ATAR Notes: Forum
Uni Stuff => Universities - Victoria => University of Melbourne => Topic started by: ChickenCh0wM1en on August 04, 2014, 10:49:50 pm
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Hi guys,
I just had a few questions about membrane potential..
1) I know that if I add K+ into the ECF, Resting membrane potential and equilibrium increases (becomes less negative) - more likely to fire but how does this occur? If we add K+ to ECF, the concentration gradient is reduced since K+ is higher in the inside of the cell - less negative charge is required to keep K+ inside the cell but how does this change anything? (i don't really see the link)
2) Would the opposite effect occur if I increase ICF K+?
3) If I add Na+ into the ECF, concentration gradient for Na+ is increased and because the inside is more negatively charged, eq potential increase, RMP increases - more likely to fire (I get that I think) - correct me if I'm wrong. Would an increase in ICF Na+ have the opposite effect?
4) What would happen to RMP if I increase # leak channels for Na+ and K+ respectively and why?
Thanks! :)
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1) I think that sort of scenario is just trying to test your understanding of RMP. If we need less negative charge to pull the K+ back into the cell then the equilibrium potential would be more positive. This doesn't actually happen during an action potential.
2) Yeah, so if we increase K+ in our cells, the concentration gradient increases and we need more negative charge so that it will equal the diffusion force. So equilibrium potential would be more negatve.
3) Correct.
4) Remember that the RMP is determined by relative permeability between K+ and Na+. Normally our RMP is at -70mV. If we increase the permeability of K+, we increase the number of K+ leak channels then more K+ is diffusing out the cell, so we need more negative charge to pull those K+ back. So the RMP would become more negative and will move closer to the equilibrium potential for K+, whichs is -90mV. If we increased permeability to Na+ then we increase the number of Na+ leak channels so more Na+ ions didfuse into the cell. We need a positive charge inside the cell to repel the Na+ and push it out, so we bring the RMP closer to the equilibrium potential for Na+ which is +60mV.
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1)Hyperpolarization (where MP becomes more negative) is basically movement of K+ from the inside of the cell (provided its there at a high concentration) to the outside of the cell. Here, since the concentration gradient is not as strong, MP becomes more +ve because less K+ is moving out of the cell. Shezn0r's explanation of the EP is good so I won't elaborate on that.
2)Yep see the first line I wrote in Q1. High conc K+ inside the cell means more K+ moves to the outside of the cell and MP becomes more -ve (as it is less +ve inside the cell with K+ ions moving out). The charge needed to bring that K+ back to the inside of the cell needs to be greater i.e. more negative because K+ is being driven out the cell with a concentration gradient.
3)Increase in ICF Na+: Concentration gradient to move sodium into the cell from the ECF decreases. Less Na+ moves into the cell. Equilibrium potential/charge needed to bring Na+ ions into the cell needs to be more -ve to attract those Na+ ions.
4)More leak channels for K+: More K+ moves from the ICF to the ECF. This is hyperpolarization so MP decreases. Charge/Equilibrium potential needed to bring K+ Into the cell needs to become more -ve to attract those K+ ions back into the cell.
More leak channels for Na+: More Na+ moves from ECF to ICF. This is depolarization so MP increases. Charge/Equilibrium potential needed to bring Na+ Into the cell becomes more +ve as the concentration gradient for Na+ is already working to bring those Na+ ions into the cell.
You will want to know everything about how different scenarios affect MP and EP & in addition, knowledge of the graph about RMP, EP for K+ and Na+ and labelling the axes for that graph in prep for the exam. Keep practicing this kind of stuff with the human phys past exams.
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Thanks guys! :)
I'm probably going to get scolded for this but what does it mean by a positive/negative equilibrium potential - it's related to the Nernst potential right?
So would a +ve EP correlate to high concentration on outside v.s inside and vice versa?
Thanks again C:
All you need to know for the equilibrium potential for physiology is that it's the charge needed to attract ions into a compartment (either the ICF or ECF). E.g. if there is a large concentration of ions in compartment 1 then compartment 2 will need to become more negative (I.e. EP becomes -ve) in order to attract those ions to compartment 2.
