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

Authors Lechin F, van der Dijs B, Pardey-Maldonado B, Rivera JE, Lechin ME, Baez S

Published 23 February 2010 Volume 2010:2 Pages 47—53


Review by Single anonymous peer review

Peer reviewer comments 4

Fuad Lechin1, Bertha van der Dijs1, Betty Pardey-Maldonado1, Jairo E Rivera1, Marcel E Lechin2, Scarlet Baez1

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

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: glutamic acid, catecholamines, noradrenaline, serotonin, sympathetic activity

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