons. 

So how does this work when it comes to generating a strong enough graded potential in the cell body to then trigger an AP along the axon? Eg say there is a specialised receptor cell like a rod or a cone that receives stimulus... the diagram we have shows that that cell synapses onto a sensory neurone but the cell body of the neurone is half way down the axon. Where is the location of the axon hillock in this situation i.e. the area in which an AP is triggered if threshold is reached?  If the axon hillock is in the cell body, which is far away from the special sense receptor, how does the information from the sense receptor get there, in order to propagate down the axon?

For these neurons, it seems the axon hillock is not near the cell body, but is located near where the graded potentials would be received.  (https://www.inkling.com/read/elseviers-integrated-neuroscience-nolte-1st/chapter-2/action-potentials)

[Starlight]

Can anyone help explain something to me?

So far I've been imagining all neurons how motoneurons look, with the cell body at one end, then the axon, and the terminals at the other end.  Heaps of other terminals synapsing onto that cell body, triggering graded potentials.  But I've just been revising a bit and have started thinking about neurons where the cell body is in the middle of the length of the neuron, like in sensory neurons. 

So how does this work when it comes to generating a strong enough graded potential in the cell body to then trigger an AP along the axon? Eg say there is a specialised receptor cell like a rod or a cone that receives stimulus... the diagram we have shows that that cell synapses onto a sensory neurone but the cell body of the neurone is half way down the axon. Where is the location of the axon hillock in this situation i.e. the area in which an AP is triggered if threshold is reached?  If the axon hillock is in the cell body, which is far away from the special sense receptor, how does the information from the sense receptor get there, in order to propagate down the axon?

Just some things about terminology:
The axon initial segment (according to my 3rd year neurophys notes) is what is considered to be the site of action potential initiation. It is the "thick, unmyelinated part of an axon that connects directly to the cell body". The axon hillock, however, "is a specialized part of the cell body (or soma) of a neuron that connects to the axon.". I think 2nd year phys is a bit behind in that sense as they talk about the axon hillock being the site of AP initiation, but current research states it's the AIS (http://en.wikipedia.org/wiki/Axon_hillock). For the purposes of human phys, you can just consider the AIS/AP being the same sort of thing with the same characteristics like high density of voltage-gated sodium channels in comparison to the rest of the axon.

In terms of your question, the bipolar neuron in the middle of this diagram shows the axon hillock after the cell body, at the side of the axon which contains the axon terminals (http://www.google.com.au/imgres?imgurl=http%3A%2F%2Fwww.cliffsnotes.com%2Fassets%2F277470.png&imgrefurl=http%3A%2F%2Fwww.cliffsnotes.com%2Fsciences%2Fanatomy-and-physiology%2Fnervous-tissue%2Fneurons&h=273&w=468&tbnid=vTy5_me1ngn8fM%3A&zoom=1&docid=Qf_m1WWmAoDBDM&ei=Div8U6mqItfn8AXCpoGQCg&tbm=isch&iact=rc&uact=3&dur=1034&page=1&start=0&ndsp=14&ved=0CBwQMygBMAE)

How the signal gets from receptor to afferent fibre varies according to the kind of sensation you are looking at. Rods and cones are too confusing to consider as an example because they hyperpolarise in response to a light stimulus. A sensation like touch would go as follows:

1. Touch stimulus causes a large mechanical deformation in that site of the skin's plasma membrane
2. Mechanosensitive receptors in that area are stimulated to open
3. Provided the touch stimulus was of a reasonably large magnitude, large amounts of mechanoreceptors are activated to allow the entry of sodium into the receptor cells
4. This large graded potential causes the mechanoreceptor MP to reach threshold (+50 mv)and thus stimulate the opening of VG sodium channels. . AP occurs and reaches the axon terminals (opening of VG calcium channels blah blah) so there is release of neurotransmitter by the mechanoreceptor cell. The neurotransmitter is depolarising as it binds to receptors that cause a depolarisation in the afferent nerve fibre (sensory neuron). These kinds of receptors on the afferent nerve fibres would contain ligand-gated ion channels.
-->These involve the neurotransmitter e.g. glutamate from the mechanoreceptor binding to the (e.g. glutamate) receptors on the afferent nerve fibre,  ligand ion-channels would change conformation and open  and there would be entry of sodium or sodium and other cations into the afferent nerve fibre. MP eventually reaches threshold in this afferent nerve fibre causing vG sodium channels to open and then the whole AP thing occurs.

