Endogenous adenosine modulation of Na-22 uptake by rat brain synaptosomes

• Type: Article in International Scientific Journal
• Date: 2003

Authors

Ribeiro, JA (Author) Other; Lobo, MGB (Author) ICBAS; Sebastiao, AM (Author) Other

Journal

Title: Neurochemical Research

Vol. 28

Pages: 1591-1595

ISSN: 0364-3190

Publisher: Springer Nature

Indexing

ISI Web of Knowledge - 2 Citations

Scopus - 2 Citations

Other information

Authenticus ID: P-000-F22

DOI: 10.1023/a:1025638929136

Abstract (EN): To evaluate if endogenous extracellular adenosine influences sodium channel activity in nerve terminals, we investigated how manipulations of extracellular adenosine levels influence Na-22 uptake by rat brain synaptosomes stimulated with veratridine (VT). To decrease extracellular adenosine levels, adenosine deaminase (ADA) that converts adenosine into an inactive metabolite was used. To increase extracellular adenosine levels, we used the adenosine deaminase inhibitor erythro-9(2-hydroxy-3-nonyl) adenine ( EHNA), as well as the inhibitor of adenosine transport, nitrobenzylthioinosine ( NBTI). ADA ( 0.1-5 U/ml) caused an excitatory effect on 22Na uptake stimulated by veratridine, which was abolished in the presence of the adenosine deaminase inhibitor erythro-9(2-hydroxy-3-nonyl) adenine ( EHNA, 25 muM). Both the adenosine uptake inhibitor nitrobenzylthioinosine (NBTI, 1 - 10 muM) and the adenosine deaminase inhibitor EHNA (10 - 25 muM) inhibited Na-22 uptake by rat brain synaptosomes. It is suggested that adenosine is tonically inhibiting sodium uptake by rat brain synaptosomes.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 5