Rapid accumulation of high molecular weight acetylcholinesterase in transected sciatic nerve

Abstract

NERVOUS tissue and muscle in rat^1–4 and chicken^5,6 contain several molecular forms of acetylcholinesterase (EC 3.1.17, AChE), distinguishable by their sedimentation coefficient in sucrose gradient⁷. In rat, several peripheral nerves and non-innervated regions of skeletal muscle^1,2 were shown to contain two molecular forms of AChE, with respective sedimentation coefficients of 4 and 10S; in addition to these two forms, a high molecular weight form with a sedimentation coefficient of 16S was found in the innervated regions of various skeletal muscles^1,2,4. After denervation, the 16S form, which we will call the H form, either disappeared from skeletal muscle² or was drastically reduced^1,4. In chicken, several nerves exhibited three molecular forms of AChE with sedimentation coefficients of 4, 6.5 and 11S, while various skeletal muscles contained an additional molecular form with a sedimentation coefficient of 19.5S (ref. 5). After denervation, the high molecular weight form 19.5S, which by analogy with the 16S of rat is referred to here as the H form, disappeared from crude extract of muscles⁵. As the H form was only found in tissues innervated by cholinergic nerve endings and disappeared or decreased drastically from denervated skeletal muscles, it has been suggested that this form of AChE is exclusively myogenic^1,3 and may constitute the specific endplate enzyme1,2,4,5. We report here that tiny amounts of the H form of AChE can be detected in crude extracts of intact sciatic nerves of rat and chicken, and that after transection of the sciatic nerve with the ensuing blockade of the axonal traffic, the H form increased rapidly at the site of injury.