L-type CaV1 channels transduce membrane excitability into dynamic Ca2+signals, such as autonomous Ca2+ oscillations, which regulate gene transcription in the nucleus critical to neurite outgrowth. Such signaling axis is defined as the coupling between CaV1 activity or Ca2+ oscillation and neurite outgrowth (i.e., CaV1-neuritogenesis coupling). In cortical neurons, stand-alone CaV1-encoded DCT (distal C-terminus) peptides are unveiled to inhibit the CaV1-neuritogenesis coupling, in contrast to the documented role of DCT as nuclear transcription factors to promote neurite outgrowth. When present in the cytosol, DCT peptides downregulate CaV1 activity, Ca2+ influx, pCREB, c-Fos, etc. Importantly, the potency of inhibition is tightly correlated with the affinity of DCT binding CaV1, quantitatively demonstrated by a series of DCT peptides of native origins (Yang 2022 Communications Biology). Autonomous Ca2+ oscillations play key roles in neural development. Specific CaV1 antagonists including DCT peptides are able to abolish oscillations, leading to their effects on neuritogenesis. Aiming at the Ca2+ oscillation-neuritogenesis coupling, with neuron-compatible GCaMP-X that our lab recently developed, we have achieved chronic GCaMP-X imaging which overcomes the toxicity of long/high expression known to conventional GCaMP. Chronic GCaMP-X imaging (∼1 month) of virus-infected cortical neurons recapitulated the tight correlation between spontaneous Ca2+ activity and neuronal development/health with quantitative insights. In support, in vivo imaging from whisker responses and spontaneous Ca2+ slow waves in live mice also demonstrated that GCaMP-X causing less toxicity outperformed GCaMP (Geng 2022 eLife).In summary, the CaV1 activity/Ca2+ oscillation-neuritogenesis coupling and its regulations/perturbations have been examined in vitro and in vivo by DCT peptides and GCaMP-X probes (versus GCaMP), both of which are expected to promote methodology development as well as mechanistic understanding.