Neurophysiology: neurons & circuits question

[MelonBar]

After the part about ion exchangers, there's a wordy slide that goes:

-neuron membrane is a barrier to ion movement,
-transporters use energy to set concentration gradients across membrane,
-at rest the membrane is selectively permeable to K+
-K+ is close to equilibrium, with little net movement due to a balance of concentration gradient and electrical gradient forces,
-this results in a membrane potential of ~65mV (interior of neuron is negative at -65mV), which is close to equilibrium potential of K+.

I am trying to make sense of this slide with 2nd year physiology, but I don't remember much so I was hoping someone could hold my hand through this

I get there are leak channels that allow the membrane to be 'selectively permeable' to K+. So, I assume K+ is able to flow down its electrical gradient into the cell, but this could only happen if there is a negative charge inside the cell - why is there a negative charge inside the cell? I also get that the Na/K pump is pumping K+ ions into the cell as well, maintaining that concentration gradient.

So, the electrical/chemical gradient keeps K+ in, giving the cell a membrane potential of -65mV? Which is close to K+'s equilibrium potential of -80mV? Is that what the slide is saying? But because -65mV > -80 mV, shouldn't K+ be flowing out?

I'm really confused, someone give me a hand here..

[nino quincampoix]

To recap: the neuron membrane is semi-permeable, and is more permeable to K+ than it is to Cl-, Na+, and Ca2+. Leak channels give rise to the selective permeability of K+, as they allow potassium to leak out of the cell. At rest, K+ is more concentrated in the cell due to its enhanced permeability (amongst other things), which means that the RMP (-65 mV) is closer to the equilibrium potential of K+ (-80 mV) than it is to the equilibrium potential of other ions, say Na+ (~ +60 mV). (Remember, there is still Na+ and Cl- inside the cell, so that would be partially why the RMP is not the same as potassium's equilibrium potential.)

The Na+/K+ pump accounts for <<10% of the concentration gradient (per Charles' lectures from PHYS20008). However, the ATPase helps establish the electrochemical gradient (and therefore potential energy) that ion exchangers/transporters use.

Even if an ion is freely permeable, the majority of the RMP is established by the leak of ions, and the cell’s inherent negative charge holds the remaining cations in the cell (again, from PHYS20008). From memory, the negative charge comes from some of the structural proteins that comprise neurons.

Since K+ has an equilibrium potential of -80 mV and is a positively charged ion, K+ wants to move into an area of that potential. As -80 mV is the potential required to keep K+ at equilibrium, K+ flows out of the cell until an RMP of -65 mV is established. Once at RMP, K+ is in a relative state of equilibrium (even though the cell is not at -80 mV, K+ leakage out of the cell means that there is less K+ concentration in the cell, and therefore is effectively at potassium's equilibrium potential).

In sum: the slide is saying that the RMP of neurons results from the selective permeability of K+, as well as potassium's equilibrium potential, therefore implying that K+ has minimal net movement as it is close to its electrochemical equilibrium. And yes, the electrochemical gradient keeps K+ in the cell at a certain concentration (or at an RMP of -65 mV).

Please let me know if I was unclear.

[MelonBar]

Thanks a lot nino for your help (also with the resonance question from a few months ago) 

Does anyone have any tips for the MST #1? There seems to be a lot of diagrams and stuff pulled from research articles, also some slides are just 'awkward'/explained scantly and it's hard to tell the level of depth you are expected to know. NB: I haven't done the 5 practice questions on the LMS but I plan to do them the night before the test.

Appreciate it 

[ferrsal]

I'm also a bit worried about the MST, particularly Joel's lectures... I remember him in HSF and he was a huge fan of testing things that he never explained but were in the textbook.

Also, Q4 in the practice test seems to not relate to anything we've been taught in lectures 1-9?

[MelonBar]

I'm also a bit worried about the MST, particularly Joel's lectures... I remember him in HSF and he was a huge fan of testing things that he never explained but were in the textbook.