Hope this makes sense

[ss12345]

Hey guys, just going Concept Check 3.
What are your thoughts for this question?

Which of the following will occur at the blood vessels leading to exercising skeletal muscles?? Select all the correct statements.

      
alpha1-adrenergic receptors on the blood vessels will be activated by sympathetic nerves.

      
beta2-adrenergic receptors on the blood vessels will be activated by adrenaline.

      
The net response will be a dilation of these blood vessels.

      
The net response will be a constriction of these blood vessels.




I am semi-confident hat option 2 and 3 and correct, and option 4 is incorrect.
But I am uncertain about option 1. Activation of the alpha-1 receptors will result in vasoconstriction, which obviously is not the NET result but I do remember Val mentioning that both effects are occurring, it is just one is more dominant. Therefore, in the exercising muscle.. vasodilation is more dominant than vasoconstriction (but vasoconstriction is still happening).

[Belgarion]

Back to the first initial posts, I know what happens to RMP if you do things like increase permeability of Na/K, if you block leak channels, add more to the ECF/ICF, etc but what confuses me is the voltage gated channels. Could someone please just quickly go over what happens to RMP if you block/ add more of these (for both Na and K)? From examples I have seen, it seems different to the leak channels

[MelonBar]

Hey guys, if you have two different arrangements of sarcomeres, where one arrangement has them lined one after the other like a long train (A), and the other arrangement has them stacked on top of each other like pancakes (B), which set will exhibit the greatest degree of shortening? Say each sarcomere shortens half a micron for the sake of explanation, and that there are 4 units in each case.

I picked A because if each sarcomere contracts in a train, the entire set of four will shorten by a total of 4 * .5 = 2 microns. If the same contraction happened in the pancakes arrangement, you only get a total shortening of .5 microns, because sarcomeres contract in only one direction if you get me. If the pancakes arrangement was of actual pancakes, then it's like cutting the stack down the middle with a knife. If you look at one stack of semicircular pancakes the total shortening is the length of half a pancake. If you have individual pancakes lined next to each other like a train, and then cut each pancake by half, the total shortening is you could say, the length of half a pancake times how many pancake carriages are in the train.

i'm blown today

sooo my question is. is that the right logic? replace the pancakes with sarcomeres

[Starlight]

Hey guys, if you have two different arrangements of sarcomeres, where one arrangement has them lined one after the other like a long train (A), and the other arrangement has them stacked on top of each other like pancakes (B), which set will exhibit the greatest degree of shortening? Say each sarcomere shortens half a micron for the sake of explanation, and that there are 4 units in each case.

I picked A because if each sarcomere contracts in a train, the entire set of four will shorten by a total of 4 * .5 = 2 microns. If the same contraction happened in the pancakes arrangement, you only get a total shortening of .5 microns, because sarcomeres contract in only one direction if you get me. If the pancakes arrangement was of actual pancakes, then it's like cutting the stack down the middle with a knife. If you look at one stack of semicircular pancakes the total shortening is the length of half a pancake. If you have individual pancakes lined next to each other like a train, and then cut each pancake by half, the total shortening is you could say, the length of half a pancake times how many pancake carriages are in the train.

i'm blown today

sooo my question is. is that the right logic? replace the pancakes with sarcomeres

Your logic for choosing A appears correct. The muscle that will produce the greatest degree of shortening has its blocks of sarcomeres arranged lengthwise, a long/lengthened muscle will allow a greater contraction/degree of shortening lengthwise. The muscle that has blocks of sarcomeres with increasing height is going to be in comparison short lengthwise, so that contraction/degree of shortening lengthwise is going to be less. This is really all the level of detail you need to know for these types of questions afaik, I don't think you will ever need to mathematically calculate the degree of shortening for a specific muscle (unless they have decided to add that in this year haha)

[MelonBar]

thanks again el!

