Cytochemical localization of acetylcholine receptors at the neuromuscular junction by means of horseradish peroxidase-labelled α-bungarotoxin

Lentz, Thomas L.; Mazurkiewicz, Joseph E.; Rosenthal, Jean

doi:10.1016/0006-8993(77)90192-5

Cited by 83 publications

(38 citation statements)

References 35 publications

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“…Binding ofa-Butx was also observed on the membrane ofthe presynaptic terminal, primarily in the portion facing the muscle fibre. Such presynaptic binding has also been observed in normal end-plates (Lentz et al 1977).…”

Section: Morphology Of Ectopic Neuromuscular Junctionssupporting

confidence: 55%

“…Specimens were processed for electronmicroscopy as described by Lentz, Mazurkiewicz & Rosenthal (1977) and stained in uranylacetate and lead citrate.…”

Section: Electronmicroscopymentioning

confidence: 99%

“…In many profiles these post-synaptic specializations extended laterally somewhat beyond the area covered by the presynaptic terminal. To study the distribution of ACh receptors along ectopically innervated fibres, the tissue was incubated in horseradish peroxidase (HRP)-labelled a-bungarotoxin (Nakane & Kawaoi, 1974;Lentz, Mazurkiewicz & Rosenthal, 1977) before fixation. P1.…”

Section: Morphology Of Ectopic Neuromuscular Junctionsmentioning

confidence: 99%

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Channel gating at frog neuromuscular junctions formed by different cholinergic neurones.

Breitschmid¹,

Brenner²

1981

The Journal of Physiology

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SUMMARY1. Drug-induced membrane current fluctuations were analysed at frog ectopic neuromuscular junctions formed de novo by somatic motoneurones and by preganglionic autonomic neurones of the vagus nerve, and at denervated end-plates reinnervated by the vagus nerve.2. At ectopic motor end-plates, the mean open time of the ion channels activated by ACh is TACh = 1P8+0'1 msec (S.E.) at -70 to -90 mV and 15-18 'C. Carbacholand suberyldicholine-induced channels have average open times TCarb = 1P0 + 0-1 msec (-80 mV, 6-8 TC) and TSub = 3-3+041 msec (-80 mV, 16-18 TC).3. The conductances y of single channels induced by ACh, carbachol and suberyldicholine are: YACh = 210+ 11 pS (+S.E.), YCarb 146+12 pS and YSub = 22 1 + 1-2 pS.4. The mean open times T of the channels is prolonged as the membrane is hyperpolarized. Their voltage dependence is similar to that of normal end-plate channels.5. The average open time of ACh-induced channels at ectopic vagus junctions is r = 1-6 + 0-2 msec (S.E.) at -70 to -80 mV and 14-15 'C. At denervated motor end-plates reinnervated by vagal neurones, the mean channel open time is T = 1P5 + 0-1 msec at -80 mV and 14-18 'C.6. At all vagus junctions, the synaptic currents are blocked by c-bungarotoxin.7. Somatic motoneurones and vagal neurones induce junctional folds in the muscle membrane where they contact it to form an ectopic end-plate. Staining the

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Section: Morphology Of Ectopic Neuromuscular Junctionssupporting

confidence: 55%

“…Specimens were processed for electronmicroscopy as described by Lentz, Mazurkiewicz & Rosenthal (1977) and stained in uranylacetate and lead citrate.…”

Section: Electronmicroscopymentioning

confidence: 99%

Section: Morphology Of Ectopic Neuromuscular Junctionsmentioning

confidence: 99%

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Channel gating at frog neuromuscular junctions formed by different cholinergic neurones.

Breitschmid¹,

Brenner²

1981

The Journal of Physiology

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“…The sciatic nerve was severed after exposing it by separating the muscles with blunt dissection; the animals were allowed to recover. Based upon the observation of Lentz et al (1977) that nerve terminals had degenerated and disappeared in a mouse hemidiaphragm denervated for 1 week, virus was injected into the footpad 7 days later. Leg muscles were examined by immunofluorescence at 1 h post-inoculation.…”

