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Hippocampal Short- and Long-Term Plasticity Are Not Modulated by Astrocyte Ca2+ Signaling
Cendra Agulhon,1,*
Todd A. Fiacco,2
Ken D. McCarthy1
Abstract:
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 Gq G protein–coupled receptor Ca2+ signaling to 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 mechanisms of gliotransmission need to be reconsidered.
1 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.
* To whom correspondence should be addressed. E-mail: cendra_agulhon{at}med.unc.edu
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