Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
Neuron. 2012 Jan 12;73(1):149-58. doi: 10.1016/j.neuron.2011.10.030.
Here we provide evidence that revises the inhibitory circuit diagram of the cerebellar cortex. It was previously thought that Golgi cells, interneurons that are the sole source of inhibition onto granule cells, were exclusively coupled via gap junctions. Moreover, Golgi cells were believed to receive GABAergic inhibition from molecular layer interneurons (MLIs). Here we challenge these views by optogenetically activating the cerebellar circuitry to determine the timing and pharmacology of inhibition onto Golgi cells and by performing paired recordings to directly assess synaptic connectivity. In contrast to current thought, we find that Golgi cells, not MLIs, make inhibitory GABAergic synapses onto other Golgi cells. As a result, MLI feedback does not regulate the Golgi cell network, and Golgi cells are inhibited approximately 2 ms before Purkinje cells, following a mossy fiber input. Hence, Golgi cells and Purkinje cells receive unique sources of inhibition and can differentially process shared granule cell inputs.
在这里，我们提供的证据修改小脑皮层的抑制性电路图。以前认为，高尔基细胞，是唯一的抑制颗粒细胞的中间神经元，通过缝隙连接专门耦合。此外，高尔基细胞被认为从分子层中间神经元（MLIs）接收 GABA 能抑制。在这里，我们通过光遗传学激活小脑回路来确定 GABA 能抑制进入高尔基细胞的时间和药理学，并通过进行配对记录来直接评估突触连接。与当前的观点相反，我们发现，高尔基细胞而不是 MLIs 对其他高尔基细胞形成抑制性 GABA 能突触。结果，MLI 反馈不调节高尔基细胞网络，并且高尔基细胞在浦肯野细胞之前大约被抑制 2ms，浦肯野细胞之后是苔藓纤维输入。因此，高尔基细胞和浦肯野细胞接收独特的抑制源，并可以对共享的颗粒细胞输入进行不同的处理。
