Control of ACh sensitivity by muscle activity in the rat

Abstract

1. Rat soleus and extensor digitorum longus (EDL) muscles were examined following complete blockade of sciatic nerve impulses with anaesthetics or diphtheria toxin for periods up to 14 days. 2. Muscles showed atrophy equivalent to that seen after similar periods of denervation. 3. Nerve blockade appeared to have little or no effect on neuromuscular transmission when tested by stimulation beyond the block. Normal spontaneous miniature end‐plate potentials were present. 4. Nerve impulse blockade caused the entire muscle membrane to become sensitive to iontophoretically applied acetylcholine. 5. The increase in sensitivity in soleus could be prevented by chronic nerve stimulation distal to the region of block. 6. Tenotomy, of 5‐12 days duration, which produced atrophy, had no effect on the sensitivity of soleus to acetylcholine. 7. Chronic direct stimulation of denervated soleus or EDL muscles could prevent the usual denervation supersensitivity, or cause it to decline towards normal once it had appeared. However, the sensitivity of the end‐plate region remained normal.

Neural Agrin Induces Ectopic Postsynaptic Specializations in Innervated Muscle Fibers

“…Colocalized with these are components seen also at the normal postsynaptic specializations and thought to be involved in their stabilization (see references in the introductory remarks). The potential of agrin to induce AChR clusters in electrically active muscle in vivo where AChR expression is suppressed (Lømo and Rosenthal, 1972;Goldman et al, 1988;Kues et al, 1995) has not been investigated.…”

Afferent influences on brain stem auditory nuclei of the chicken: Neuron number and size following cochlea removal

“…Unfortunately, there are only a few direct measurements of overall activity changes due to lid suture or dark conditions (Rodieck, 1967;Burke and Hayhow, 1968), and essentially nothing is known about ongoing activity levels under such conWhile the effects of denervating muscles can be largely reversed by direct electrical stimulation, certain properties, such as acetylcholinesterase enzyme levels, do not return to normal (Lomo and Rosenthal, 1972). For this reason, presynaptic activity is thought to be important, independent of its role in evoking action potentials in the postsynaptic target.…”

Effects of drug‐induced paralysis and depolarisation on acetylcholine receptor and cyclic nucleotide levels of chick muscle cultures

“…With adrenal medullary cells, temporary changes in CAMP are known to suffice for eliciting tyrosine hydroxylase induction [28]. In accord with such a model of regulation are the observations [8,29] that rather rare electrical stimulation (10 Hz for 10 s every 5.5 h) suffices to reduce the extrasynaptic acetylcholine sensitivity of denervated rat muscle, provided the stimuli are given in trains of high frequency.…”

“…Different investigators showed that the developmental localisation of AChR to the postsynaptic part of the sarcolemma involves: (i) The aggregation of receptors under the nerve terminal [3,4]; (ii) The repression of the synthesis of extrasynaptic AChR [S-7]. Several lines of evidence suggest the latter process to be mediated by neurally-induced muscle activity: (1) Electrical stimulation of adult denervated muscle prevents appearance of extrasynaptic AChd [8] and blocks the incorporation of radiolabelled amino acids into the receptor protein [9]; (2) Chronic paralysis of the motor endplate by cholinergic antagonists increases the synthesis of extrasynaptic AChR in adult and embryonic myofibers [6,10,11]; (3) In muscle cell cultures, the rate of AChR synthesis is decreased by electrical stimulation or depolarising agents [ 12,131; under the same conditions, paralysis of the spontaneously contracting myotubes by tetrodoxin leads to an increase of newly synthesized receptor molecules.…”