Neurotrophic control of the transmembrane Cl? pump in mammalian muscle fibers

Urazaev, A. Kh.; Surovtsev, Valeriy A.; Chikin, A. V.; Волков, Е. М.; Poletaev, G. I.; Khamitov, Kh. S.

doi:10.1007/bf01056921

Cited by 2 publications

(5 citation statements)

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“…These changes include the development of the early denervation depolarization of muscle (Albuquerque et al. 1971) as activation of sarcolemma Na + ,K + ,2Cl – ‐transport occurs in the absence of nitric oxide synthase activity (Urazaev et al. 1987, 1999).…”

Section: Discussionmentioning

confidence: 99%

Glutamate regulation of non‐quantal release of acetylcholine in the rat neuromuscular junction

Malomouzh

Mukhtarov

Nikolsky

et al. 2003

Journal of Neurochemistry

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Glutamate, previously demonstrated to participate in regulation of the resting membrane potential in skeletal muscles, also regulates non-quantal acetylcholine (ACh) secretion from rat motor nerve endings. Non-quantal ACh secretion was estimated by the amplitude of endplate hyperpolarization (H-effect) following blockade of skeletal muscle post-synaptic nicotinic receptors by (+)-tubocurarine and cholinesterase by armin (diethoxy-p-nitrophenyl phosphate). Glutamate was shown to inhibit non-quantal release but not spontaneous and evoked quantal secretion of ACh. Glutamate-induced decrease of the H-effect was enhanced by glycine. Glycine alone also lowered the H-effect, probably due to potentiation of the effect of endogenous glutamate present in the synaptic cleft. Inhibition of N-methyl-D-aspartate (NMDA) receptors with (+)-5-methyl-10,11-dihydro-5H-dibenzocyclohepten-5,10-imine (MK801), DL-2-amino-5-phosphopentanoic acid (AP5) and 7-chlorokynurenic acid or the elimination of Ca It is well known that glutamate serves as a neurotransmitter at invertebrate neuromuscular junctions (Lunt and Olsen 1988) whereas acetylcholine (ACh) serves that role in the vertebrate. However, investigations during the last decade indicate a role for glutamate as a signalling molecule at the neuromuscular junction of vertebrates (see for review Grozdanovic and Baumgarten 1999). In support of this notion, glutamate transporter mRNA has been shown to be present in the cytoplasm of rat spinal motoneurones along with a glutamate-like immunoreactivity (Meister et al. 1993). Glutamate has been found in nerve terminals of rat motoneurones in association with synaptic vesicles (Waerhaug and Ottersen 1993) and evidence that it is co-released with ACh in cholinergic nerve terminals has been documented (Vyas and Bradford 1987;Israel et al. 1993;Meister et al. 1993). In addition, N-methyl-D-aspartate (NMDA) and Received August 15, 2002; revised manuscript received November 20, 2002; accepted December 19, 2002. Address correspondence and reprint requests to Dr Albert K. Urazaev, Department of Physiology, The Brody School of Medicine, East Carolina University, Greenville, NC 27858, USA. E-mail: urazaeva@mail.ecu.eduAbbreviations used: ACh, acetylcholine; AP5, DL-2-amino-5-phosphopentanoic acid; D-NAME, N G -nitro-D-arginine methyl ester; EPP, endplate potentials; L-NAME, N G -nitro-L-arginine methyl ester; mEPP, miniature endplate potentials; MK801, (+)-5-methyl-10,11-dihydro-5H-dibenzocyclohepten-5,10-imine; NO, nitric oxide; ODQ, 1H [1,2,4] oxadiazolo [4,3-a]quinoxalin-1-one.

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Section: Discussionmentioning

confidence: 99%

Glutamate regulation of non‐quantal release of acetylcholine in the rat neuromuscular junction

Malomouzh

Mukhtarov

Nikolsky

et al. 2003

Journal of Neurochemistry

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“…1982) through muscarinic M1 receptor (M 1 AChR)‐mediated (Urazaev et al . 2000) suppression of the activity of the furosemide‐sensitive Na + ,K + ,2Cl – ‐cotransport in sarcolemma (Urazaev et al . 1987b, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…1996), and NO synthase inhibition in vivo (Khairova et al . 2002, 2003) eliminate the negative control of active Cl – cotransport, leading to an elevation of sarcoplasm Cl – and a decrease in the Cl – equilibrium potential (Urazaev et al . 1987b).…”

