LRRTM4 is a transsynaptic adhesion protein regulating glutamatergic synapse assembly on dendrites of central neurons. In the mouse retina, we find that LRRTM4 is enriched at GABAergic synapses on axon terminals of rod bipolar cells (RBCs). Knockout of LRRTM4 reduces RBC axonal GABAA and GABAC receptor clustering and disrupts presynaptic inhibition onto RBC terminals. LRRTM4 removal also perturbs the stereotyped output synapse arrangement at RBC terminals. Synaptic ribbons are normally apposed to two distinct postsynaptic "dyad" partners, but in the absence of LRRTM4, "monad" and "triad" arrangements are also formed. RBCs from retinas deficient in GABA release also demonstrate dyad mis-arrangements but maintain LRRTM4 expression, suggesting that defects in dyad organization in the LRRTM4 knockout could originate from reduced GABA receptor function. LRRTM4 is thus a key synapse organizing molecule at RBC terminals, where it regulates function of GABAergic synapses and assembly of RBC synaptic dyads.

中文翻译：

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LRRTM4：视网膜双极细胞的突触前抑制和丝带突触安排的新型调节器。

LRRTM4是一种突触粘附蛋白，可调节中枢神经元树突上的谷氨酸能突触装配。在小鼠视网膜中，我们发现LRRTM4在杆状双极细胞（RBCs）轴突末端的GABA能突触中富集。LRRTM4的敲除减少了RBC轴突GABAA和GABAC受体的聚集，并破坏了对RBC末端的突触前抑制。LRRTM4的删除也会干扰RBC终端上的定型输出突触排列。突触带通常与两个不同的突触后“双性体”伴侣并置，但在没有LRRTM4的情况下，也会形成“单核”和“三联体”排列。缺乏GABA释放的视网膜红细胞也显示出二元错配，但维持LRRTM4表达，提示LRRTM4基因敲除的二联体组织缺陷可能源于GABA受体功能降低。因此，LRRTM4是RBC末端的关键突触组织分子，在该分子中它调节GABA能突触的功能和RBC突触二元的组装。