The Effects of Atropine and Oxotremorine on Acetylcholine Release in Rat Phrenic Nerve‐diaphragm Preparations

Abbs, E.T.; Joseph, Daniel

doi:10.1111/j.1476-5381.1981.tb10446.x

Cited by 57 publications

(30 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In some experiments, muscarinic agonists have inhibited ACh release from motor nerve terminals, whereas in others, ACh release was increased (Abbs and Joseph, 1981;Wessler et al, 1987;Arenson, 1991;Robitaille et al, 1997;Santafé et al, 2007). At the vertebrate NMJ, the activation of m2 AChR reduced the release, whereas the activation of m1/m3 AChR facilitated the release (Slutsky et al, 2001;Minic et al, 2002;Oliveira et al, 2002Oliveira et al, , 2009Dudel, 2007).…”

Section: Discussionmentioning

confidence: 99%

Schwann Cells Sense and Control Acetylcholine Spillover at the Neuromuscular Junction by α7 Nicotinic Receptors and Butyrylcholinesterase

Петров¹,

Girard²,

Nikitashina³

et al. 2014

J. Neurosci.

View full text Add to dashboard Cite

Terminal Schwann cells (TSCs) are key components of the mammalian neuromuscular junction (NMJ).How the TSCs sense the synaptic activity in physiological conditions remains unclear. We have taken advantage of the distinct localization of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) at the NMJ to bring out the function of different ACh receptors (AChRs). AChE is clustered by the collagen Q in the synaptic cleft and prevents the repetitive activation of muscle nicotinic AChRs. We found that BChE is anchored at the TSC by a proline-rich membrane anchor, the small transmembrane protein anchor of brain AChE. When BChE was specifically inhibited, ACh release was significant depressed through the activation of ␣7 nAChRs localized on the TSC and activated by the spillover of ACh. When both AChE and BChE were inhibited, the spillover increased and induced a dramatic reduction of ACh release that compromised the muscle twitch triggered by the nerve stimulation. ␣7 nAChRs at the TSC may act as a sensor for spillover of ACh adjusted by BChE and may represent an extrasynaptic sensor for homeostasis at the NMJ. In myasthenic rats, selective inhibition of AChE is more effective in rescuing muscle function than the simultaneous inhibition of AChE and BChE because the concomitant inhibition of BChE counteracts the positive action of AChE inhibition. These results show that inhibition of BChE should be avoided during the treatment of myasthenia and the pharmacological reversal of residual curarization after anesthesia.

show abstract

Section: Discussionmentioning

confidence: 99%

Schwann Cells Sense and Control Acetylcholine Spillover at the Neuromuscular Junction by α7 Nicotinic Receptors and Butyrylcholinesterase

Петров¹,

Girard²,

Nikitashina³

et al. 2014

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…It was suggested that the myenteric plexus in guineapig ileum had a muscarinic receptor which modulated ACh release by a negative feed-back mechanism (Kilbinger & Wagner, 1975;Sawynok & Jhamandas, 1977; Kilbinger, 1977;Fosbraey & Johnson, 1978; Kilbinger & Wagner, 1979;Gustafsson, Hasqvist & Lundgren 1980;Kilbinger & Wessler, 1980a,b;Fosbraey & Johnson, 1980;Kilbinger & Kruel, 1981). Furthermore, it has been suggested that similar presynaptic muscarinic receptors exist in cerebral cortex of the cat (Dudar & Szerb, 1969), in central cholinergic nerves of rat (Polak, 1967;Szerb & Somogyi, 1973;Kato, Collier, Ilson & Wright, 1975;Szerb, Hadhazy & Dudar, 1977;Szerb, 1977;Nordstrom & Bartfai, 1980), in the electric organ of Torpedo (Michaelson, Avissar, Kloog & Sokolovsky, 1979;Dunant & Walker, 1981) and in rat phrenic nerve-diaphragm prepara-0007-1188/82/090075-08 $01.00 tions (Abbs & Joseph, 1981). On the other hand, Kato et al (1975) found that the cat superior cervical ganglion did not have such a presynaptic muscarinic receptor.…”

Section: Introductionmentioning

confidence: 99%

Presynaptic Muscarinic Receptors Inhibiting Active Acetylcholine Release in the Bullfrog Sympathetic Ganglion

Koketsu

Yamada

1982

British J Pharmacology

View full text Add to dashboard Cite

The effects of bethanechol and atropine on the release of acetylcholine (ACh) from bullfrog sympathetic preganglionic nerve terminals were examined electrophysiologically. Bethanechol (1 mm) caused no depolarization of sympathetic preganglionic nerve terminals, whereas carbachol or ACh in the same concentration induced marked depolarizations of these terminals. Bethanechol (10 μm) depressed the amplitude of fast excitatory postsynaptic potentials (e.p.s.ps) recorded in low Ca2+‐high Mg2+ solution, without depolarizing ganglion cells. The quantal content measured from these fast e.p.s.ps by the variance method showed a significant reduction. Amplitudes of both miniature e.p.s.ps and ACh‐potentials induced by iontophoresis of ACh were not affected by addition of bethanechol (10 μm). The depressant effect of bethanechol (10 μm) on fast e.p.s.ps disappeared in the presence of atropine (3 μm). Atropine (3 μm) increased the quantal content measured from fast e.p.s.ps recorded in low Ca2+‐high Mg2+ solution. The depressant effect of bethanechol (10 μm) on fast e.p.s.ps was unaffected by α‐adrenoceptor blocking agents (phenoxybenzamine (10 μm) or phentolamine (10 μm)). These results suggest that presynaptic nerve terminals in bullfrog sympathetic ganglia possess a muscarinic receptor which inhibits active release of ACh.

show abstract

“…The type of cholinoceptor sites involved in the feedback regulation however, is controversial. Muscarinic inhibitory (Duncan & Publicover, 1979;Michaelson et al, 1979;Abbs & Joseph, 1981;Somogyi et al, 1987) and excitatory (Das et al, 1978;Wali et al, 1987;Wessler et al, 1987) prejunctional cholinoceptors have been reported at vertebrate neuromuscular junctions and in the Torpedo electric organ. In the presence of tubocurarine, a frequency-dependent decrease of evoked ACh release was obtained which suggested the presence of nicotinic prejunctional cholinoceptors mediating a positive feedback control of evoked transmitter release (Glavinovic, 1979a;Magleby et al, 1981;Wessler et al, 1986;Matzner et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Phenthonium, a quaternary derivative of (−)−hyoscyamine, enhances the spontaneous release of acetylcholine at rat motor nerve terminals

Fann

Souccar

Lapa

1990

British J Pharmacology

View full text Add to dashboard Cite

show abstract

The Effects of Atropine and Oxotremorine on Acetylcholine Release in Rat Phrenic Nerve‐diaphragm Preparations

Cited by 57 publications

References 9 publications

Schwann Cells Sense and Control Acetylcholine Spillover at the Neuromuscular Junction by α7 Nicotinic Receptors and Butyrylcholinesterase

Schwann Cells Sense and Control Acetylcholine Spillover at the Neuromuscular Junction by α7 Nicotinic Receptors and Butyrylcholinesterase

Presynaptic Muscarinic Receptors Inhibiting Active Acetylcholine Release in the Bullfrog Sympathetic Ganglion

Phenthonium, a quaternary derivative of (−)−hyoscyamine, enhances the spontaneous release of acetylcholine at rat motor nerve terminals

Contact Info

Product

Resources

About