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Transgenic mice expressing a dominant mutation in the gene for the phototransduction molecule rhodopsin undergo retinal degeneration similar to that experienced by patients with the retinal degenerative disease, retinitis pigmentosa (RP). Although the mutation is thought to cause photoreceptor degeneration in a cell-autonomous manner, the fact that rod photoreceptor degeneration is slowed in chimeric wild-type/mutant mice suggests that cellular interactions are also important for maintaining photoreceptor survival. To more fully characterize the nature of the cellular interactions important for rod degeneration in the RP mutant mice, we have used an in vitro approach. We found that when the retinas of the transgenic mice were isolated from the pigmented epithelium and cultured as explants, the rod photoreceptors underwent selective degeneration with a similar time course to that observed in vivo. This selective rod degeneration also occurred when the cells were dissociated and cultured as monolayers. These data indicate that the mutant rod photoreceptors degenerate when removed from their normal cellular relationships and without contact with the pigmented epithelium, thus confirming the relative cell autonomy of the mutant phenotype. We next tested whether normal retinal cells could rescue the mutant photoreceptors in a coculture paradigm. Coculture of transgenic mouse with wild-type mouse or rat retinal cells significantly enhanced transgenic rod photoreceptor survival; this survival-promoting activity was diffusible through a filter, was heat labile, and not present in transgenic retinal cells. Several peptide growth factors known to be present in the retina were tested as the potential survival-promoting molecule responsible for the effects of the conditioned medium; however, none of them promoted survival of the photoreceptors expressing the Pro23His mutant rhodopsin. Nevertheless, we were able to demonstrate that the mutant photoreceptors could be rescued by an antagonist to a retinoic acid receptor, suggesting that the endogeneous survival-promoting activity may function through this pathway. These data thus confirm and extend the findings of previous work that local trophic interactions are important in regulating rod photoreceptor degeneration in retinitis pigmentosa. A diffusible factor found in normal but not transgenic retinal cells has a protective effect on the survival of rod photoreceptors from Pro23His mutant rhodopsin mice.

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* BACKGROUND AND OBJECTIVE: Previous studies investigating the accuracy of digital palpation through the eyelids to estimate intraocular pressure (IOP) have shown disappointing results. In this study, the accuracy of digital assessment of IOP by palpation of the bare cornea is investigated. * MATERIALS AND METHODS: The IOP of a cadaveric eye model was varied from 5 to 40 mm Hg in increments of 5 mm Hg. Two examiners, one experienced and one inexperienced, digitally palpated the corneas and estimated IOP. The results were compared before and after a 1-hour training session. * RESULTS: Prior to the training session, the experienced examiner guessed correctly 46% of the time and was correct within 5 mm Hg 100% of the time. The inexperienced examiner guessed correctly 21% of the time and was within 5 mm Hg 62% of the time. After the training session, the experienced examiner's score did not significantly change, whereas the inexperienced examiner improved significantly (38% correct, 88% within 5 mm Hg, P = .05.) * CONCLUSIONS: Digital assessment of IOP by palpation of bare cornea is accurate when performed by experienced individuals. A minimal amount of training using the eye model may improve one's accuracy. [Ophthalmic Surg Lasers 1998;29:754-757.]