B. Walmsley et al., SERIAL E-M AND SIMULATION STUDY OF PRESYNAPTIC INHIBITION ALONG A GROUP IA COLLATERAL IN THE SPINAL-CORD, Journal of neurophysiology, 74(2), 1995, pp. 616-623
1. A muscle spindle primary afferent (group Ia) was physiologically id
entified and labeled intracellularly with the use of horseradish perox
idase (HRP) in the cat lumbar spinal cord. Serial-section electron mic
roscopy (EM) was used to examine and reconstruct an entire axon collat
eral and its branches within Clarke's column. In the present study the
existence and location of presynaptic contacts on Ia afferent boutons
along these collateral branches were determined from examination of t
he serial-section electron-micrographs. 2. Of 36 Ia boutons examined i
n serial sections along the branches of the same collateral, 3 presyna
ptic contacts were found. Two of these contacts were made with Ia bout
ons in a complex nodal region consisting of two unmyelinated side bran
ches exhibiting a total of six Ia boutons. The other presynaptic conta
ct was made with a Ia bouton in a nodal region consisting of two Ia bo
utons connected by a thin unmyelinated bridge. 3. Computer simulations
, based directly on the serial-section reconstructions, were used to i
nvestigate the possible effects of these presynaptic contacts on membr
ane potential and on a propagating action potential along the Ia colla
teral. The effect of a presynaptic contact was modeled by a sustained
gamma-aminobutyric acid-A (GABA(A))-activated chloride conductance. 4.
The simulation results indicated that the effect of a presynaptic con
tact on membrane potential and action-potential amplitude is likely to
extend beyond the contacted bouton to other boutons occurring along t
he short unmyelinated branches arising from the same node. However, de
spite a large reduction of the action-potential amplitude within such
a nodal region, the action potential was relatively unaffected at prio
r and subsequent nodes along the myelinated collateral. 5. Simulations
of action-potential generation, based on different densities of volta
ge-dependent sodium and potassium conductances and the resting membran
e leak conductance, indicated that a very large sustained chloride con
ductance compared with known synaptically mediated GABA, conductances
was required to significantly reduce the action-potential amplitude, i
n agreement with a recent theoretical study on presynaptic inhibition
by B. Graham and S. J. Redman. The possibility that presynaptic inhibi
tion operates via a depolarization-induced inactivation of presynaptic
calcium channels and the role of GABAB receptor activation is discuss
ed.