Calcium channels in retinal photoreceptors

第一视觉突触的信息传递由L型电压门控Cav1.4 Ca ~（2+）介导 渠道这些通道集中在带状物下方的突触末端， 利用紧张性神经递质释放的突触特征的细胞器。突变 Cav1.4改变神经传递，但也可以阻止突触发育。此类缺陷可 表现为各种视觉疾病，包括先天性静止性夜盲或视锥-视杆细胞营养不良。在这个建议中，我们将测试假设，Cav1.4（目标1）和它的辅助 亚基β2（Aim 2）和α2δ4（Aim 3）在突触的各种方式中都是必不可少的。 光感受器的发展。这项工作将使用一个互补的阵列来完成， 电生理学、遗传学、生物化学和细胞生物学方法。这个结果 研究应该通过改变Cav1.4通道的概念来产生广泛的影响， 有助于突触功能和疾病引发的重塑。

Communication at the first visual synapse is mediated by L-type voltage-gated Cav1.4 Ca2+ channels. These channels are concentrated in the synaptic terminal beneath the ribbon, an organelle characteristic of synapses employing tonic neurotransmitter release. Mutation of Cav1.4 alters neurotransmission but can also prevent synaptic development. Such defects can present as a variety of visual diseases, including congenital stationary night blindness or cone-rod dystrophy. In this proposal, we will test the hypothesis that Cav1.4 (Aim 1) and its auxiliary subunits, β2 (Aim 2) and α2δ4 (Aim 3), are each essential in various ways for synaptic development in photoreceptors. This work will be accomplished using a complementary array of electrophysiological, genetic, biochemical, and cell biological approaches. The outcomes of this research should have a broad impact by transforming the concept of how Cav1.4 channels contribute to synapse function and disease-triggered remodeling.