Again, using the examples above:
"if I add K+ into the ECF". Under resting conditions, the concentration of K+ is higher in the ICF than the ECF. By adding K+ into the ECF, you are decreasing the concentration gradient by which K+ moves from the ICF to the ECF. Therefore the EP becomes more positive as the ICF doesn't need to attract those ions as much.
"if I add K+ into the ICF" Under resting conditions, the concentration of K+ is higher in the ICF than the ECF. By adding K+ into the ICF, you are increasing the concentration gradient by which K+ moves from the ICF to the ECF. Therefore the EP becomes more negative as the ICF needs to have more of a negative charge to attract those ions back into that compartment.
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You're a legend mate, thanks so much.
Ugh I feel so stupid not understanding this before, gotta brush up and fully wrap my head around it :(
No probs. Don't worry, it's a bit difficult to get your head around at first but by the time you are revising for the MST & the exam you will find that interpreting these membrane potential scenarios isn't too bad at all!
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Osmotic equilibrium means that osmolarity is the same inside and outside the cell, which is the concentration of both penetrating and non-penetrating solutes ?? If that is true, then the total number of particles on either side of the membrane can vary, because the volume of water/fluid can change the concentration of ions etc whether it is inside the cell or outside the cell - is this correct?
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ty men. physo is hard as... harder than anatomy and biochem?
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ty men. physo is hard as... harder than anatomy and biochem?
I never once thought physiology was harder than anatomy & biochem :l
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Hi guys,
in the attached screenshot, I'm kind of confused about one thing.
If you look at the yellow area (the active area where the Na channels are open) you can see that the polarity across the membrane is reversed (negative outside, positive inside).
Is this really accurate?
So, I understand that the -90mV charge that holds K+ inside the cell at RMP is due to negatively charged proteins and stuff like that (I actually wish they didn't gloss over it so much, because its pretty confusing to just say "the cell has a negative charge". Like, what?).
But at the peak of a action potential, is it REALLY a negative charge on the outside of the membrane? Or did they just draw it like that for illustrative purposes? I don't really understand how the polarity totally swaps - I understand that the concentration gradient across the membrane gets reduced, but to have it switch polarity completely?
Does anyone know what I'm on about? I'm confused.
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Hi guys,
in the attached screenshot, I'm kind of confused about one thing.
If you look at the yellow area (the active area where the Na channels are open) you can see that the polarity across the membrane is reversed (negative outside, positive inside).
Is this really accurate?
So, I understand that the -90mV charge that holds K+ inside the cell at RMP is due to negatively charged proteins and stuff like that (I actually wish they didn't gloss over it so much, because its pretty confusing to just say "the cell has a negative charge". Like, what?).
But at the peak of a action potential, is it REALLY a negative charge on the outside of the membrane? Or did they just draw it like that for illustrative purposes? I don't really understand how the polarity totally swaps - I understand that the concentration gradient across the membrane gets reduced, but to have it switch polarity completely?
Does anyone know what I'm on about? I'm confused.
So the definition of an AP is that it should go from -50 mV(threshold) to around -70 mV, where after-hyperpolarization is expected to kick in. In the resting state, the RMP of the cell is expected to be at -70 mV (correspond to the inside of the cell membrane having negative charges). As soon as RMP reaches threshold (-50 mv) i.e. when the trigger event occurs, the activation gate of the VG sodium channel rapidly opens. As is shown in the active area of the diagram, sodium ions rush into the cell from the ECF and hence take their positive charges into the cell. The active area in the picture is representing the peak of the action potential, i.e. just before the inactivation gate closes the VG sodium channel and the potassium VG channel is triggered to open and allow K+ ions to exit from the ICF to the ICF.
Basically I think the reason there are + charges lining the inner membrane of the active area is because of the fact that this area of the cell is at a MP ranging anywhere from 0 to +30 mV during the AP event(here the example is at peak potential: +30 mV). The adjacent inactive area still has negative charges lining the inner membrane because although sodium ions are flowing from the active area to that region to stimulate a depolarization, the AP event has not occurred and so it does not have a positive MP in that area yet.
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I think I must have expressed my question badly because I was talking about the -ve charges on the outside of the membrane (ECF) that are still within the active area... not the -ve charges adjacent.
However I think you still answered my question inadvertently!
I think it's definitely more about thinking of it like a relative charge difference thing rather than absolute.
