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Lechin F, van der Dijs B, Pardey-Maldonado B, et al. Effects of an oral dose of l-glutamic acid on circulating neurotransmitters: Possible roles of the C1(Ad) and the A5(NA) pontomedullary nuclei. J Exp Pharmacol. 2010;2:47-53doi: 10.2147/jep.s9410.
Lechin, F., van der Dijs, B., Pardey-Maldonado, B., Rivera, J. E., Lechin, M. E., & Baez, S. (2010). Effects of an oral dose of l-glutamic acid on circulating neurotransmitters: Possible roles of the C1(Ad) and the A5(NA) pontomedullary nuclei. Journal of experimental pharmacology, 247-53. https://doi.org/10.2147/jep.s9410
Lechin, Fuad, et al. "Effects of an oral dose of l-glutamic acid on circulating neurotransmitters: Possible roles of the C1(Ad) and the A5(NA) pontomedullary nuclei." Journal of experimental pharmacology vol. 2 (2010): 47-53. doi: https://doi.org/10.2147/jep.s9410
Lechin F, van der Dijs B, Pardey-Maldonado B, Rivera JE, Lechin ME, Baez S. Effects of an oral dose of l-glutamic acid on circulating neurotransmitters: Possible roles of the C1(Ad) and the A5(NA) pontomedullary nuclei. J Exp Pharmacol. 2010 Feb 20;2:47-53. doi: 10.2147/jep.s9410. eCollection 2010. PMID: 27186090; PMCID: PMC4863285.
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J Exp Pharmacol. 2010 Feb 20;2:47-53. doi: 10.2147/jep.s9410. eCollection 2010.

Effects of an oral dose of l-glutamic acid on circulating neurotransmitters: Possible roles of the C1(Ad) and the A5(NA) pontomedullary nuclei.

Journal of experimental pharmacology

Fuad Lechin, Bertha van der Dijs, Betty Pardey-Maldonado, Jairo E Rivera, Marcel E Lechin, Scarlet Baez

Affiliations

  1. Department of Physiological Sciences, Sections of Neuroendocrinology, Neuropharmacology, and Neurochemistry, Instituto de Medicina Experimental, Faculty of Medicine, Universidad Central de Venezuela, Caracas, Venezuela.
  2. Department of Internal Medicine, Texas A & M Health Science Center, College of Medicine, Texas, USA.

PMID: 27186090 PMCID: PMC4863285 DOI: 10.2147/jep.s9410

Abstract

OBJECTIVE: Investigation of the effects of an oral administration of a small dose of l-glutamic acid on the two peripheral sympathetic branches (neural and adrenal) of the autonomic nervous system.

RESEARCH DESIGN AND METHODS: Circulating neurotransmitters and cardiovascular parameters were assessed in 28 healthy volunteers before and after the administration of 500 mg of l-glutamic acid or placebo.

RESULTS: The drug triggered a significant and sustained enhancement of the noradrenaline and dopamine circulating levels which were paralleled and positively correlated with the diastolic blood pressure increases. Conversely, both platelet and plasma serotonin showed significant falls throughout the test. Significant positive correlations were registered between noradrenaline, dopamine, and noradrenaline/dopamine ratio versus diastolic blood pressure but not versus systolic blood pressure or heart rate.

CONCLUSION: The above results allowed us to postulate that the drug provoked a significant enhancement of peripheral neural sympathetic activity and the reduction of adrenal sympathetic and parasympathetic drives. Both sympathetic branches are positively correlated with the A5 noradrenergic and the C1 adrenergic pontomedullary nuclei, which interchange inhibitory axons that act at post-synaptic α2 inhibitory autoreceptors. In addition, we discussed the mechanisms able to explain why the drug acted preferentially at the A5 noradrenergic rather than the C1 adrenergic nuclei.

