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- From: knowled@ccsmtp.ccf.org (Doug Knowles)
- Subject: Re: primary afferent depolarization
- Message-ID: <knowled.14.727980754@ccsmtp.ccf.org>
- Lines: 42
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- Organization: Cleveland Clinic Foundation
- References: <9301251254.AA21883@xray1.cshl.org>
- Distribution: bionet
- Date: Mon, 25 Jan 1993 16:52:34 GMT
-
- In article <9301251254.AA21883@xray1.cshl.org> anderson@CSHL.ORG (John Anderson) writes:
- >From: anderson@CSHL.ORG (John Anderson)
- >Subject: primary afferent depolarization
- >Date: 25 Jan 93 12:54:59 GMT
- >
- ....
-
- >Could someone please explain this statement? How does presynaptic
- >depolarization reduce the presynaptic spike amplitude? Seems like it
- >should enhance it.
- >
- >-------
- >John E. Anderson
- >W. M. Keck Structural Biology Laboratory
- >Cold Spring Harbor Laboratory
-
-
- The amount of transmitter released is dependent on the amount of
- calcium which enters the presynaptic terminal, which is dependent
- on the amplitude of the action potential in the presynaptic
- terminal. Prior depolarization of the terminal (e.g. by inceased
- extracellular K+) reduces the difference between the (depolarized)
- resting potential and the peak of the action potential, thus
- reducing the action potential amplitude. This causes less calcium
- entry, less transmitter release, and a smaller postsynaptic
- potential.
-
- I'm not sure why the calcium entry is dependent on the amplitude
- of the action potential, rather than absolute membrane potential
- difference. Probably because of the time and voltage dependence
- of the calcium channels. I'll have to defer to my more informed
- biophysics colleagues (Bill?).
-
- W. Douglas Knowles, Ph.D. E-mail: knowled@ccsmtp.ri.ccf.org
- Department of Neurosciences voice: (216) 444-3870
- Cleveland Clinic Foundation FAX: (216) 444-7927
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- Cleveland, OH 44195 USA other: hey, you!
-
- quote: "We need not all give our whole time to the currently more glamorous
- "molecular biology"; it will doubtless come soon enough." I.H. Page 1962
-
-