ATP- and Adenosine-Mediated Signaling in the Central Nervous System: Adenosine Stimulates Glutamate Release From Astrocytes via A2a Adenosine Receptors

• Main Author: Tomoyuki Nishizaki (Author)
• Format: Book
• Published: Elsevier, 2004-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 1347-8613; 10.1254/jphs.94.100
• Keywords: Therapeutics. Pharmacology; RM1-950
• Source: Journal of Pharmacological Sciences, Vol 94, Iss 2, Pp 100-102 (2004)

Adenosine enhanced intracellular Ca2+ concentrations in astrocytes via A2a adenosine receptors involving protein kinase A (PKA) activation. The Ca2+ rise is inhibited by brefeldin A, an inhibitor of vesicular transport; but not by neomycin and U73122, phospholipase C inhibitors; xestospongin, an IP3-receptor inhibitor; ryanodine, a ryanodine-receptor inhibitor; TMB-8, an endoplasmic reticulum calcium-release blocker; octanol, a gap-junction inhibitor; or cadmium, a non-selective, calcium-channel blocker. Adenosine stimulates astrocytic glutamate release via an A2a adenosine receptors/PKA pathway, and the release is inhibited by the vesicular transport inhibitors brefeldin A and bafilomycin A1. A2a adenosine receptors and the ensuing PKA events, thus, are endowed with vesicular Ca2+ release from an unknown intracellular calcium store and vesicular glutamate release from astrocytes. Keywords:: adenosine, A2a receptor, glutamate release, Ca2+, astrocyte