Calcium channels in retinal photoreceptors

第一视觉突触的信息传递由L型电压门控钙通道Cav1.4Ca~(2+)介导 频道。这些通道集中在突触终末的功能区下，一个 使用紧张性神经递质释放的突触的细胞器特征。基因突变 Cav1.4改变神经传递，但也可以阻止突触发育。这类缺陷可能 表现为各种视觉疾病，包括先天性静止性夜盲或视锥细胞杆营养不良。在这个提议中，我们将检验Cav1.4(目标1)及其辅助元素的假设 β2(Aim 2)和α2δ4(Aim 3)亚基在不同的方式下对突触是必不可少的 光感受器的发展。这项工作将使用一组互补的 电生理学、遗传学、生化和细胞生物学方法。这样做的结果是 研究应该产生广泛的影响，改变Cav1.4渠道的概念 有助于突触功能和疾病触发的重塑。

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.