Purchase this article with an account.
Cameron Atkinson, Dao-Qi Zhang; Melanopsin mediates dopamine neuron light-evoked responses in rd1 retinas. Invest. Ophthalmol. Vis. Sci. 2013;54(15):301.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Dopamine released from retinal dopaminergic neurons plays an imperative role in a variety of retinal functions. We previously found that some dopamine neurons remain light-responsive in rd1 retinas although rods and most cones have degenerated (Zhang et al., 2008); the source of this activity is unclear. Our study aims to elucidate the origin of preserved dopamine neuron light responses in rd1 retinas and determine the underlying mechanisms of dopamine neurotransmission in retinal dystrophy.
We utilized an rd1 mouse in which dopamine neurons are transgenically labeled by RFP; these animals were used in combination with a knock-out mouse for melanopsin. Patch-clamp recordings were conducted on dopamine neurons presented with various light stimuli.
Approximately 2% of dopamine neurons were labeled by RFP in rd1 retinas; our recordings were made from this small proportion of the total cells. 30 out of 33 (~91%) rd1 dopamine cells tested were responsive to 375, 470, or 525 nm light. Conversely, in melanopsin knock-out rd1 retinas, 0 out of 19 (0%) cells tested were light-responsive. In addition, experiments were performed in rd1 mice across ages P40 to P182. Dopamine neuron light responses were found to strengthen with age in rd1 retinas; the younger mice had dopamine neuron light responses characterized by a long latency period (1.95 ± 0.12 s; n = 5) and low frequency (9.7 Hz; n = 5) whereas older mice exhibited short latency (0.94 ± 0.14 s; n = 5), high frequency (85.8 Hz; n = 5) responses.
The dopamine neuron light responses in rd1 retinas were mediated exclusively by melanopsin, not by surviving cones. In rd1 mice, the retina undergoes extensive remodeling during disease progression resulting in strengthened melanopsin neurotransmission to dopamine neurons.
This PDF is available to Subscribers Only