A Serial E-M and Simulation Study of Pre-synaptic Inhibition along a group Ia Collateral in the Spinal Cord. Walmsley, Bruce, Bruce Graham, and Madeleine Jane Nicol. The Neuroscience Group, Faculty of Medicine, University of Newcastle, Callaghan, NSW, Australia and Division of Neuroscience, The John Curtin School of Medical Research, The Australian National University, Canberra, A.C.T., Australia.
APStracts 2:0096N, 1995.
SUMMARY AND CONCLUSIONS
1. A muscle spindle primary afferent (group Ia) was physiologically identified and labelled intracellularly using HRP in the cat lumbar spinal cord. Serial-section electron microscopy (EM) was used to examine and reconstruct an entire axon collateral and its branches within Clarke's column. In the present study, the existence and location of pre-synaptic contacts on Ia afferent boutons along these collateral branches was determined from examination of the serial-section electron-micrographs. 2. Of 36 Ia boutons examined in serial-sections along the branches of the same collateral, 3 pre- synaptic contacts were found. Two of these contacts were made with Ia boutons in a complex nodal region consisting of two unmyelinated side-branches exhibiting a total of 6 Ia boutons. The other pre-synaptic contact was made with a Ia bouton in a nodal region consisting of 2 Ia boutons connected by a thin unmyelinated bridge. 3. Computer simulations, based directly on the serial-section reconstructions, were used to investigate the possible effects of these pre-synaptic contacts on membrane potential and on a propagating action potential along the Ia collateral. The effect of a pre-synaptic contact was modelled by a sustained GABA A -activated chloride conductance (Graham and Redman,1994). 4. The simulation results indicated that the effect of a pre- synaptic contact on membrane potential and action potential amplitude is likely to extend beyond the contacted bouton to other boutons occurring along the short unmyelinated branches arising from the same node. However, despite a large reduction of the action potential amplitude within such a nodal region, the action potential was relatively unaffected at prior and subsequent nodes along the myelinated collateral. 5. Simulations of action potential generation, based on different densities of voltage-dependent sodium and potassium conductances and the resting membrane leak conductance, indicated that a very large sustained chloride conductance compared with known synaptically mediated GABA A conductances, was required to significantly reduce the action potential amplitude, in agreement with a recent theoretical study on pre-synaptic inhibition by Graham and Redman (1994). The possibility that pre-synaptic inhibition operates via a depolarisation induced inactivation of pre-synaptic calcium channels and the role of GABA B receptor activation is discussed. 

Received 6 July 1994; accepted in final form 20 March 1995.
APS Manuscript Number J402-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.