Cplx4, or Complexin 4, is a SNARE regulator that plays a crucial role in regulating the speed and Ca(2+) sensitivity of SNARE-mediated synaptic vesicle fusion, especially at retinal ribbon synapses [2,3,4]. It is involved in the visual information processing pathway, contributing to the overall function of the retina [1,2,4]. Genetic models, such as knockout mouse models, are valuable tools for studying its function.

Studies on Cplx3 and Cplx4 single-and double-knockout mice have revealed significant impacts on retinal function and structure. In the retinae of Cplx3 and Cplx4 double-knockout mice, there was a disorganized outer plexiform layer, with a significant proportion of photoreceptor terminals containing spherical free-floating ribbons. This led to aberrant adjustment and fine-tuning of transmitter release at the photoreceptor ribbon synapse, alterations in transmission at bipolar cell terminals, changes in the temporal structure of synaptic processing in the inner plexiform layer of the retina, and perturbed vision [2]. The loss of Cplx3 and Cplx4 also differentially impacted the ON and OFF pathways in the mouse retina. Under photopic conditions, the cone ON pathway responses were diminished, while under scotopic conditions, both ON and OFF response rates were reduced and high-sensitivity OFF responses were missing [5].

In conclusion, Cplx4 is essential for the normal function of retinal ribbon synapses, playing a role in maintaining the structure and function of the retina and the proper transmission of visual signals. The study of Cplx4 knockout mouse models has provided valuable insights into its role in vision-related processes, contributing to our understanding of how disruptions in this gene can lead to visual deficits.