Section: Virusesmentioning

confidence: 99%

Entry of Rabies Virus into the Peripheral Nerves of Mice

Watson

Tignor

Smith

1981

Journal of General Virology

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SUMMARYYoung adult mice were inoculated in the hind limb with rabies virus or Sindbis virus. Rabies 1820B virus antigen was detected in leg sections by immunofluorescence at 1 h post-inoculation at sites comparable in form and distribution to cholinesterase-positive sites, which represent motor end-plates (MEPs). Sites which were rabies virus antigen-positive by immunofluorescence were also cholinesterasepositive on double-stained slides. Rabies CVS virus detected by autoradiography was similarly distributed at 6 h post-inoculation. Uptake of rabies virus at motor nerve endings was confirmed by the detection of rabies antigen by immunofluorescence in ventral horn cells in the spinal cord at 20 h post-inoculation before involvement of dorsal root ganglia. Rabies virus antigen could not be detected at MEPs if the virus had been inactivated by beta propiolactone or mixed with antibody prior to injection or if the sciatic nerve had been cut 7 days earlier; similarly treated groups of mice survived for the observation period of 6 weeks. Rabies virus antigen was found at MEPs in mice given antibody 24 h before virus injection, but virus antigen was not found in the spinal cord, and mice similarly treated survived. Sindbis virus strain At86, which like rabies virus is neurotropic in adult mice, was also found at MEPs and in peripheral nerves by autoradiography at 6 h post-inoculation. In contrast to results with rabies virus-infected mice, stimulation of the sciatic nerve for the first hour post-inoculation prevented mortality. Sindbis virus strain Ar339, which is not neurotropic in adult mice, could not be detected at MEPs by immunofluorescence or autoradiography and mice injected with virus survived. The results presented here suggest that rabies virus and perhaps other neurotropic viruses can use the motor axon terminal at the neuromuscular junction as a site of entry into the nervous system.

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“…It was subsequently proposed (Blaber & Karczmar, 1967;Webb & Bowman, 1974;Bowman, 1980a, b) that this action of ACh was mediated by cholinoceptors located either at the nerve terminal or at the first node of Ranvier. Binding studies in rats (Lentz, Mazurkiewicz & Rosenthal, 1977) and mice (Daniels & Vogel, 1975) have provided direct evidence for the existence of prejunctional nicotinic cholinoceptors at motor endplates. Webb & Bowman (1974) suggested that the prejunctional cholinoceptors were of the ganglionic nicotinic type since in cat hind limb muscles exposed to neostigmine, hexamethonium, a selective antagonist of ACh in autonomic ganglia, could suppress ADF without affecting twitch potentiation or the normal twitch response.…”

Section: Introductionmentioning

confidence: 99%

Effects of pancuronium and hexamethonium on paraoxon‐induced twitch potentiation and antidromic firing in rat phrenic nerve diaphragm preparations

Clark

Hobbiger

Terrar

1983

British J Pharmacology

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1The actions of pancuronium, a selective antagonist of acetylcholine (ACh) at nicotinic cholinoceptors at motor endplates, and hexamethonium, a selective antagonist of ACh at nicotinic cholinoceptors in autonomic ganglia, have been studied in rat phrenic nerve diaphragm preparations. The effects on paraoxon-induced twitch potentiation and antidromic firing (ADF) in the phrenic nerve, were compared with the effects on normal twitch tension and intracellularly recorded miniature endplate potentials (m.e.p.ps) and endplate potentials (e.p.ps.) 2 In preparations exposed to paraoxon, pancuronium was found to be approximately 10 times more effective in reducing the potentiated component of the twitch than the component which corresponded to the pre-paraoxon twitch. A similar result was obtained with hexamethonium. 3 Pancuronium and hexamethonium, in concentrations which reduced paraoxon-induced twitch potentiation but had no effect on the twitch tension of preparations not treated with paraoxon, reduced paraoxon-induced ADF. The lowest concentrations of pancuronium and hexamethonium required for this also reduced the amplitude of m.e.p.ps and e.p.ps. 4 Dithiothreitol, a disulphide bond reducing agent which reduces the affinity of ACh for nicotinic cholinoceptors, enhanced the potency of pancuronium 2 to 3 fold. The same also applied for hexamethonium. 5 It is concluded that the experiments failed to provide evidence for an action of ACh on prejunctional nicotinic cholinoceptors of the ganglionic-type being involved in the initiation by paraoxon of twitch potentiation and ADF. Furthermore, the results obtained can be explained by pancuronium and hexamethonium reducing the action of ACh at the postjunctional membrane.

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Cytochemical localization of acetylcholine receptors at the neuromuscular junction by means of horseradish peroxidase-labelled α-bungarotoxin

Cited by 83 publications

References 35 publications

Channel gating at frog neuromuscular junctions formed by different cholinergic neurones.

Channel gating at frog neuromuscular junctions formed by different cholinergic neurones.

Entry of Rabies Virus into the Peripheral Nerves of Mice

Effects of pancuronium and hexamethonium on paraoxon‐induced twitch potentiation and antidromic firing in rat phrenic nerve diaphragm preparations

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