Section: Discussionmentioning

confidence: 99%

“…NO diffuses from muscle fibers to the cytoplasm of the nerve ending to attenuate the non-quantal secretion of ACh through a cGMP-dependent mechanism (Urazaev et al 1996(Urazaev et al , 1997Mukhtarov et al 2000). Non-quantal ACh maintains high resting membrane potential in the muscle fibers (Bray et al 1982) through muscarinic M1 receptor (M 1 AChR)-mediated suppression of the activity of the furosemide-sensitive Na + ,K + ,2Cl -cotransport in sarcolemma (Urazaev et al 1987b(Urazaev et al , 1999. In addition, non-quantal ACh modulates its own release through a negative feedback mechanism that involves activation of voltage-dependent Ca 2+ channels (CaCh) in muscle membrane and synthesis of NO in the sarcoplasm (Urazaev et al 1997;Mukhtarov et al 2000).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, non-quantal ACh modulates its own release through a negative feedback mechanism that involves activation of voltage-dependent Ca 2+ channels (CaCh) in muscle membrane and synthesis of NO in the sarcoplasm (Urazaev et al 1997;Mukhtarov et al 2000). Both muscle denervation, which impairs non-quantal ACh release (Stanley and Drachman 1986;Nikolsky et al 1996), and NO synthase inhibition in vivo (Khairova et al 2002(Khairova et al , 2003 eliminate the negative control of active Clcotransport, leading to an elevation of sarcoplasm Cland a decrease in the Clequilibrium potential (Urazaev et al 1987b). This causes early denervation depolarization of muscle fibers (Albuquerque et al 1971;Urazaev et al 1999).…”

Section: Discussionmentioning

confidence: 99%

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Effect of N‐acetylaspartylglutamate (NAAG) on non‐quantal and spontaneous quantal release of acetylcholine at the neuromuscular synapse of rat

Malomouzh

Nikolsky

Lieberman

et al. 2005

Journal of Neurochemistry

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N-Acetylaspartylglutamate (NAAG), known to be present in rat motor neurons, may participate in neuronal modulation of nonquantal secretion of acetylcholine (ACh) from motor nerve terminals. Non-quantal release of ACh was estimated by the amplitude of the endplate membrane hyperpolarization (H-effect) caused by inhibition of nicotinic receptors by (+)-tubocurarine and acetylcholinesterase by armin (diethoxyp-nitrophenyl phosphate). Application of exogenous NAAG decreased the H-effect in a dose-dependent manner. The reduction of the H-effect by NAAG was completely removed when N-acetyl-b-aspartylglutamate (bNAAG) or 2-(phosphonomethyl)-pentanedioic acid (2-PMPA) was used to inhibit glutamate carboxypeptidase II (GCP II), a presynaptic Schwann cell membrane-associated ectoenzyme that hydrolyzes NAAG to glutamate and N-acetylaspartate. Bath application of glutamate decreased the H-effect similarly to the action of NAAG but N-acetylaspartate was without effect.Inhibition of NMDA receptors by DL-2-amino-5-phosphopentanoic acid, (+)-5-methyl-10,11-dihydro-5H-dibenzocyclohepten-5,10-imine (MK801), and 7-chlorokynurenic acid or inhibition of muscle nitric oxide synthase (NO synthase) by N G -nitro-L-arginine methyl ester and 3-bromo-7-nitroindazole completely prevented the decrease of the H-effect by NAAG. These results suggest that glutamate, produced by enzymatic hydrolysis of bath-applied NAAG, can modulate non-quantal secretion of ACh from the presynaptic terminal of the neuromuscular synapse via activation of postsynaptic NMDA receptors and synthesis of nitric oxide (NO) in muscle fibers. NAAG also increased the frequency of miniature endplate potentials (mEPPs) generated by spontaneous quantal secretion of ACh, whereas the mean amplitude and time constants for rise time and for decay of mEPPs did not change.

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Neurotrophic control of the transmembrane Cl? pump in mammalian muscle fibers

Cited by 2 publications

References 11 publications

Glutamate regulation of non‐quantal release of acetylcholine in the rat neuromuscular junction

Glutamate regulation of non‐quantal release of acetylcholine in the rat neuromuscular junction

Effect of N‐acetylaspartylglutamate (NAAG) on non‐quantal and spontaneous quantal release of acetylcholine at the neuromuscular synapse of rat

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