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I think I must have expressed my question badly because I was talking about the -ve charges on the outside of the membrane (ECF) that are still within the active area... not the -ve charges adjacent.
However I think you still answered my question inadvertently!
I think it's definitely more about thinking of it like a relative charge difference thing rather than absolute.
Haha whoops. Yeah I think i think you are right about it being a case of relative charge difference. The sodium ions are rushing from the ECF to the ICF and you are taking away positive ions from the ECF in the active zone during the AP. The negativity on the outside is further enhanced from 0 to +30 mV because the potassium VG channels are not yet open to allow K+ to go from the ICF into the ECF and reverse that negative charge on the outside that has been established whilst the cell is undergoing an AP :)
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Anyone have any tips for the physiology blogs ??
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Anyone have any tips for the physiology blogs ??
Post frequently, i'd aim for about 5 good-quality posts. Try commenting on posts made by other members of the blog.
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RMP = -70mV, equilibrium potential for K+ = -90mV. Over time then, the concentration gradient would disappear as potassium ions regularly leave the cell through the K+ leak channels. But this is countered by the action of Na+/K+ pumps that drive sodium and potassium ions against their concentration gradient, thereby maintaining the relative ion concentrations and the RMP.
Is this correct?
edit: also when we say the positive charge is pulled along the membrane attracted by the negative charge that lines the cell during an AP (activation gate of VG sodium channel opens) --- what exactly is this negative charge? Why is it there... what is it
Btw thank you El etc for helping out.
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What do you define as good quality? Is it like 2-3 sentences or a full paragraph etc?
You'll kind of get an indication from each blog i.e what is required. Just say what you want to say in each post, each post can be of different lengths. I think you can imagine if you were a moderator of the blog posts that 2 sentences is not really going to be a good indication of what you have learnt from the course/blog topic.
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Hi guys,
in the attached screenshot, I'm kind of confused about one thing.
If you look at the yellow area (the active area where the Na channels are open) you can see that the polarity across the membrane is reversed (negative outside, positive inside).
Is this really accurate?
So, I understand that the -90mV charge that holds K+ inside the cell at RMP is due to negatively charged proteins and stuff like that (I actually wish they didn't gloss over it so much, because its pretty confusing to just say "the cell has a negative charge". Like, what?).
But at the peak of a action potential, is it REALLY a negative charge on the outside of the membrane? Or did they just draw it like that for illustrative purposes? I don't really understand how the polarity totally swaps - I understand that the concentration gradient across the membrane gets reduced, but to have it switch polarity completely?
Does anyone know what I'm on about? I'm confused.
Also dont forget that it just involves the ions at the very surface of the membrane. There are still millions of of ions on either side of the membrane that do not move
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Hey guys,
Just going the Week 4 Concept Check quiz and having some confusion over one question....
Which of the following could potentially inhibit an alpha motor neuron?? Select all that apply
The golgi tendon organ reflex
The muscle spindle reflex
Inputs from the brain motor cortex
Inputs from the cerebellum
Local spinal cord interneurons
What do you think? I know GTO reflex will definitely inhibit AM neurons. I thought no to muscle spindle reflex at first but then I realised while this results in excitation of some AM neurons, it will cause inhibition in the antagonistic muscle... therefore it also applies. Local spinal cord interneurons I suspect is correct but really not sure about the brain motor cortex and the cerebellum!! Any ideas?? :)
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hey mate i defo think local cord interneurons is one, but dunno about muscle spindle/motor cortex/cerebellum. i know the motor cortex can defo activate alpha MNs, and the cerebellum is involved in muscle memory and balance according to charles. there might be more info in the pre-reading textbook refs or modules.
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carn fellas motor cortex?? cerebellum?
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carn fellas motor cortex?? cerebellum?
I think all of these are correct:
The golgi tendon organ reflex
The muscle spindle reflex
Inputs from the brain motor cortex
Inputs from the cerebellum
Local spinal cord interneurons
The reasoning for GTO, muscle spindle & interneurons has already been mentioned.
According to my neuroscience notes: Motor cortex contains upper motor neurons that control the excitability of lower motor neurons (alpha motor neurons).
