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. 2017 Oct 18;37(42):10085–10096. doi: 10.1523/JNEUROSCI.1093-17.2017

Figure 6.

Figure 6.

IN terminal fields in RNm do not overlap with inhibitory somata. A, Schematic of experimental setup. AAV1.mCherry or BDA 10K was injected into the IN of either Gad1-Cre or GlyT2.eGFP mice. B, In situ hybridization showing Gad1 and Gad2 mRNA expression at the level of RNm from the Allen Brain Atlas (Lein et al., 2007; http://mouse.brain-map.org). Note absence of label within putative RNm. Scale bars, 200 μm. Right, Zoom of RNm border. C, Injection site of BDA into the Cbn of a Gad1.Cre animal, dashed line delineating CbN. D, GFP-expressing cells at the level of RNm (dashed line) driven by Gad1.Cre. E, BDA-labeled IN terminals in RNm, delineated with Nissl counterstain. F, Merged channels from C and D showing IN terminals in area devoid of somatic Gad1-GFP label (n = 5). Scale bar, 100 μm. G, Injection site of AAV.mCherry into the CbN, dashed line. H, GFP-expression in GlyT2-GFP mouse at the level of RNm (dashed line). I, mCherry labeled IN terminals target RNm, delineated with Nissl counterstain (right). J, Merged channels from H and I showing IN terminals in RNm do not overlap with GlyT2-GFP somata (n = 3). Scale bar, 100 μm. Right, IN terminals wrap around RNm somata counterstained with Nissl. Scale bar, 10 μm. CbN, Cerebellar nuclei; D, dorsal; M, medial; CBX, cerebellar cortex.