1994
DOI: 10.1523/jneurosci.14-05-02953.1994
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Beta-adrenergic receptor-mediated regulation of extracellular adenosine in cerebral cortex in culture

Abstract: Adenosine is an important inhibitory neuromodulator in the CNS, yet the sources of extracellular adenosine have yet to be well characterized. In this study we show that beta-adrenergic stimulation of cortical cultures results in the extracellular accumulation of cAMP as well as adenosine, and that the extracellular adenosine derives from extracellular cAMP. The concentration dependence of isoproterenol in evoking cAMP secretion was determined by radioimmunoassay, and the EC50 for this effect was found to be ap… Show more

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Cited by 84 publications
(72 citation statements)
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“…Because the extracellular conversion of cAMP to adenosine requires first an extracellular phosphodiesterase capable of converting cAMP into adenosine-5 0 -monophosphate (AMP), we performed experiments with the phosphodiesterase inhibitor Ro 20-1724 (Brundege et al, 1997;Rosenberg et al, 1994), and cAMP transport inhibitor probenecid (Henderson and Strauss, 1991;Rosenberg et al, 1994). In agreement with previous studies (Brundege et al, 1997), Ro20-1724 significantly increased the amplitude of the EPSC (126.3 6 13%, P < 0.05).…”
Section: Activation Of Presynaptic Adenosine Receptors Modulates Transupporting
confidence: 77%
“…Because the extracellular conversion of cAMP to adenosine requires first an extracellular phosphodiesterase capable of converting cAMP into adenosine-5 0 -monophosphate (AMP), we performed experiments with the phosphodiesterase inhibitor Ro 20-1724 (Brundege et al, 1997;Rosenberg et al, 1994), and cAMP transport inhibitor probenecid (Henderson and Strauss, 1991;Rosenberg et al, 1994). In agreement with previous studies (Brundege et al, 1997), Ro20-1724 significantly increased the amplitude of the EPSC (126.3 6 13%, P < 0.05).…”
Section: Activation Of Presynaptic Adenosine Receptors Modulates Transupporting
confidence: 77%
“…In THC-tolerant mice, activation of the cAMP/PKA pathway by forskolin or by brief tetanic stimulation induces an adenosine A1R-mediated inhibition of synaptic release, instead of triggering LTP. Adenylyl cyclase activation by forskolin causes intracellular cAMP accumulation, transport, and conversion into adenosine by extracellular phosphodiesterase activity (Rosenberg and Dichter, 1989;Rosenberg et al, 1994;Rosenberg and Li, 1995). Adenosine, originating from the metabolism of intracellular cAMP, may also be released after synaptic stimulation (Mitchell et al, 1993).…”
Section: Discussionmentioning
confidence: 99%
“…Of the neurotransmitter receptors present in astrocytes, b-ARs occupy a special place, because unequivocal evidence suggests that astroglial cells may be the targets of the central noradrenergic system (48). These receptors have multifarious functions that include regulating astroglial glycogen metabolism (41), stimulating the expression of cytokines (49), inducing gene expression of neurotrophic factors (50), modulating glial inwardly rectifying potassium channels (51), and regulating the extracellular concentration of adenosine (52). Additionally, the b-AR system has a profound effect on the differentiation and maturation of astrocytes (53,54).…”
Section: Discussionmentioning
confidence: 99%