Poster
# 20
Poster |
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6th Internet World Congress for Biomedical Sciences |
María Dolores Mayas-Torres(1), José Manuel Martínez-Martos(2), María Jesús Ramírez-Expósito(3), María Jesús García-López(4), Isabel Prieto-Gómez(5), Garbiñe Arechaga-Maza(6), Manuel Ramírez-Sánchez(7)
(1)(2)(4)(5)(6)(7)Unit of Physiology. University of Jaén - Jaén. Spain
(3)Unit of Physiology. University of Jaen - Jaén. Spain
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[Endocrinology] |
[Neuroscience] |
[Pharmacology] |
[Physiology] |
[Toxicology] |
Brain aminopeptidases (AP) have been implicated in the enzymatic activation and degradation of several neuropeptides(1). These two actions may regulate not only their role as neuromodulators2 but may also modify the free amino acid pool through the release of N-terminal amino acids, some of which, such as glutamate and aspartate, are particularly active in the central nervous system (CNS)(3,4). The aminopeptidase A activity (AP-A) (GluAP and AspAP) has a quick action on the N-terminal aspartic and glutamic acids of biologically active peptides and polypeptides, regulating their activities1. Therefore, changes in AspAP and/or GluAP may contribute to or reflect modifications in excitatory amino acid turnover. One of the mechanisms responsible for neurodegenerative processes affecting the CNS is the hyperexcitability of amino-acid neurotransmitters, particularly glutamic and aspartic acids. This hyperexcitability of excitatory neurotransmitters make themself strong endogenous toxins which induce degeneration and neurone death(5,6,7,8,9,10,11,12,13).
The purpose of this work was to study the influence of a neurotoxic agent, ethanol, on the AP-A activity on basal and stimulated conditions, in a synaptic transmission model by using synaptosomes.
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[Endocrinology] |
[Neuroscience] |
[Pharmacology] |
[Physiology] |
[Toxicology] |
