T-Type Ca²⁺ Channels Boost Neurotransmission in Mammalian Cone Photoreceptors

Abstract

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 Ca 21 channels serve as a crucial link for the coding of membrane potential variations into neurotransmitter release. Ca v 1.4 L-type Ca 21 channels are expressed in photoreceptor terminals, but the complete pool of Ca 21 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 Ca 21 currents are composed of low-(T-type Ca 21 channels) and high-(L-type Ca 21 channels) voltage-activated components. Furthermore, Ca 21 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 Ca 21 chelators revealed that T-type Ca 21 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 v 3.2 T-type Ca 21 channels in cone photoreceptors but not in rod photoreceptors. Altogether, we found several crucial functions of T-type Ca 21 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 Ca 21 levels, and boost synaptic transmission.