Cabp4, also known as calcium-binding protein 4, is a neuronal Ca2+-binding protein. It participates in many cellular processes by regulating the concentration of free Ca2+ ions, and is essential for the development and maintenance of the photoreceptor synapse in the retina [2,3]. It may also be involved in the regulation of voltage-gated Ca(v)1 Ca(2+) channels [4].

In Cabp4 knockout mice, the thickness of the outer plexiform layer and the number of photoreceptor terminals were reduced. The amplitude and sensitivity of the b-wave in double Cabp4/rod alpha-transducin knockout (Cabp4(-/-)Gnat1(-/-)) mice, which lack the rod-mediated component of electrophysiologic responses, were severely attenuated, indicating severe disruption of cone synaptic function [3]. In addition, a missense mutation (p.G155D) in Cabp4 in mice led to an imbalance in protein expression in brain regions and an increase in the frequency of micro-excitatory post-synaptic currents in layer II/III cortical pyramidal cells, suggesting its role in seizure onset [1].

In conclusion, Cabp4 is crucial for signal transmission from rods and cones to second-order neurons in the retina. The gene knockout mouse models have revealed its important role in retinal function and provided insights into its potential involvement in epilepsy-related mechanisms [1,3].