| Summary: | (1) Background: High-tension glaucoma damages the peripheral vision dominated by rods. How mechanosensitive channels (MSCs) in the outer retina mediate pressure responses is unclear. (2) Methods: Immunocytochemistry, patch clamp, and channel fluorescence were used to study MSCs in salamander photoreceptors. (3) Results: Immunoreactivity of transient receptor potential channel vanilloid 4 (TRPV4) was revealed in the outer plexiform layer, K<sup>+</sup> channel TRAAK in the photoreceptor outer segment (OS), and TRPV2 in some rod OS disks. Pressure on the rod inner segment evoked sustained currents of three components: (A) the inward current at <−50 mV (<i>I</i><i><sub>pi</sub></i>), sensitive to Co<sup>2+</sup>; (B) leak outward current at ≥−80 mV (<i>I</i><i><sub>po</sub></i>), sensitive to intracellular Cs<sup>+</sup> and ruthenium red; and (C) cation current reversed at ~10 mV (<i>I</i><i><sub>pc</sub></i>). Hypotonicity induced slow currents like <i>I<sub>pc</sub></i>. Environmental pressure and light increased the FM 1-43-identified open MSCs in the OS membrane, while pressure on the OS with internal Cs<sup>+</sup> closed a Ca<sup>2+</sup>-dependent current reversed at ~0 mV. Rod photocurrents were thermosensitive and affected by MSC blockers. (4) Conclusions: Rods possess depolarizing (TRPV) and hyperpolarizing (K<sup>+</sup>) MSCs, which mediate mutually compensating currents between −50 mV and 10 mV, serve as an electrical cushion to minimize the impact of ocular mechanical stress.
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