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Updated: Apr 23, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
Published on: March 20, 2014
Purinergic receptor activation facilitates astrocytic GABAB receptor calcium signalling
Miho Terunuma1, Philip G Haydon2, Menelas N Pangalos3
1Department of Cell Physiology and Pharmacology, College of Medicine, Biological Sciences and Psychology, University of Leicester, University Road, Leicester LE1 9HN, UK.
Abstract:
Gamma-aminobutyric acid B receptors (GABABRs) are heterodimeric G-protein coupled receptors, which mediate slow synaptic inhibition in the brain. Emerging evidence suggests astrocytes also express GABABRs, although their physiological significance remains unknown. To begin addressing this issue, we have used imaging and biochemical analysis to examine the role GABABRs play in regulating astrocytic Ca(2+) signalling. Using live imaging of cultured cortical astrocytes loaded with calcium indicator Fluo-4/AM, we found that astrocytic GABABRs are able to induce astrocytic calcium transients only if they are pre-activated by P2 purinoceptors (P2YRs). The GABABR-mediated calcium transients were attenuated by the removal of extracellular calcium. Furthermore, P2YRs enhance the phosphorylation of astrocytic GABABR R2 subunits on both serine 783 (S783) and serine 892 (S892), two phosphorylation sites that are well known to regulate the activity and the cell surface stability of GABABRs. Collectively these results suggest that P2YR mediated signalling is an important determinant of GABABR activity and phosphorylation in astrocytes.
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