[Starlight]

thanks again el!

Haha no worries, all these questions are a repeat from last year's course for which I have physiology notes for. Though, from time to time I might wait a while to answer a question (unless urgent) because it's probably more beneficial for current physiology students to discuss possible answers

[MelonBar]

What was the answer for the broken c5 question?

[hobbitle]

Debate on the Facebook site is leaning towards "parasympathetic control of the heart" (will be maintained) but that's the only question no one can give a concrete answer on.

[MelonBar]

It's prob right then. My friends had heart as well. I think I put adrenal glands cos i thought the neurohormone from the pituitary can stimulate it.

and the myosin head releases from actin when atp-bound correct?

i maintain that phys is the harder of the 3 premed subjects

[hobbitle]

Yes re myosin/ATP.
I haven't found it too bad so far to I thought Valerians lectures were the hardest to get my head around but I also spent least time on them.

[MelonBar]

yeah fair enough. it's harder than biochem and anatomy imo because you need to have a deep understanding of all the concepts to proof yourself against all the integration/application questions. i'm less sure about neuro major now...

[MelonBar]

Hey all,

i'm having some trouble with this week's concept check.

2. which of the following could be used to decrease acid levels in the stomach?
a histamine blocker, somatostatin, a pepsinogen blocker, acetylcholine, cholecystokinin (CCK)

i think histamine blocker, somatostatin and acetylcholine are defo ones, but what about a pepsinogen blocker and CCK? I know pepsin helps digest proteins, but does it contribute to stomach acid levels? CCK i know can contract the gallbladder to release bile salts, but could it have a role in stomach acid level?

3. ‘Pancreatic insufficiency’ is a disease involving inadequate release of pancreatic enzymes.  which of the following would you most expect to see in a patient suffering from this condition? (Choose one)

reduced bile production, reduced intestinal contractions, undigested fat in the faeces, increased gastric acid levels, or two of the above are correct.

I'm pretty sure about undigested fat, because the pancreas releases pancreatic lipase to finish off fat digestion - i don't think the first two options are correct, but i'm not sure about gastric acid levels.

[hobbitle]

Hey all,

i'm having some trouble with this week's concept check.

2. which of the following could be used to decrease acid levels in the stomach?
a histamine blocker, somatostatin, a pepsinogen blocker, acetylcholine, cholecystokinin (CCK)

i think histamine blocker, somatostatin and acetylcholine are defo ones, but what about a pepsinogen blocker and CCK? I know pepsin helps digest proteins, but does it contribute to stomach acid levels? CCK i know can contract the gallbladder to release bile salts, but could it have a role in stomach acid level?

3. ‘Pancreatic insufficiency’ is a disease involving inadequate release of pancreatic enzymes.  which of the following would you most expect to see in a patient suffering from this condition? (Choose one)

reduced bile production, reduced intestinal contractions, undigested fat in the faeces, increased gastric acid levels, or two of the above are correct.

I'm pretty sure about undigested fat, because the pancreas releases pancreatic lipase to finish off fat digestion - i don't think the first two options are correct, but i'm not sure about gastric acid levels.

For 1,
I believe acetylcholine will increase stomach acid levels. Acetylcholine is released by the parasympathetic NS. It also triggers release of gastrin and histamine both of which increase gastric acid secretion.
I don't think CCK or pepsinogen have any affect on stomach acid levels.

I think you are correct on the second questions with the undigested fat.

I didn't get 100% on that concept check though and couldn't see what I got wrong.