Course:NRSC500

NRSC 500 2010 Discussion board

This is a page for the students of NRSC 500 in the 2010 year to post up questions they might have regarding course content, help with assignments, and midterm/final-related questions.

Just click on the edit tab at the top to post.

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Finally got this thing uploaded properly! Anyways... old midterm with some answers that Ricardo got his hands on... a lot of the stuff written on them appears to be notes taken during an exam review session.

File:NRSC500 Old Midterm exam.pdf

Also, there were a few topics from the old midterm that we had issues with...

There are VGCCs located in the soma, meaning that even when recording from the soma we will still see the activation of Ca-activated K channels and a resulting longer AHP.

From the workshop unit on chapter 1, Lynn Raymond stated that Ca channels open during an AP have pretty much no effect on the peak amplitude of the AP because Na current is so much greater (due to higher concentration). However, it will likely prolong the AP peak during the normal falling phase of the AP. This is when Na current drops very quickly meaning the effect of Ca will be much more noticeable.

Inward rectifiers are primarily activated in astrocytes... in this location they act to take up K when extracellular levels rise (note, this causes Ek to become much less negative)... so the primary role of inward rectifiers is not relevant to this question Instead the effects will be:

1) faster AP propagation

2) higher resting membrane potential

Explanation:

Normally, we would not see inward rectifiers actually allowing any current into a cell. This is because the resting membrane potential is typically above Ek... hence, we would need some outside force to hyperpolarize the membrane beyond Ek.

[Note: I talked to MacVicar today for some context. Inward rectifiers aren't really expressed on neurons since they aren't very useful unless you get below Ek.]

There are two ways to hyperpolarize the cell beyond Ek in an endogenous cell: active ion pumps and chloride channels

i) During the AHP of an action potential, the increased K conductance will hyperpolarize the cell beyond the resting potential, but not beyond Ek. However, the Na-K-ATPase will hyperpolarize the cell beyond the Ek. Hence, inward rectifiers, which will be open at this time, will reduce the AHP duration and amplitude by minimizing the hyperpolarizing effect of Na/K-ATPase.

ii) A lower Ecl than Ek... there is variability in both equilibrium potentials depending on ion gradients, so this could occur in some cells (even though I'm pretty sure Ecl is usually higher than Ek). If Ecl is lower than Ek, then outward Cl current could hyperpolarize the cell beyond Ek, allowing inward flow of K+ ions through the inward rectifiers.