Adenosine is essential for energy metabolism and acts as a neuromodulator in the central nervous system. The retina is a highly energy-demanding neural tissue, and dysregulation of adenosine metabolism contributes to retinal diseases. Although adenosine pathways form extensive compensatory networks, the dynamics of ecto-5'-nucleotidase (CD73), a key enzyme for extracellular adenosine generation, remain elusive. Here, we map its spatiotemporal profile from development to adulthood using two transgenic mouse lines. We found that CD73 became expressed in the rod-photoreceptor lineage by postnatal day (P) 3 and appeared in the inner nuclear layer from P7 onward. Moreover, CD73 was transiently expressed in the astrocyte lineage between embryonic day 16.5 and P3 and the descendants accumulated in the retinal periphery. Functionally, CD73 deletion delayed rod-response recovery and shortened the implicit time in scotopic electroretinography under dim light. These findings suggest that physiological cues such as light and hypoxia may influence CD73 expression and retinal function. Our work lays the groundwork for investigating how genetic and environmental risk factors may alter adenosine metabolism in retinal diseases.
Ishii et al. (Wed,) studied this question.