Abstract
Endogenous adenosine can enter the extracellular space either by direct release or via formation from adenine nucleotides. We have compared the effects of substances blocking the ecto-5'-nucleotidase with a, b-methylene adenosine 5'-diphosphate (AOPCP) or adenosine kinase with iodotubercidin (Itu) on field potentials in the hippocampus and the neostriatum in vitro evoked by stimulation of the stratum radiatum or the cortico-striatal pathway respectively. AOPCP enhanced the amplitude of the population spikes by 34% in the hippocampus and by 26.5% in the neostriatum. DPCPX, a selective A1-receptor antagonist, increased the amplitude of the population spikes by 68% in the hippocampus and by 53.5% in the neostriatum. Thus both, release of adenosine from the intracellular space and, extracellular dephosphorylation of adenine nucleotides to a lesser extent, contribute to the effective levels of adenosine in the extracellular space in hippocampus and neostriatum.
Highlights
Adenosine is released metabolically from active brain cells and is generated extracellular by degradation of adenosine triphosphate (ATP) [1], and to provide a scientific data for present research
We have examined the relative importance of the two sources of extracellular adenosine in neural tissue: extracellular adenine nucleotides and adenosine released from the intracellular space
We have determined the effect of ectonucleotidase and adenosine kinase on field potentials from hippocampal and neostriatal slices, in order to estimate the relative contributions of adenosine direct release and nucleotides as sources of extracellular adenosine
Summary
Adenosine is released metabolically from active brain cells and is generated extracellular by degradation of adenosine triphosphate (ATP) [1], and to provide a scientific data for present research. It needs to explain how adenosine was released from sources in the striatum. Intra- and extracellular adenosine concentrations are kept in equilibrium by means of bidirectional nucleoside transporters. Some of these carrier mechanisms can be inhibited by drugs such as dipyridamole, nitrobenzylthioinosine and dilazep [11] [12]. The direction of adenosine transport depends on its concentration gradient between the cytosol and the extracellular space
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