Publication Date
8-1-2025
Journal
American Journal of Physiology-Cell Physiology
DOI
10.1152/ajpcell.00028.2025
PMID
40549549
PMCID
PMC12515377
PubMedCentral® Posted Date
10-13-2025
PubMedCentral® Full Text Version
Author MSS
Abstract
Pannexin 1 (Panx1) forms large-pore, single-membrane channels that connect the intracellular and extracellular environments, permitting the passage of ions and small molecules such as ATP. Panx1 channels are involved in diverse signaling pathways that contribute to various physiological processes, including sensory processing, although their precise mechanisms of action remain incompletely understood. This study reveals a Panx1-mediated mechanism regulating visual signal processing in the amphibian retina. Using immunolabeling and confocal imaging, we localized Panx1 channels in the cone-dominated On-bipolar cells, specifically at both somas and axon terminals. Whole-cell patch-clamp recordings showed that these channels have high permeability to Cl⁻ ions, which can be blocked by 10Panx1 peptide, carbenoxolone, and mefloquine, all recognized as Panx1 inhibitors. Blocking Panx1 channels or reducing external Cl⁻ concentrations significantly increased bright light-induced delayed spontaneous excitatory responses in ganglion cells, indicating an inhibitory role of Panx1 channels at the bipolar cell synaptic release. These delayed spontaneous responses in ganglion cells, known as rebound currents, are associated with afterimage signals in the retina. Our findings suggest that Panx1 channels help prevent over-excitation associated with bright light-induced afterimage phenomena.
Keywords
Animals, Connexins, Retina, Retinal Bipolar Cells, Nerve Tissue Proteins, Retinal Ganglion Cells, Signal Transduction, Xenopus laevis, Pannexin, retina, bipolar cells, ganglion cells, afterimages
Published Open-Access
yes
Recommended Citation
Liu, Yufei; Libian, Nick; Jiang, Zheng; et al., "Contribution of Pannexin Channels to Afterimage Signals in the Amphibian Retina" (2025). Faculty and Staff Publications. 5525.
https://digitalcommons.library.tmc.edu/baylor_docs/5525