The Effect of Ethidium Bromide on Purinergic Modulation of Myoneural Transmission and Skeletal Muscle Contraction

Capa

Citar

Texto integral

Acesso aberto Acesso aberto
Acesso é fechado Acesso está concedido
Acesso é fechado Somente assinantes

Resumo

The problem of changes in myoneural transmission in the presence of an intercalating agent, ethidium bromide, which has a known inhibitory effect on neuromuscular transmission, has been investigated, but the nature of such an effect remains unclear. To solve the question of the possible participation in this process of known modulators of synaptic transmission – purines (ATP and adenosine), we evaluated their effects in the presence of this agent. After holding the neuromuscular frog preparation in a perfusing solution containing ethidium bromide, the amplitude of postsynaptic responses and muscle contraction forces decreased. Under these conditions, both purines additionally exerted their usual suppressive effect on both the amplitude of postsynaptic responses and the strength of skeletal muscle contraction. Thus, the inhibitory effect of ethidium bromide on neuromuscular transmission is not associated with an increase in the inhibitory effect of endogenous purines caused by the quantum release of the neurotransmitter.

Sobre autores

A. Gorshunova

Kazan Law Institute of the Ministry of Internal Affairs of Russia

Kazan, Russia

A. Teplov

Kazan State Medical University

Kazan, Russia

S. Grishin

Kazan State Medical University

Kazan, Russia

R. Mukhamedzyanov

Kazan State Medical University

Kazan, Russia

A. Khairullin

Kazan State Medical University; Kazan Federal University

Email: khajrulli@ya.ru
Kazan, Russia

Bibliografia

  1. Sigmon J. and Larcom L. L. The effect of ethidium bromide on mobility of DNA fragments in agarose gel electrophoresis. Electrophoresis, 17 (10), 1524—1527 (1996). doi: 10.1002/elps.1150171003
  2. Перечень химических и биологических веществ, прошедших государственную регистрацию. Токсикологич. вестн., 1 (142), 48 (2007).
  3. Liu J., Li X., and Ke A. High-mobility group box-1 induces mechanical pain hypersensitivity through astrocytic connexin 43 via the toll-like receptor-4/JNK signaling pathway. Synapse, 75 (2), e22184 (2020). doi: 10.1002/syn.22184
  4. Dong R., Han Y., Jiang L., Liu S., Zhang F., Peng L., Wang Z., Ma Z., Xia T., and Gu X. Connexin 43 gap junction-mediated astrocytic network reconstruction attenuates isoflurane-induced cognitive dysfunction in mice. J. Neuroinflammation, 19 (1), 64 (2022). doi: 10.1186/s12974-022-02424-y
  5. Komatsu K., Uchida K., and Satoh S. Neurotrophic influences are not affected by miniature end-plate potentials. Exp. Neurol., 83 (1), 33—41 (1984). doi: 10.1016/0014-4886(84)90043-8
  6. Smith K. J., Felts P. A., and John G. R. Effects of 4-ami-nopyridine on demyelinated axons, synapses and muscle tension. Brain, 123 (1), 171-184 (2000). doi: 10.1093/brain/123.1.171
  7. Sterz R., Hermes M., Peper K., and Bradley R. J. Effects of ethidium bromide on the nicotinic acetylcholine receptor. Eur. J. Pharmacol., 80 (4), 393-399 (1982). doi: 10.1016/0014-2999(82)90085-1
  8. Dreyer F., Peper K., Sterz R., Bradley R. J., and Müller K.
  9. D. Drug-receptor interaction at the frog neuromuscular junction. Prog. Brain Res., 49, 213-223 (1979). doi: 10.1016/S0079-6123(08)64635-X
  10. Peper K., Bradley R. J., and Dreyer F. The acetylcholine receptor at the neuromuscular junction. Physiol. Rev., 62 (4), 1271-1340 (1982). doi: 10.1152/physrev.1982.62.4.1271
  11. Dreyer F., Peper K., and Sterz R. Determination of doseresponse curves by quantitative ionophoresis at the frog neuromuscular junction. J. Physiol., 281, 395-419 (1978). doi: 10.1113/jphysiol.1978.sp012430
  12. Bostock H., Sherratt R. M., and Sears T. A. Overcoming conduction failure in demyelinated nerve fibres by prolonging action potentials. Nature, 274 (5669), 385-387 (1978). doi: 10.1038/274385a0
  13. Sherratt R., Bostock H., and Sears T. Effects of 4-amino-pyridine on normal and demyelinated mammalian nerve fibres. Nature, 283, 570-572 (1980). doi: 10.1038/283570a0
  14. Bostock H., Sears T. A., and Sherratt R. M. The effects of 4-aminopyridine and tetraethylammonium ions on normal and demyelinated mammalian nerve fibres. J. Physiol., 313, 301-315 (1981) doi: 10.1113/jphysiol.1981.sp013666
  15. Hansebout R. R., Blight A. R., Fawcett S., and Reddy K. 4-Aminopyridine in chronic spinal cord injury: a controlled, double-blind, crossover study in eight patients. J. Neurotrauma, 10 (1), 1-18 (1993). doi: 10.1089/neu.1993.10.1
  16. Hayes K. C., Blight A. R., Potter P. J., Allatt R. D., Hsieh J. T., Wolfe D. L., Lam S., and Hamilton J. T. Pre-clinical trial of 4-aminopyridine in patients with chronic spinal cord injury. Paraplegia, 31 (4), 216-224 (1993). doi: 10.1038/sc.1993.40
  17. Hansebout R. R., Blight A. R., Fawcett S., and Reddy K. 4-Aminopyridine in chronic spinal cord injury: a controlled, double-blind, crossover study in eight patients. J. Neurotrauma, 10 (1), 1-18 (1993). doi: 10.1089/neu.1993.10.1
  18. Grishin S., Shakirzyanova A., Giniatullin A., Afzalov R., and Giniatullin R. Mechanisms of ATP action on motor nerve terminals at the frog neuromuscular junction. Eur. J. Neurosci., 21 (5), 1271-1279 (2005). doi: 10.1111/j.1460-9568.2005.03976.x
  19. Burnstock G., Knight G. E., and Greig A. V. Purinergic signaling in healthy and diseased skin. J. Invest. Dermatol., 132 (3), 526-546 (2012). doi: 10.1038/jid.2011.344
  20. Burnstock G. Purines and sensory nerves. Handb. Exp. Pharmacol., 194, 333-392 (2009). doi: 10.1007/978-3-540-79090-7_10
  21. Khairullin A. E., Grishin S. N., and Ziganshin A. U. Pre-synaptic purinergic modulation of the rat neuro-muscular transmission. Curr. Issu. Mol. Biol., 45, 8492-8501 (2023). doi: 10.3390/cimb45100535
  22. Bravo D. T., Kolmakova N. G., and Parsons S. M. New transport assay demonstrates vesicular acetylcholine transporter has many alternative substrates. Neurochem. Int., 47 (4), 243-247 (2005). doi: 10.1016/j.neuint.2005.05.002
  23. Khairullin A. E., Teplov A. Y., Grishin S. N., and Ziganshin A. U. ATP causes contraction of denervated skeletal muscles. Biochemistry (Moscow) — Suppl. Ser. A: Membr. Cell. Biol., 17 (1), 73-77 (2023). doi: 10.1134/s1990747823060065

Arquivos suplementares

Arquivos suplementares
Ação
1. JATS XML
Baixar

Declaração de direitos autorais © Russian Academy of Sciences, 2024