Carbachol-induced pigment granule dispersion
The retinal pigment epithelium (RPE) is a monolayer of pigmented, simple cuboidal epithelium with long apical processes that interdigitate with photoreceptors. In teleosts, the RPE aids in light adaptation through pigment granule movements. In the bright light, pigment granules are dispersed into the long apical processes thereby shielding rods from excessive light. The opposite occurs in dark conditions; pigment granules are aggregated into the cell body of the RPE allowing the maximal exposure of the rods to incoming light. Using isolated bluegill (Lepomis macrochirus) RPE, I examined the effects that carbachol and acetylcholine analog, has on pigment granule dispersion in a dose-dependent manner, and the maximum effects of carbachol were observed at concentrations as low as 10 nM. Atropine was highly effective in blocking carbachol-induced dispersion. The role of specific muscarinic receptor subtypes (Ml-M3) in mediating carbachol-induced dispersion was investigated. The M1 and M3 blockers pirenzepine and 4-DAMP, respectively, were effective in blocking carbachol-induced dispersion. The M2 antagonist, AFDX-116, did not block carbachol-induced dispersion. Consistent with these results, the M1 agonist, 4-chlorophenyl stimulated pigment granule dispersion, while arecaidine, an M2 agonist, did not. I conclude that carbachol-induced pigment granule dispersion is mediated via M1 and M3 but not M2 subtypes of the muscarinic receptor family.
rhodopsin, bluegill, epithelium, muscarinic receptors, dispersion
González, A. (2000). Carbachol-induced pigment granule dispersion (Unpublished thesis). Southwest Texas State University, San Marcos, Texas.