In article <Pine.SOL.3.91.941214122851.14287C-100000 at welchlink.welch.jhu.edu> "TAO T. WANG" <toddwang at welchlink.welch.jhu.edu> writes:
>1. If increasing the concentration of glutamate, what will be caused
>in its receptor channel (NMDA or non-NMDA) current.
This depends on the concentration of glutamate relative to its affinity for
the receptor. If glutamate is already at saturating concentrations at steady
state then doubling the concentration will have no additional effect. If the
concentration of glutamate is between threshold and maximum then the
alteration in the response should be governed by standard pharmacological
principles to be found in any pharmacology textbook.
>2-fold increase in the concentration of glutamate release will cause:
>(a) 2-fold increase in the current of *single* receptor channel?
Definitely not this - channel openings are all-or-none
>(b) 2-fold increase in the number of open channel?
This is more reasonable with some caveats.
>2. If the concentration of glutamate has a fast change, for example,
>the glutamate concentration is changed only for 2 ms, or even less,
>this kind of transient change will also cause some change in its receptor
This is probably the way that glutamate works at typical synapses - a very
rapid increase to millimolar concentrations for very brief periods (<10msec).
As NMDA receptors clearly participate in at least some forms of synaptic
transmission it seems reasonable to suppose that brief large changes in
glutamate are sufficient to activate NMDA receptors.
To understand how glutamate activates NMDA receptors over this time frame you
could do a lot worse than check out the work of Craig Jahr who has published
several nice papers on the subject recently