Hippocampal Short- and Long-Term Plasticity Are Not Modulated by Astrocyte Ca~(2+) Signaling

摘要

The concept that astrocytes release neuroactive molecules (gliotransmitters) to affect synaptic transmission has been a paradigm shift in neuroscience research over the past decade. This concept suggests that astrocytes, together with pre- and postsynaptic neuronal elements, make up a functional synapse. Astrocyte release of gliotransmitters (for example, glutamate and adenosine triphosphate) is generally accepted to be a Ca~(2+)-dependent process. We used two mouse lines to either selectively increase or obliterate astrocytic G_q G protein-coupled receptor Ca~(2+) signaling to further test the hypothesis that astrocytes release gliotransmitters in a Ca~(2+)-dependent manner to affect synaptic transmission. Neither increasing nor obliterating astrocytic Ca~(2+) fluxes affects spontaneous and evoked excitatory synaptic transmission or synaptic plasticity. Our findings suggest that, at least in the hippocampus, the mechanisms of gliotransmission need to be reconsidered.