Neuronal activity elicits increases in intracellular Ca2+ in astrocytes, wh
ich in turn can elevate neuronal Ca2+ and potentiate the efficacy of excita
tory synaptic transmission. Therefore, understanding the modulation of astr
ocyte Ca2+ elevations by neurotransmitters should aid in understanding astr
ocyte-neuronal interactions. On cultured hippocampal microislands containin
g only astrocytes, activation of metabotropic glutamate receptors (mGluRs)
with the specific agonist 1S,3R-ACPD triggers Ca2+ elevations that are pote
ntiated by adenosine A1 receptor activation. A1 receptor modulation of mGlu
R-induced Ca2+ elevations is blocked by pertussis toxin and is mimicked by
the wasp venom peptide mastoparan, suggesting that potentiation occurs by m
eans of a G(i/o) mechanism. Surprisingly, on microislands containing only a
strocytes, A1 receptor antagonism or adenosine degradation suppresses mGluR
-triggered Ca2+ elevations, strongly suggesting that astrocytes are a sourc
e of physiologically relevant concentrations of adenosine. GLIA 33:24-35, 2
001. (C) 2001 Wiley-Liss, Inc.