Abstract
Adenosine is a major non-peptide neuromodulator in the central nervous system (CNS). Numerous reviews have been written on this subject with detailed accounts of the receptor heterogeneity, localization and functionality (Fredholm et. al 1980, Marangos et. al 1985). Existing information paints a clear picture regarding the importance of the adenosine system in CNS functions. There are few neurotransmitter or neuromodulator systems that have been characterized as well as that for adenosine. The prevailing view is that not only do adenosine receptors modulate c-AMP levels in both directions but that perhaps more importantly they regulate both K+ and Ca++ ion fluxes across neural membranes (Michaelis et. al 1988). It appears that these latter adenosine mediated processes (i. e. Stimulation of K+ efflux or inhibition of Ca++ influx) serve to shorten the action potential and thereby inhibit the release of a number of neurotransmitters. The inhibition of Ca+-dependent neurotransmitter release by adenosine has been consistently observed in a number of laboratories (for review see Marangos et. al 1985, Fredholm et. al, 1980) and is thought to be the most functionally relevant action of the purine riboside.
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Marangos, P.J., Lubitz, D.V., Miller, L.P., Daval, J.L., Deckert, J. (1990). The Central Adenosine System as a Therapeutic Target in Stroke. In: Jacobson, K.A., Daly, J.W., Manganiello, V. (eds) Purines in Cellular Signaling. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3400-5_17
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DOI: https://doi.org/10.1007/978-1-4612-3400-5_17
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