Keywords: catecholamines; glutamic acid; noradrenaline; serotonin; sympathetic activity

References

  1. Psychoneuroendocrinology. 2004 Jun;29(5):669-85 - PubMed
  2. Brain Res. 1982 Jun 17;242(1):125-35 - PubMed
  3. Brain Res. 1997 Jul 18;763(1):56-62 - PubMed
  4. Clin Sci (Lond). 1979 Dec;57(6):509-14 - PubMed
  5. Brain Res Bull. 1989 Dec;23(6):519-40 - PubMed
  6. Brain Res. 2003 Jan 24;961(1):109-20 - PubMed
  7. Brain Res. 1999 Jan 9;815(2):227-36 - PubMed
  8. Dig Dis Sci. 2009 Mar;54(3):458-70 - PubMed
  9. Neurosci Lett. 1993 Apr 16;153(1):1-4 - PubMed
  10. Brain Res. 1982 Jun 10;241(2):271-8 - PubMed
  11. Brain Res Bull. 1990 Jan;24(1):33-9 - PubMed
  12. J Comp Neurol. 1996 Jan 15;364(3):402-413 - PubMed
  13. Brain Res. 1986 Jun 4;375(1):117-25 - PubMed
  14. Am J Physiol. 1996 Nov;271(5 Pt 2):R1304-10 - PubMed
  15. Prog Neuropsychopharmacol Biol Psychiatry. 2006 Jun;30(4):565-85 - PubMed
  16. J Auton Nerv Syst. 1988 Aug;23(2):161-74 - PubMed
  17. Brain Res. 1997 Feb 14;748(1-2):211-8 - PubMed
  18. J Comp Neurol. 1984 Sep 10;228(2):168-85 - PubMed
  19. Am J Physiol. 1997 Nov;273(5 Pt 2):H2280-9 - PubMed
  20. Brain Res. 1991 Oct 18;562(1):126-35 - PubMed
  21. Eur J Pharmacol. 1985 Feb 12;109(1):91-6 - PubMed
  22. Clin Sci (Lond). 1995 Apr;88(4):439-46 - PubMed
  23. Am J Physiol. 1984 Jul;247(1 Pt 1):E35-40 - PubMed
  24. Am J Physiol. 1980 Sep;239(3):H349-58 - PubMed
  25. Neurosci Lett. 1990 Oct 16;118(2):141-6 - PubMed
  26. Neurosci Lett. 2002 Oct 31;332(2):107-10 - PubMed
  27. Neuropharmacology. 1983 Sep;22(9):1071-9 - PubMed
  28. J Comp Neurol. 1987 Jul 22;261(4):529-42 - PubMed
  29. Brain Res. 1999 Mar 27;823(1-2):42-8 - PubMed
  30. Neuroscience. 1989;30(1):199-214 - PubMed
  31. Am J Physiol. 1994 Mar;266(3 Pt 2):H1075-86 - PubMed
  32. Br J Pharmacol. 1985 Aug;85(4):733-5 - PubMed
  33. Curr Neurovasc Res. 2006 Nov;3(4):307-25 - PubMed
  34. Clin Exp Pharmacol Physiol. 1988 Feb;15(2):147-55 - PubMed
  35. J Cardiovasc Pharmacol. 1987;10 Suppl 12:S22-5 - PubMed
  36. Eur Respir J. 1999 Sep;14(3):642-9 - PubMed
  37. Neuroendocrinology. 2006;84(4):222-34 - PubMed
  38. Brain Res. 1976 May 7;107(2):407-11 - PubMed
  39. Brain Res Bull. 1993;31(3-4):273-8 - PubMed
  40. Eur J Pharmacol. 2002 Jun 7;445(1-2):37-42 - PubMed
  41. Am J Physiol. 1997 Jan;272(1 Pt 2):R249-58 - PubMed
  42. Am J Physiol. 1984 Jan;246(1 Pt 2):H44-51 - PubMed
  43. Brain Res. 1984 Jun 11;303(1):31-40 - PubMed

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