Cerebellum outputs are to the motor cortex (so for example it could inhibit the upper motor neurons to in turn inhibit the LMNs for tasks e.g. controlling balance).
So i'd say all 5 are correct (keeping in mind that the cerebellum indirectly inhibits lower motor neurons via the upper motor neurons)
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Thanks heaps for the help!!!
I just submitted the test and yep you were correct, all five of those options were correct. :)
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Thanks heaps for the help!!!
I just submitted the test and yep you were correct, all five of those options were correct. :)
Hey dude, with the muscle spindle, with the alpha motor neuron that is stimulated (reflex excitation), is another alpha motor neuron inhibited?
Also, with the end plate potential at the NMJ, is that also counted as a graded potential? (I think it is but not 100% sure).
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^^
Excitation pathway:
1) Increased muscle stretch--> Detection by muscle spindles--> Muscle spindles fire afferent APs to muscle spindle cell bodies in the dorsal root ganglia -> Cell bodies make direct synaptc connections with alpha motor neurons --> Alpha motor neurons are excited -> a-M neurons excite the agonist/synergist muscle (that was stretched & which contains the muscle spindle receptors) -> Muscle contracts to promote the reflex (opposite) response
Inhibition pathway:
2) Increased muscle stretch--> Detection by muscle spindles--> Muscle spindles fire afferent APs to muscle spindle cell bodies in the dorsal root ganglia -> Cell bodies make direct synaptc connections with inhibitory interneurons -> Alpha motor neurons are inhibited -> a-M neurons inhibit the antagonist muscle (that does not contain the muscle spindle receptors that detected the stretch in the synergist muscle) -> Antagonist muscle is relaxed/inhibited from contracting to prevent it from opposing the contractile response of the agonist muscle
Also, the end plate potential is just one huge graded potential event that always results in a contraction of the connected muscle. (for reasons that outlined in the textbook/ charles from lectures)
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El, you're insane. In the best way.
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el2012 is my hero
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Thanks El :) you da best!
El, you're insane. In the best way.
el2012 is my hero
Happy to help folks!
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Thanks heaps for the help!!!
I just submitted the test and yep you were correct, all five of those options were correct. :)
I ticked all 5 as well and got 10/10. apparently if you unticked muscle spindles you still got marks for the question, hmm.
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Yeah I lost one mark because I didn't check spindles
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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?
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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)
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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
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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).
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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
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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
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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)
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thanks again el!
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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 :)
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What was the answer for the broken c5 question?
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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.
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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
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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.
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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...
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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.
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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.
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thanks, good point about the acetylcholine. for the first question, I'm thinking the vagus nerve has to do with gastric motility, so severing that would mean no motility in the lower GI tract.
the other options are, stop salivating at the sight of food (incorrect I believe, cranial nerve does this), increased production of gastric juices normally associated with eating would be delayed until food reached the stomach, the increase of chyme from the stomach into the small intestine would become impaired, and all smooth muscle sphincters would lock in the closed position - what do we think?
ehhh the ENS is still in tact, didn't consider that one
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Comparative Animal Physiology's theory component seems so much more straightforward than Human Phys, ahahahaha (though the four lab reports are a big pain). I actually think I'd appreciate it a lot more; we didn't cover any digestive physiology at all, other than a little bit of comparison between various animals and their digestion techniques :( also CHARLES
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Obviously too late because the concept check has closed but might be worth a discussion anyway:
for the first question, I'm thinking the vagus nerve has to do with gastric motility, so severing that would mean no motility in the lower GI tract.
As you say below, the ENS is still in tact, so motility would continue presumably.
the other options are, stop salivating at the sight of food (incorrect I believe, cranial nerve does this),
Actually the "Vagus Nerve" slide says that the Vagus Nerve does trigger this kind of anticipatory response (long reflex). what do you think?
increased production of gastric juices normally associated with eating would be delayed until food reached the stomach,
Yeah this would probably happen if vagus nerve was severed, as Vagus nerve stimulates acid secretion in anticipation of food entering stomach.
the increase of chyme from the stomach into the small intestine would become impaired,
Hmm sounds too far down the GI tract for the vague nerve to have effect, I think it works from the stomach and above? Notes do say that the vagus nerve has an affect on the gastro-esophagael sphincter but the pyloric sphincter isn't mentioned.
and all smooth muscle sphincters would lock in the closed position - what do we think?
