CONTINUOUS LOW-AMPLITUDE DIRECT-CURRENT STIMULATION OF THE CRUSHED PERIPHERAL-NERVE ACCELERATES THE EARLY RECOVERY OF CHOLINE-ACETYLTRANSFERASE BUT NOT OF ACETYLCHOLINESTERASE ACTIVITY IN FAST AND SLOW MUSCLES
S. Ribaric et al., CONTINUOUS LOW-AMPLITUDE DIRECT-CURRENT STIMULATION OF THE CRUSHED PERIPHERAL-NERVE ACCELERATES THE EARLY RECOVERY OF CHOLINE-ACETYLTRANSFERASE BUT NOT OF ACETYLCHOLINESTERASE ACTIVITY IN FAST AND SLOW MUSCLES, Restorative neurology and neuroscience, 7(2), 1994, pp. 89-94
We investigated if continuous 1 mu A direct current stimulation of the
injured nerve, with the cathode electrode at the distal end of the ne
rve crush injury (cathode stimulation), accelerated the recovery of ch
oline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activit
y in transiently denervated extensor digitorum longus (EDL) and soleus
(SOL) rat muscles. ChAT is a specific marker of cholinergic nerve ter
minals and may reflect axon ingrowth, and AChE reflects the re-establi
shment of neuromuscular junctions and recovery of muscle activity. Com
pared to sham operated animals, the cathode (CA) stimulated rats had a
statistically significant larger ChAT activity in the EDL and SOL mus
cles on days 12 and 14 after nerve crush (P < 0.01, n = 6). The differ
ence in ChAT activity between the groups decreased thereafter. Regardi
ng recovery of muscle AChE, CA stimulation of the crushed sciatic nerv
e did not detectably accelerate the normalization of activity and patt
ern of AChE molecular forms in the EDL and SOL muscles. This means tha
t the early rise in ChAT muscle activity in CA stimulated rats was not
followed by an accelerated normalization of the neuromuscular transmi
ssion in the same group. It is more likely that the higher ChAT activi
ty observed after cathode stimulation indicates a higher ChAT content
in regenerating motor nerve endings, rather than a greater number of m
otor axons entering the muscles. It seems possible that cathode stimul
ation increased ChAT axonal transport, causing the early increase of C
hAT content in the nerve endings. This raised the possibility that the
axon transport and subsequent secretion of a trophic factor(s) from t
he nerve to the reinnervated muscle are enhanced as well, thus shorten
ing the overall time of muscle force recovery in the absence of an app
reciable acceleration of recovery of the neuromuscular transmission.