Acetylcholinesterase (AChe) molecular forms were studied in hindlimb skeletal muscles from adult male Fischer 344 rats subjected to treadmill exercise for periods ranging between 1 and 30 days. Groups of three animals were exercised for 1 h/day at a treadmill speed of 8.5 m/min, with 1-min sprints at 15 m/min every 10 min. This exercise protocol led to a significant increase in the activity of G4 AChe in fast-twitch (gracilis and tibialis) but not in slow-twitch (soleus) muscles. Other AChe forms and muscle protein content remained unaltered. Such a selective enzymatic change was detected after a single exercise session, became more apparent after three daily sessions, and persisted for at least 30 days of exercise. A larger increment in G4 AChe activity was observed in gracilis muscle end-plate vs. non-end-plate regions. These findings show a specific adaptive reaction of fast-twitch muscles to enhanced motor activity, suggest that individual AChe forms in motor end plates are regulated through separate mechanisms, and support the hypothesis that membrane-bound G4 AChe plays an essential role in neuro-muscular transmission.

Fast axoplasmic transport of labeled proteins as well as the ultrastructure was studied in the vagus nerves of cats treated chronically with vincristine sulfate (VCR) and in normal nerves exposed in vitro to vincristine. Transport was partially blocked in nerves of somc neuropathic cats, and nerves of all neuropathic animals showed a small accelerated transport peak, probably reflecting a reactive or regenerative process. In vitro, vincristine induced a dose-related partial blockage of fast axoplasmic transport, with concurrent disappearance of microtubules and appearance of paracrystals.Green We have reexamined fast axoplasmic transport and ultrastructural changes in chronic VCR neuropathy in cats. Using certain modifications of the customary techniques for studying transport, we found that fast transport is impaired in some neuropathic animals and that the impairment is associated with ultrastructural abnormalities. Methods

Microtubule (MT) number, axonal area, and MT density were examined in unmyelinated axons of rat cervical vagus nerve. Study of nerve regions proximal (1-5 mm) and distal (35-40 mm) to the nodosum ganglion in controls (incubation at 37 degrees C for 1 h) showed that the number of MT per axon is significantly less in distal than in proximal nerve regions. Cooling (incubation at 0 degree C for 1 h) caused a significant reduction in the number of MT per axon in both nerve regions. The unmyelinated axons from both nerve regions showed a comparable reduction in MT number by cooling, indicating that axonal MT stability to cold was not significantly different between these two nerve regions. In these nerves no detectable changes were found in cross-axonal area of unmyelinated axons between distal and proximal nerve regions. In another experimental series, in distal nerve regions (35-40 mm from the nodosum ganglion) the number of MT was not further reduced in nerves incubated at 0 degree C by increasing the incubation time. Similar results were obtained from colchicine treated nerves (incubation at 37 degrees C, with 10 mM colchicine for 1 and 2 h). Distal nerve regions (35-40 mm from the nodosum ganglion) showed a similar reduction in the number of MT per axon when nerves were incubated at 0 degree C or with colchicine, suggesting that this drug, as well as cold, may be affecting a similar population of axonal MT, i.e., MT susceptible to anti-MT agents. These results indicate that approximately one-half of the axonal MT are stable to cold as well as to colchicine in rat unmyelinated axons.

No abstract