Also, Q4 in the practice test seems to not relate to anything we've been taught in lectures 1-9?

that's concerning, i was def going to use the TB for his ear part but I might just go through everything with the text to be safe. 25% is a lot to feel sorry for. also... subject is hard. my head hurts from learning...

[ChickenCh0wM1en]

sigh...

I'm finding L8 to be a massive pain in the ass tbh
Don't really understand how all these techniques work - e.g. patch clamp vs. voltage clamp etc.

[nino quincampoix]

Re Q4 of the practice test.

See slide 14 of lecture 3.
I.e., vesicular glutamate transporters (VGLUT2) package glutamate into vesicles for release at the synaptic terminal onto the postsynaptic cell.


Re patch clamp and voltage clamp.

Info on these recording devices can be found in Neuroscience (Purves).

[ferrsal]

In lecture 6 regarding the proprioception, I understand everything written on the slides and the existence of the group Ia, II and Ib primary afferents, their different firing speed, and how they're related to either muscle length or tension, but the lecturer delved into a really indepth explanation. I listened to it about 20 times and read up on it in the neuroscience book, but am still a little ?!!!! about it. Can someone explain the difference between these and WHEN they actually fire potentials? Would really appreciate it

[nino quincampoix]

In lecture 6 regarding the proprioception, I understand everything written on the slides and the existence of the group Ia, II and Ib primary afferents, their different firing speed, and how they're related to either muscle length or tension, but the lecturer delved into a really indepth explanation. I listened to it about 20 times and read up on it in the neuroscience book, but am still a little ?!!!! about it. Can someone explain the difference between these and WHEN they actually fire potentials? Would really appreciate it

The following is from my notes that I took during the lecture. I think it would be advisable to double check in the textbook because I could have misheard or misunderstood the lecture material myself.

Muscle spindles have group Ia and group II afferents.

• Group Ia afferent terminals are deformed when the muscle itself stretches. As per most mechanoreceptors, deformation of the nerve terminals causes them to fire; in this case, the spindle fires when the muscle stretches.
• Group II afferents fire when the spindle itself is stretched and their firing follows the level of stretch within the spindle.

Moreover, group Ia afferents have rapidly adapting responses to changes in muscle length, whereas group II afferents produce sustained responses to constant muscle lengths (from Neuroscience, Purves). This is for proprioception, as group Ia afferents "report" on the dynamics of the limb, while group II afferents "report" on the static position of the limb.


Golgi tendon organs have group Ib afferents.

• When the muscle either lengthens or contracts, the Golgi tendon organs stretch. In either case, potentials are fired due to mechanoreceptor deformation.

[ferrsal]

Thank you, this clarifies a lot!

[Pup]

Just a clarification: For the convergence of rods and cones with bipolar cells:

In response to light, the photoreceptors (more specifically the cones being more at the centre at the fovea) hyperpolarizes and there is a reduced  glutamate release. reduced glutamate depolarises the on centre bipolar cells and subsequently the on centre ganglion cells. The off centre bipolar cells are hyper polarised and are essentially switched off.


In response to darkness, the photoreceptors (more specifically the rods) depolarises and there is an increase in glutamate release. Increased glutamate release depolarises the off centre bipolar cells and subsequently activates the off centre ganglion cells. The on centre bipolar cells are hyper polarised and are essentially switched off.

So essentially, in low light, the peripheral region of the eye is more activated, whereas, in bright light, the fovea of the eye is more activated. I don't know if my logic and reasoning is correct.  let me know if there is something wrong thanks!

[MelonBar]

Wtf joel

[ChickenCh0wM1en]

Wtf joel

Struggled hard with his questions....
A lot of questions I was second guessing myself - had 2 choices but didn't know which one to choose... :S

[MelonBar]

Yeah I know what you mean, do you remember the first line (2 blanks)  on the very last question btw? I was tossing up putting primary afferent then another answer, or the other way around with primary afferent on 2nd blank... it was wack.

[nino quincampoix]

The neurophys MST results are now on the LMS (for me at least). There were 34 questions on the test, but my score is out of 32. Does anybody else have the same thing?