In article <1993Jan26.123642.11726 at ringer.cs.utsa.edu>,
senseman at lucy.brainlab.utsa.edu (David M. Senseman) writes:
>> PAD (primary afferent depolarization) isn't all that mysterious.
> Why would expect depolarization to ENHANCE transmitter release?
> Assuming that the axonal spike completely invades all the terminals,
> (probably a reasonable assumption for most systems Eva was
> referring to), then depolarization would DECREASE syanptic release
> simply because the membrane potential of the presynaptic terminal
> would be closer to V which is going to be somewhere above +100 mv.
>> (Hard to do subscripts :)
>> That means the electrical force driving Ca inward would be reduced
> so that calcium entry during the terminal spike would be reduced.
> Since transmitter release is dependent on entry of external Ca,
> less transmitter release would occur.
>> If you get enough PAD so that the terminal membrane is really
> depolarized, then additional factors could come into to play
> such as channel inactivation.
> David M. Senseman, Ph.D. | Imagine the Creator as a low
> (senseman at lonestar.utsa.edu) | comedian, and at once the world
> Center for Information Visualization | becomes explicable.
> University of Texas at San Antonio | H.L. Mencken
You are forgetting that when the terminal membrane is depolarized, Calcium
channels would tend to open (It is, after all voltage sensitive, and that's
the mechanism for normal release when the AP invades the terminals). So
your reasons are not valid, since there would be a steady calcium inward
current at rest.
The reason PAD seems to work is thought to be due to the property of Calcium
channels (at least some type of calcium channels anyway). They seem to be
inactivated by a high concentration of internal calcium concentration.
This calcium dependent inactivation of calcium channels would keep the resting
Review your Hille.
mvcy at cornella.cit.cornell.edu