It is a commonly accepted view that light stimulation of mammalian photoreceptors causes a graded change in membrane potential instead of developing a spike. The presynaptic Ca²⁺ channels serve as a crucial link for the coding of membrane potential variations into neurotransmitter release. Ca_v1.4 L-type Ca²⁺ channels are expressed in photoreceptor terminals, but the complete pool of Ca²⁺ channels in cone photoreceptors appears to be more diverse. Here, we discovered, employing whole-cell patch-clamp recording from cone photoreceptor terminals in both sexes of mice, that their Ca²⁺ currents are composed of low- (T-type Ca²⁺ channels) and high- (L-type Ca²⁺ channels) voltage-activated components. Furthermore, Ca²⁺ channels exerted self-generated spike behavior in dark membrane potentials, and spikes were generated in response to light/dark transition. The application of fast and slow Ca²⁺ chelators revealed that T-type Ca²⁺ channels are located close to the release machinery. Furthermore, capacitance measurements indicated that they are involved in evoked vesicle release. Additionally, RT-PCR experiments showed the presence of Ca_v3.2 T-type Ca²⁺ channels in cone photoreceptors but not in rod photoreceptors. Altogether, we found several crucial functions of T-type Ca²⁺ channels, which increase the functional repertoire of cone photoreceptors. Namely, they extend cone photoreceptor light-responsive membrane potential range, amplify dark responses, generate spikes, increase intracellular Ca²⁺ levels, and boost synaptic transmission.

SIGNIFICANCE STATEMENT Photoreceptors provide the first synapse for coding light information. The key elements in synaptic transmission are the voltage-sensitive Ca²⁺ channels. Here, we provide evidence that mouse cone photoreceptors express low-voltage-activated Ca_v3.2 T-type Ca²⁺ channels in addition to high-voltage-activated L-type Ca²⁺ channels. The presence of T-type Ca²⁺ channels in cone photoreceptors appears to extend their light-responsive membrane potential range, amplify dark response, generate spikes, increase intracellular Ca²⁺ levels, and boost synaptic transmission. By these functions, Ca_v3.2 T-type Ca²⁺ channels increase the functional repertoire of cone photoreceptors.

一种普遍接受的观点是，哺乳动物光感受器的光刺激会导致膜电位发生分级变化，而不是产生尖峰。突触前 Ca ²⁺通道充当将膜电位变化编码为神经递质释放的关键环节。Ca _v 1.4 L 型 Ca ²⁺通道在感光器末端表达，但锥形感光器中完整的 Ca ²⁺通道池似乎更加多样化。在这里，我们发现，采用全细胞膜片钳记录来自两种性别小鼠的锥形光感受器末端，它们的 Ca ^{2+电流由低（T 型 Ca 2+}通道）和高（L 型）组成钙²⁺通道）电压激活元件。此外，Ca ²⁺通道在暗膜电位中发挥自生尖峰行为，并且尖峰响应光/暗转换而产生。^{快速和慢速 Ca 2+}螯合剂的应用表明 T 型 Ca ²⁺通道靠近释放机制。此外，电容测量表明它们参与诱发的囊泡释放。_{此外，RT-PCR 实验表明，Ca v} 3.2 T 型 Ca ²⁺通道存在于视锥细胞中，但不存在于视杆细胞中。总之，我们发现了 T 型 Ca ^{2+的几个关键功能}通道，增加视锥光感受器的功能库。也就是说，它们扩展了锥形光感受器光响应膜电位范围，放大暗响应，产生尖峰，增加细胞内 Ca ²⁺水平，并促进突触传递。

意义声明光感受器提供编码光信息的第一个突触。突触传递的关键要素是电压敏感的 Ca ²⁺通道。在这里，我们提供的证据表明，除高压激活的 L 型Ca ^{2+通道外，小鼠视锥光感受器还表达低压激活的 Ca} _v 3.2 T 型Ca ²⁺通道。锥形光感受器中T 型 Ca ²⁺通道的存在似乎扩展了它们的光响应膜电位范围，放大暗响应，产生尖峰，增加细胞内 Ca ²⁺水平，并促进突触传递。通过这些功能，Ca _v 3.2 T 型 Ca ²⁺通道增加了视锥光感受器的功能库。