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S. Thompson, E. L. Nylen, J. S. East, R. H. Kardon, L. H. Pinto, V. C. Sheffield, S. F. Stasheff, R. F. Mullins, E. M. Stone; Different Bipolar Cell Input Pathways for Negative Masking and the Pupil Light Reflex in Mice. Invest. Ophthalmol. Vis. Sci. 2010;51(13):669.
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© ARVO (1962-2015); The Authors (2016-present)
Separate from spatial vision, irradiance-coding circuits of the eye detect light to regulate many aspects of physiology and behavior. Despite the importance of this function of the eye, there is only limited understanding of the neuroethology of the different forms of irradiance coding circuit, and associated responses to light. The purpose of this study was to investigate bipolar cell pathways (BCs) mediating rod-cone photoreceptor input to functionally distinct irradiance responses.
The pupil light reflex and a behavioral response to light termed negative masking were measured in: C57BL/6J mice with intact rod-cone photoreceptor input, Nob4 mice with selective absence of rod-cone input via on-bipolar cells, and rd1 mice with no identifiable rod-cone input via on or off-BCs.
The sensitivity of the pupil light reflex was reduced in line with absent photoreceptor input, being more severely reduced in rd1 than Nob4 mice. As previously demonstrated, there was enhanced sensitivity of negative masking with loss of photoreceptor input in rd1. Unlike the pupil light reflex, the negative masking phenotype in Nob4 mice was identical to that seen in rd1.
Both on and off BCs mediate rod-cone input to the pupil light reflex. By contrast, the observed modulation of negative masking can be fully mediated by on-BCs. In context of the findings of others, we predict that retinal input to negative masking is via M1 melanopsin ganglion cells that receive on-BC input. If M1 melanopsin ganglion cells do not transmit substantial off-BC signals, the off-BC mediated input to the pupil light reflex is presumably via either M2 melanopsin ganglion cells, or by ganglion cells that project to the olivary pretectal nucleus but do not express melanopsin.
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