Hippocampal Short- and Long-Term Plasticity Are Not Modulated by Astrocyte Ca²⁺ Signaling

Cendra Agulhon,^1,* Todd A. Fiacco,²Ken D. McCarthy¹

The concept that astrocytes release neuroactive molecules (gliotransmitters)to affect synaptic transmission has been a paradigm shift inneuroscience research over the past decade. This concept suggeststhat astrocytes, together with pre- and postsynaptic neuronalelements, make up a functional synapse. Astrocyte release ofgliotransmitters (for example, glutamate and adenosine triphosphate)is generally accepted to be a Ca²⁺-dependent process. We usedtwo mouse lines to either selectively increase or obliterateastrocytic G_q G protein–coupled receptor Ca²⁺ signalingto further test the hypothesis that astrocytes release gliotransmittersin a Ca²⁺-dependent manner to affect synaptic transmission.Neither increasing nor obliterating astrocytic Ca²⁺ fluxes affectsspontaneous and evoked excitatory synaptic transmission or synapticplasticity. Our findings suggest that, at least in the hippocampus,the concept of gliotransmission need to be reconsidered.

Department of Pharmacology, University of North Carolina at Chapel Hill, Genetic Medicine Building, CB 7365, Chapel Hill, NC 27599, USA.
² Department of Cell Biology and Neuroscience, University of California Riverside, Riverside, CA 92521, USA.