Nah don't think so............ as you say, ENS still in tact?
Hmm Digestive System is quite confusing!
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Totes vasoconstricting the crap out of my sprained ankle with this ice pack.
But not too much you know because we don't want to disrupt the... physiology n stuff.
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What happens if voltage gated Sodium channels can't open at all, is it possible to fire an AP at all, ever? Will APs be impossible?
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^I think it's impossible
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What happens if voltage gated Sodium channels can't open at all, is it possible to fire an AP at all, ever? Will APs be impossible?
^I think it's impossible
Agreed. The real stimulus for an AP is opening the VG sodium channels at threshold.
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So I'm just turning this thread into a general PHYS20008 study thread.
I have a few questions where I'm not confident in my answers. Can we discuss?
1) In which of the following scenarios would peripheral chemoreceptors most likely be dominant over central chemoreceptors in regulating ventilation?
A. When locked in a sealed environment
B. At high altitudes
C. During Exercise
D. At extremely low temperatures
2. How would removing inactivation gates from all Na+ Volatage Gated channels affect the MAXIMUM FREQUENCY at which a neurone can fire?
A. Increase frequency
B. Decrease frequency
C. No Change
D. Not enough information
3. How would blocking voltage-gated K+ channels affect the MAXIMUM FREQUENCY at which a neurone can fire?
A. Increase frequency
B. Decrease frequency
C. No Change
D. Not enough information
4. What affect on the likelihood of the axon hillock reaching threshold potential would this have: Synchronising IPSPs arriving from different sources so they arrive at the same time.
A. More likely
B. Less likely
C. No difference
D. Not enough Information
5. AP firing frequency is determined by an inward Na+/Ca2+ current called I Funny in which muscle cells? Cardiac auto rhythmic cells?
6. EC coupling is dependant on Ca2+ binding to calmodulin in which muscle cells? Smooth muscle?
7. Which muscle cell type has no t-tubules? I have no idea - smooth muscle?
Do you all disagree or agree with my Bold answers?
My last question related to ventilation and I am having a TONNE of trouble getting my head around questions like the one I've attached. Does anyone have any ideas or good ways of visualising/conceptualising what happens? I seem to THINK I get it but then always seem to get the complete opposite answers. Halp!
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So I'm just turning this thread into a general PHYS20008 study thread.
I have a few questions where I'm not confident in my answers. Can we discuss?
1) In which of the following scenarios would peripheral chemoreceptors most likely be dominant over central chemoreceptors in regulating ventilation?
A. When locked in a sealed environment
B. At high altitudes
C. During Exercise
D. At extremely low temperatures
2. How would removing inactivation gates from all Na+ Volatage Gated channels affect the MAXIMUM FREQUENCY at which a neurone can fire?
A. Increase frequency
B. Decrease frequency
C. No Change
D. Not enough information
3. How would blocking voltage-gated K+ channels affect the MAXIMUM FREQUENCY at which a neurone can fire?
A. Increase frequency
B. Decrease frequency
C. No Change
D. Not enough information
4. What affect on the likelihood of the axon hillock reaching threshold potential would this have: Synchronising IPSPs arriving from different sources so they arrive at the same time.
A. More likely
B. Less likely
C. No difference
D. Not enough Information
5. AP firing frequency is determined by an inward Na+/Ca2+ current called I Funny in which muscle cells? Cardiac auto rhythmic cells?
6. EC coupling is dependant on Ca2+ binding to calmodulin in which muscle cells? Smooth muscle?
7. Which muscle cell type has no t-tubules? I have no idea - smooth muscle?
Do you all disagree or agree with my Bold answers?
My last question related to ventilation and I am having a TONNE of trouble getting my head around questions like the one I've attached. Does anyone have any ideas or good ways of visualising/conceptualising what happens? I seem to THINK I get it but then always seem to get the complete opposite answers. Halp!
For the first one i would say at high altitudes b/c peripheral chemoreceptors respond more to O2 (central more to CO2) and at high altitudes there is a significant reduction in P(O2). During exercise, unless it is extreme exercise, O2 doesnt have much of an effect. All the other ones i agree with
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Oh! Clever. Yes. Agree. Thankyou.