Movement of choline acetyltransferase in axons disconnected from their cell bodies

Abstract

SUMMARY1. Phrenic nerves of rats were cut out and divided into two parts of equal length, one proximal and one distal. The activity of choline acetyltransferase of the two pieces was estimated. Four groups of rats were studied: (1) normal rats, and rats in which 3 days earlier, (2) the right nerve had been cut in the uppermost part of the thorax, (3) a ligature had been tied round the right nerve just above the diaphragm, and (4) these two procedures had been combined.2. In normal rats the activity of the enzyme was about the same in proximal and distal pieces. Ligation of the nerve caused an increase of the activity, of about 50 %, in the distal but not in the proximal segment.3. After section of the nerve the activity below the section was 18 % of normal in the proximal, and 9 % in the distal piece.4. When the nerve was both cut and tied the activity decreased to the same level in both pieces, and this was about the level of the proximal piece after mere section of the nerve.5. It is concluded that choline acetyltransferase can move for some time along the axons to the nerve terminals even when the connexion with the soma has been interrupted.

Neurotrophic control of 16S acetylcholinesterase at the vertebrate neuromuscular junction

“…A similar explanation has been given for the denervation-induced decrease of muscle ChE activity which occurs later than that of the presynaptic junctional ChE (Csillik, 1975;Ranish and Dettbarn, 1978). Compatible with this possibility are experiments showing that 16S-AChE is conveyed by fast axonal transport (DiGiamberardino and Couraud, 1978;Festoff and Fernandez, 1978), a process which continues in isolated nerve stumps (Edstrom and Emmelin, 1971;Ochs and Ranish, 1969) and may provide a source for the enzyme found at the endplates (Ochs, 1972;Fernandez et al, 1978). Also, total AChE activity, though not the 16s form specifically, is known to be released into the extracellular space by injured motor neurons (Kreutzberg and Toth, 1974), released from nerve terminals in response to nerve stimulation (Skau and Brimijoin, 1978), and, synthesized by spinal cord cells in culture with its subsequent release into the culture medium (Oh et al, 1977).…”

Slow accumulation of choline acetyltransferase in crushed sciatic nerves of the rat

“…Earlier investigations have shown that ChAc activity decreases markedly, distal to a cut several days after operation (Hebb and Silver, 1961;Ekstrom and Emmelin, 1971). This loss in ChAc activity is likely to have been due to degeneration of the axons.…”

The relationship of choline acetyltransferase activity at the neuromuscular junction to changes in muscle mass and function

“…According to current concepts ChAc is a soluble enzyme (Fonnum, 1968) which is produced in cell bodies of cholinergic neurones and transported by slow axoplasmic flow to cholinergic nerve endings (Hebb & Silver, 1961;Frizell, Hasselgren & Sjbstrand, 1970; Ekstrdm & Emmelin, 1971; Saunders, Dziegielewska, Haggendal & Dahlstr6m, 1973). High rates of ChAc activity are found in the soluble fraction from nerve endings in brain (Whittaker, 1965;Diamond & Milfay, 1972) and from innervated portions of skeletal muscle (Hebb, Krnjevic & Silver, 1964;Emmelin, Nordenfelt & Perec, 1966;McCamen, Stafford & Skinner, 1967;Tucek, 1968;Flood, Fonnum & Storm-Mathisen, 1970).…”