Adenosine deaminase increases release of excitatory amino acids through a mechanism independent of adenosine depletion

Maria V. Catania, Maria A. Sortino, L. Rampello, P. L. Canonico, F. Nicoletti

Risultato della ricerca: Contributo su rivistaArticolo in rivistapeer review

Abstract

Addition of adenosine deaminase to cultured cerebellar neurones, led to large increases in the influx of 45Ca2+ and hydrolysis of polyphosphoinositide. These effects were inhibited or attenuated by glutamate receptor antagonists (AP5 or MK-801) and were not observed in cells stimulated by maximum concentrations of glutamate or quisqualate. Stimulation of the influx of 45Ca2+ and hydrolysis of phosphoinositide by adenosine deaminase may be secondary to an enhanced release of endogenous glutamate that in turn activates specific excitatory amino acid receptors. Accordingly, adenosine deaminase potently increased release of D-[3H]aspartate, an effect that requires the presence of extracellular Na+ and is insensitive to inhibition by MK-801. None of the effects of adenosine deaminase may be simply related to a fall in endogenous adenosine. In fact, the action of adenosine deaminase was neither reversed by agonists (L-PIA or NECA), nor mimicked by antagonists (IBMX or theophylline) of adenosine receptors. It is speculated that adenosine deaminase stimulates release of neurotransmitter through a mechanism independent of depletion of adenosine. A possible direct action of adenosine deaminase should be taken into account when the enzyme is used to unmask the effects of endogenous adenosine.

Lingua originaleInglese
pagine (da-a)153-159
Numero di pagine7
RivistaNeuropharmacology
Volume30
Numero di pubblicazione2
DOI
Stato di pubblicazionePubblicato - feb 1991
Pubblicato esternamente

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