M. Enriquez et al., CHANGES IN PAD PATTERNS OF GROUP-I MUSCLE AFFERENTS AFTER A PERIPHERAL-NERVE CRUSH, Experimental Brain Research, 107(3), 1996, pp. 405-421
In the anesthetized cat we have analyzed the changes in primary affere
nt depolarization (PAD) evoked in single muscle spindle and tendon org
an afferents at different times after their axons were crushed in the
periphery and allowed to regenerate. Medial gastrocnemius (MG) afferen
ts were depolarized by stimulation of group I fibers in the posterior
biceps and semitendinosus nerve (PBSt), as soon as 2 weeks after crush
ing their axons in the periphery, in some cases before they could be a
ctivated by physiological stimulation of muscle receptors. Two to twel
ve weeks after crushing the MG nerve, stimulation of the PBSt produced
PAD in all MG fibers reconnected with presumed muscle spindles and te
ndon organs. The mean amplitude of the PAD elicited in afferent fibers
reconnected with muscle spindles was increased relative to values obt
ained from Ia fibers in intact (control) preparations, but remained es
sentially the same in fibers reconnected with tendon organs. Quite une
xpectedly, we found that, between 2 and 12 weeks after crushing the MG
nerve, stimulation of the bulbar reticular formation (RF) produced PA
D in most afferent fibers reconnected with muscle spindle afferents. T
he mean amplitude of the PAD elicited in these fibers was significantl
y increased relative to the PAD elicited in muscle spindle afferents f
rom intact preparations (from 0.08 +/- 0.4 to 0.47 +/- 0.34 mV). A sub
stantial recovery was observed between 6 months and 2.5 years after th
e peripheral nerve injury. Stimulation of the sural (SU) nerve produce
d practically no PAD in muscle spindles from intact preparations, and
this remained so in those afferents reconnected with muscle spindles i
mpaled 2-12 weeks after the nerve crush. The mean amplitude of the PAD
produced in afferent fibers reconnected with tendon organs by stimula
tion of the PBSt nerve and of the bulbar RF remained essentially the s
ame as the PAD elicited in intact afferents. However, SU nerve stimula
tion produced a larger PAD in afferents reconnected with tendon organs
2-12 weeks after the nerve crush (mean PAD changed from 0.05 +/- 0.04
to 0.32 +/- 0.17 mV). The results obtained indicate that the PAD patt
erns of the afferent fibers reconnected with muscle spindle and tendon
organ afferents are changed after crushing their axons in the periphe
ry: stimulation of the bulbar RF appears to produce larger PAD in fibe
rs reconnected with muscle spindles, and stimulation of cutaneous affe
rents produces larger PAD in fibers reconnected with tendon organs. It
is suggested that these alterations in the patterns of PAD of muscle
afferents result from central changes in the balance of excitatory and
inhibitory influences acting on the segmental pathways mediating the
PAD. Although the functional role of these changes has not been establ
ished, they may reflect compensatory changes aimed to adjust informati
on arising from damaged afferents.