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Differential changes of neuroactive amino acids in samples obtained from discrete rat brain regions after systemic administration of saxitoxin

Aspartic acid, glutamic acid, γ-amino-n-butyric acid (GABA) and 2-aminoethanesulfonic acid are neuroactive amino acids. They are found in the central rat nervous system. Here, we have studied if a relationship exists between the presence of saxitoxin (STX) a paralytic poisoning shellfish (PSP) and t...

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Published in:Neurochemistry international 2009-05, Vol.54 (5), p.308-313
Main Authors: Cianca, Rosa Carmina Cervantes, Barbosa, Rafael Durán, Faro, Lilian Rosana Ferreira, Adan, Lucia Vidal, Gago-Martínez, Ana, Pallares, Miguel Alfonso
Format: Article
Language:English
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Summary:Aspartic acid, glutamic acid, γ-amino-n-butyric acid (GABA) and 2-aminoethanesulfonic acid are neuroactive amino acids. They are found in the central rat nervous system. Here, we have studied if a relationship exists between the presence of saxitoxin (STX) a paralytic poisoning shellfish (PSP) and the neuroactive amino acids. Samples of striatum (S), hypothalamus (H), mid brain (MB), frontal cortex (FC), brain stem (BS), right hemisphere (RH) and left hemisphere (LH) of rat brain were collected and analyzed for neuroactive amino acids (AAn t) by Aswad method (1984). Experiments, consisting of intraperitoneal injection of SXT (5 and 10 μg kg −1 body weight) to young male rats, evoked significant changes in AAn t above basal values. Aspartic and glutamic acid significantly increased for RH and LH (after 30 min the increased was 116% and 210%, P ≤ 0.001 over basal values, respectively). On the other hand, aspartic, glutamic, taurine and GABA significantly decreased for S (after 30 min the decreased was 77.4%; 84%; 93.8% and 95.3%, P ≤ 0.001 over basal values, respectively). These results suggest that STX alters AAn t. It is produced at least in part, because STX blocks voltage-gated sodium channels and this blockade could decrease AAn t release by exocytotic dependent mechanism of depolarization.
ISSN:0197-0186
1872-9754
DOI:10.1016/j.neuint.2008.12.014