Department of Pharmacology, University of North Carolina at Chapel Hill, Genetic Medicine Building, CB 7365, Chapel Hill, NC 27599, USA.
Science. 2010 Mar 5;327(5970):1250-4. doi: 10.1126/science.1184821.
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 Ca2+-dependent process. We used two mouse lines to either selectively increase or obliterate astrocytic Gq G protein-coupled receptor Ca2+ signaling to further test the hypothesis that astrocytes release gliotransmitters in a Ca2+-dependent manner to affect synaptic transmission. Neither increasing nor obliterating astrocytic Ca2+ 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.
在过去十年的神经科学研究中，星形胶质细胞释放神经活性分子（神经递质）以影响突触传递的概念是一个范式转变。这个概念表明，星形胶质细胞与突触前和突触后神经元元件一起构成了一个功能性突触。星形胶质细胞释放神经递质（例如谷氨酸和三磷酸腺苷）通常被认为是一个 Ca2+依赖的过程。我们使用两种小鼠品系，选择性地增加或消除星形胶质细胞 Gq G 蛋白偶联受体 Ca2+信号，以进一步检验这样一个假设，即星形胶质细胞以 Ca2+依赖的方式释放神经递质以影响突触传递。增加或消除星形胶质细胞 Ca2+流都不会影响自发和诱发的兴奋性突触传递或突触可塑性。我们的研究结果表明，至少在海马体中，需要重新考虑神经递质传递的机制。
