Modulation by Nitric Oxide (NO) of the Intensity of Non-Quantum Mediator Secretion in Neuromuscular Junctions in Rats
Tóm tắt
Experiments on rat diaphragm muscle showed that the nitric oxide (NO) donors sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP), as well as L-arginine, a substrate for NO synthesis, decreased the level of muscle fiber hyperpolarization (the H effect) after blockade of cholinoceptors on the postsynaptic membrane by d-tubocurarine in conditions of irreversible inhibition of acetylcholinesterase with armine. Conversely, disruptions to NO synthesis in muscle fibers by the NO synthase blocker NG-nitro-L-arginine methyl ester (L-NAME) led to increases in the H effect both in vitro and in vivo. Inactivated solutions of sodium nitroprusside and inactive forms of arginine and NAME (D-arginine, D-NAME) had no effect on the magnitude of the H effect, while hemoglobin, which efficiently binds NO molecules, blocked the inhibitory effects of sodium nitroprusside, SNAP, and L-arginine on the magnitude of the H effect. All these points provide evidence that NO can function as a modulator of non-quantum mediator release in the neuromuscular junctions of warm-blooded animals.
Tài liệu tham khảo
E. E. Nikol'skii, V. A. Voronin, and T. I. Oranskaya, “The dynamics of changes in spontaneous quantum and non-quantum secretion of acetylcholine from motor nerve endings after nerve section,” Dokl. Akad. Nauk SSSR, 281, No. 3, 762–764 (1985).
A. Kh. Urazaev and A. L. Zefirov, “The physiological role of nitric oxide,” Usp. Fiziol. Nauk, 30, No. 1, 54–72 (1999).
E. X. Albuquerque, F. T. Schun, and F. C. Kaufman, “Early membrane depolarization of the fast mammalian muscle after denervation,” Pflüger's Arch., 328, No. 1, 36–50 (1971).
M. Barinaga, “Is nitric oxide the 'retrograde messenger'?” Science, 29, No. 11, 1296–1297 (1991).
G. A. Bohme, C. Bon, M. Lemaire, M. Reibaid, O. Piot, J.-M. Stuzmann, A. Doble, and J.-C. Blanchard, “Altered synaptic plasticity and memory formation in nitric oxide synthase inhibitor-treated rats,” Proc. Natl. Acad. Sci. USA, 90, 9191–9194 (1993).
J. J. Bray, J. W. Forrest, and J. I. Hubbard, “Evidence for the role of non-quantal acetylcholine in the maintenance of the membrane potential of rat skeletal muscle,” J. Physiol. (London), 326, 285–296 (1982).
D. S. Bredt and S. H. Snyder, “Nitric oxide, a novel neuronal messenger,” Neuron, 8, No. 1, 3–11 (1992).
D. B. Drachman, E. F. Stanley, A. Pestronk, J. W. Griffin, and D. L. Price, “Neurotrophic regulation of two properties of skeletal muscle by impulse-dependent and spontaneous acetylcholine transmission,” J. Neurosci., 2, 232–243 (1982).
M. G. Garry, J. D. Richardson, and K. M. Hargreaves, “Sodium nitroprusside evokes the release of immunoreactive calcitonin gene related peptide and substance P from dorsal horn slices via nitric oxide-dependent and nitric oxide-independent mechanisms,” J. Neurosci., 14, No. 7, 4329–4337 (1994).
J. Hu and E. E. El-Fakahany, “The calmodulin antagonist calmidazolium stimulates release of nitric oxide in neuroblastoma NIE-115 cells,” NeuroReport, 2, 198–200 (1993).
B. Katz and R. Miledi, “Transmitter leakage from motor nerve endings,” Proc. Roy. Soc. London, 196, 59–72 (1977).
S. A. Lindgren and M. W. Laird, “Nitroprusside inhibits neurotransmitter release at the frog neuromuscular unction,” NeuroReport, 5, No. 16, 2205–2208 (1994).
S. T. Meller and G. F. Gebhart, “Nitric oxide (NO) and nociceptive processing in the spinal cord,” Pain, 52, 127–136 (1993).
J. F. Mitchell and A. Silver, “The spontaneous release of acetylcholine from the denervated hemidiaphragms of the rat,” J. Physiol. (London), 66, 657–669 (1963).
E. E. Nikolsky, V. A. Voronin, T. I. Oranska, and F. Vyskocil, “The dependence of non-quantal acetylcholine release on the choline-uptake system in the mouse diaphragm,” Pflüger's Arch., 418, 74–78 (1991).
E. E. Nikolsky, T. I. Oranska, and F. Vyskocil, “Non-quantal acetylcholine release in the mouse diaphragm after phrenic nerve crush and during recovery,” Exp. Physiol., 81, 341–348 (1996).
L. Oliver, O. Goreau, Y. Curtois, and M. Vigny, “Accumulation of NO synthase (type-1) at the neuromuscular junctions in adult mice,” NeuroReport, 7, 924–926 (1996).
M. B. Reid, “Reactive oxygen and nitric oxide in skeletal muscle,” News Physiol. Sci., 11, 114–119 (1996).
E. M. Schuman and D. V. Madison, “Nitric oxide and synaptic function,” Ann. Rev. Neurosci., 17, 153–183 (1994).
Y.-A. Sun and M.-M. Poo, “Non-quantal release of acetylcholine at a developing neuromuscular synapse in culture,” J. Neurosci., 5, No. 3, 634–642 (1985).
A. Kh. Urazaev, “Nitric oxide is the retrograde messenger providing the neurotrophic control of membrane potential in muscle fibres of rats,” Neurosci., 12, No. 2, 75–76 (1995).
A. Kh. Urazaev, N. V. Naumenko, G. I. Poletaev, E. E. Nikolsky, and F. Vyskocil, “Acetylcholine and carbachol prevent muscle depolarization in denervated rat diaphragm,” NeuroReport, 8, No. 2, 403–406 (1997).
A. Kh. Urazaev, N. V. Naumenko, E. E. Nikolsky, and F. Vyskocil, “The glutamate and carbachol effects on the early post-denervation depolarization in rat diaphragm are directed towards furosemide-sensitive chloride transport,” Neurosci. Res., 33, No. 2, 81–86 (1999).
S. R. Vincent and B. T. Hope, “Neurones that say NO,” Trends Neurosci., 15, 108–113 (1992).
F. Vyskocil and P. Iles, “Non-quantal release of transmitter at mouse neuromuscular junction and its dependence on the activity of Na+,K+-ATPase,” Pflüger's Arch., 370, 295–297 (1977).
F. Vyskocil, E. Nikolsky, and C. Edwards, “An analysis of the mechanisms underlying the non-quantal release of acetylcholine at the mouse neuromuscular junction,” Neurosci., 9, 429–435 (1983).
F. Vyskocil and G. Vrbova, “Non-quantal release of acetylcholine affects polyneuronal innervation on developing rat muscle fibres,” Eur. J. Neurosci., 5, 1677–1683 (1993).
T. Wang, Z. Xie, and B. Lu, “Nitric oxide mediates activity-dependent synaptic suppression at developing neuro-muscular synapses,” Nature, 374, No. 16, 262–266 (1995).
S. H. Young and M.-M. Poo, “Spontaneous release of transmitter from growth cones of embryonic neurones,” Nature, 305, 634–637 (1983).