Sample comment: I was going over my notes on neurotransmission and my notes said that glutamate receptors only produce direct changes in channel conductance. However, I remember that you said that glutamate bound to a receptor that activated Phospholipase C. Which is correct my memory or my notes.
Reply :Glutamate does activate a receptor called the metabotropic glutamate receptor. This receptor does increase the activity of PLC and thus can activate PKC. Activation of PKC can lead to changes in membrane permeabiltity by activating or inactivating ion channels through phosphorylation. It can also change the kinetics of NT receptors thus changing the response of a postsynaptic cell to a given release of NT from a presynaptic cell.

What exactly is the "P-domain" (ie, what is it's structure) and how does it work? Is it another subunit?
Reply: The P-domain is not a separate subunit. It is a string of amino acids between the 5th and 6th transmembrane portions of a voltage dependent channel. This string of amino acids sits inside the pore of the channel and is responsible for conferring ion selectivity upon a given channel.

What exactly is the difference between the parallel conductance equation and the GHK equation, if any?
Reply:The major difference is in how they are derived and what values are used in the equation. In the parallel conductance model the value used for defining ion flow across the membrane is conductance. In the GHK permeability is used as a measure of the ability of a particular ion to flow across the membrane. Furthermore, in the parallel conductance model the Nernst or equilibrium potential factors in differently than it does for the GHK model. Basically, the difference deals with what variables you have at hand to calculate Vm. If you have conductances you would use the parallel conductance model. If you are given permeabilities then you would use the GHK equation.

How does the release of Calcium from the voltage dependent calcuim channels lead to neurosecretion?
Reply: At this stage of the game what I would like you to know is that there is an interaction between the proteins that are involved in docking and calcium such that the vesicle fuses with the axon terminal membrane and the contents of the vesicle are released into the space.  One possible mechanism that was mentioned in class was that synaptotagmin, which has 2 calcium binding sites, might regulate this process by becoming less tightly bound to neurexin and NSF in the presence of calcium.

I am confused about the whole NSF, SNAp, SRARE thing when the vessicle is fusing with the membrane. Could you go over this again?
See Reply to Q5

How do 2nd messenger proteins figure into the whole classical Neurotransmitter process from synthesis in the pre-synaptic axon terminal to binding in the post-synaptic membrane? They are Kineses or G-proteins? Or is kinase one of the 17 G-proteins?
Reply: Hopefully, thursday's lecture cleared everything up! If not come to the review session on tues.

Do both K+ and Na+ produce depolarization? Do they have differnt functions? Do you think you could breifly summarize the roles of each of the differnt ions in action potentials? Thanks.
Reply: Both are voltage dependent i.e. they are opened in response to depolarization.  Sodium channels are opened very quickly while potassium channels are opened slowly.  The opening of sodium channels will depolarize the cell, while the opening of potassium channels will hyperpolarize the cell.  Since sodium channels open first in response to depolarization the cell first depolarizes and then, when the potassium channels open the cell repolarizes (hyperpolarizes). Hope this helps. If it doesn't come to the review session or look at the textbooks I've put on reserved for the course.

What is the significance of molecular motors such as kinesin and dynein?
Reply:  moving molecules around the cell.  One moves them in a retrograde fashion and the other in an anterograde fashion.

When is the Nernst equation value negative? Is it due to the valence? What produces a negative value for the valence?
REply: The valence has something to do with it. Valence reflects the charge on a ion eg. potassium is +1.  Also remember that the ln of a given number can be negative.

do we have to memorize the equations for nernst, ghk, and parallel conductance?
REply: Good question. YES!!

What are shunting and noting?
Reply:  I believe you are referring to the 3 results of changing ion conductances - depolarization, hyperpolarization and nothing.  When nothing happens in response to opening a given channel it is sometimes referred to as shunting.  This concept was not dealt with any further ecxept to say that just because the membrane potenial doesn't change in response to the opening of channels does not mean nothing is happening.  What is really happening is a process that is referred to as shunting.

Is the p-domain related to the n-terminal or globular protein that swings in to close the channel? If so, how? Also, the picure that shows 4 circles with 4 things sticking towards the center -- what is this a picture of?
Reply:  No the P-domain is a region between the 5th and 6th transmembrane segments of a voltage dependent channel's subunit.  It's hard to say because I don't know which picture you're referring to.

what happens when Vm = 0? does it happen? is it a bad thing?
(4/3/98, 11:07:03 PM) () wrote:

what happens when Vm = 0? does it happen? is it a bad thing?
Reply: in and of itself it is not bad.  It could mean a number of things 1) all channels have been closed - not likely. 2) the balance of sodium and potassium conductances is such that Vm = 0.  This does in fact does happen. 3)  there is no chemical gradient.

What is the membrane potential at the peak of an action potential?
Reply:  The exact potential depends on the ratio of the sodium to potassium conductance at the moment.  In practice it is usually slightly above 0 i.e. +10-+20

When you were talking about voltage dependent calcuim channels, you said that they in turn open up potassium channels which have greater conductivity than the delayed rectifiers which are normally open. However, accompanying this in my notes is a diagram of a more depolarized bump than before. Wouldn't greater gK result in a hyperpolarized cell? Which is correct, the diagram or what I wrote?
Reply: Yes opening K channels would hyperpolarize the cell.  What I was getting at was that the opening of calcium channels can lead to an opening of calcium dependent potassium channels which will terminate the depolarization and the calcium signal by hyperpolarizing the cell.

which proteins make up the SNARE? Is it just synaptobrevin, syntaxin, a and the SNAPs? Or does it also include synaptotagmin and neurexin?
Reply: Synaptotagmin and neurexin are not part of the SNARE.

in lecture you said that ACh is found in dorsal motor cells in the spine. But aren't the motor cells in the spin located ventrally?
REply: You are correct motor neurons are found in the ventral horn. They release Ach.

are the alpha and beta receptors for norepinephrine connected directly to ion channels, or to G-proteins?
Reply: both are connected to g-proteins

Submit your own questions and/or comments to appear above:

E-mail the professor directly.