IUBio

Primary Afferent Depolarisation & Presynaptic Inhibition.

falvarez at desire.wright.edu falvarez at desire.wright.edu
Mon Feb 6 13:22:46 EST 1995


In article <Pine.SUN.3.91.950203193255.1121A-100000 at apus.cus.cam.ac.uk> "S. Chakrabarty" <sc203 at cus.cam.ac.uk> writes:
>From: "S. Chakrabarty" <sc203 at cus.cam.ac.uk>
>Subject: Primary Afferent Depolarisation & Presynaptic Inhibition.
>Date: Fri, 3 Feb 1995 19:47:05 +0000

>Dear netters,
>        I am fresh in this field and would like to know more about these 
>above mentioned phenomenons within the Vertebrate Sensory-motor system.
>        I have been going through ano. of papers by Rudomin P. & of 
>course the classics by Eccles ,& Llyod. But they kind of leave things 
>unclear.
>        So, I shall be grateful if anyone of you outthere have any clues 
>about it, and would post it to me either by E-mail OR post. I need it for 
>the submission of a proposal for grants.
>        thanking you in anticipation.
>S.Chakrabarty                           e-mail : sc203 at cus.cam.ac.uk
>Downing Street                          Tel:    01223 333757
>Cambridge CB2 3DY                       Fax:01223 333786
>U.K.

As you might now PAD is believed to be a consequence of presynaptic inhibition 
of primary afferent terminals through GABAA receptors. The depolarization is a 
consequence of an inward Cl- current due to the net movement of Cl- ions out 
of the primary afferent terminals following the concentartion gradient imposed 
by very effective Cl- pumps in the primary afferents. This depolarization 
imposes a shunt in the terminals thereby decreasing the effect of incoming 
action potentials over Ca2+-driven synaptic vesicle exocytosis and therefore 
reducing neurotransmitter release. This in brief is the current hypothetical 
frame-work to explain the phenomenon. Unfortunately nobody has yet recorded 
from intact "in vivo" primary afferent terminals in the spinal cord and 
therefore there is no direct confirmation. The hypothesis stands over a wealth 
of information (is an old field in some aspects) on the anatomy and 
electrophysiology of the system confirming the existence of GABA 
synapses over primary afferent terminals and the existence of PAD in intact 
spinal cords, and also in the presence of active GABAA receptors in the DRG 
cell somas. If you are lookin Rudomin refs. you are in the right track for 
much what is to know about the triggering and consequences of PAD.

Two freqeuently cited reviews of the PAD phenomena are:
Nicoll and Alger, International Rev. of Neurobiol. (1979) 21:217-258
Burke and Rudomin, (1977) Handbook of Physiology (Vol 1 -Nervous system) 
American pHysiological Society. pp 877-944.

Very interesting, but tough reading articles, have just appeared on various 
simulation models of this system. Try

Graham and Redman J. of Neurophysiol (1994) 71:538-549
for a feel of the field.
Good Luck!!

Francisco J. Alvarez
Res. Ass. Prof.
Wright State University
Dayton, OH
 



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