A neuroprotective role for adenosine is commonly assumed. Recent studies re
vealed that adenosine may unexpectedly, under certain circumstances, have t
he opposite effects contributing to neuronal damage and death. The basis fo
r this duality may be the activation of distinct subtypes of adenosine rece
ptors, interactions between these receptors, differential actions on neuron
al and glial cells, and various time frames of adenosinergic compounds admi
nistration. If these aspects are understood, adenosine should remain an int
eresting target for therapeutical neuroprotective approaches after all. (C)
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