Effects of amantadine on circulating neurotransmitters in healthy subjects

Considering that glutamatergic axons innervate the C1(Ad) medullary nuclei, which are responsible for the excitation of the peripheral adrenal glands, we decided to investigate catecholamines (noradrenaline, adrenaline and dopamine) plus indolamines (plasma serotonin and platelet serotonin) at the b...

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Bibliographic Details
Published in:Journal of Neural Transmission 2010-03, Vol.117 (3), p.293-299
Main Authors: Lechin, Fuad, van der Dijs, Bertha, Pardey-Maldonado, Betty, Rivera, Jairo E., Baez, Scarlet, Lechin, Marcel E.
Format: Article
Language:English
Subjects:
Adult
Amantadine - pharmacology
Basic Neurosciences
Basic Neurosciences, Genetics and Immunology - Original
Blood Platelets - drug effects
Blood Platelets - metabolism
Blood Pressure - drug effects
Dopamine - blood
Dopamine - metabolism
Epinephrine - blood
Epinephrine - metabolism
Excitatory Amino Acid Antagonists - pharmacology
Female
Genetics and Immunology - Original Article
Heart Rate - drug effects
Humans
Male
Medicine
Medicine & Public Health
Middle Aged
Neurology
Neurosciences
Neurotransmitter Agents - blood
Neurotransmitter Agents - metabolism
Norepinephrine - blood
Norepinephrine - metabolism
Plasma - drug effects
Plasma - metabolism
Psychiatry
Serotonin - blood
Serotonin - metabolism
Time Factors
Tryptophan - blood
Tryptophan - metabolism
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Summary:Considering that glutamatergic axons innervate the C1(Ad) medullary nuclei, which are responsible for the excitation of the peripheral adrenal glands, we decided to investigate catecholamines (noradrenaline, adrenaline and dopamine) plus indolamines (plasma serotonin and platelet serotonin) at the blood level, before and after a small oral dose of amantadine, a selective NMDA antagonist. We found that the drug provoked a selective enhancement of noradrenaline plus a minimization of adrenaline, dopamine, plasma serotonin and platelet serotonin circulating levels. Significant enhancement of diastolic blood pressure plus reduction of systolic blood pressure and heart rate paralleled the circulating parameter changes. The above findings allow us to postulate that the drug was able to enhance the peripheral neural sympathetic activity. Minimization of both adrenal sympathetic and parasympathetic activities was also registered after the amantadine challenge. The above findings supported the postulation that this drug should be a powerful therapeutic tool for treating diseases affected by adrenal sympathetic hyperactivity.
ISSN:0300-9564
1435-1463
DOI:10.1007/s00702-010-0371-1