Light-adaptive effects of retinoic acid on receptive field properties of retinal horizontal cells.
Besides its role in ocular development, retinoic acid (RA), which is a light-correlated byproduct of the phototransduction cycle, was recently shown to affect light-driven synaptic plasticity in the outer plexiform layer of the adult fish retina. Tuning by ambient light conditions of the retinal network properties is very prominent in outer plexiform layer circuits, and we therefore examined whether RA could affect cone horizontal cell physiology similar to ambient light. Performing intracellular recordings and dye injections in the dark-adapted inverted eyecup preparation of the carp, we found that RA reduced the receptive fields of horizontal cell somata and impaired gap junctional communication. This action was not observed among coupled axon terminals of horizontal cells and appeared to be stereospecific because it could only be attributed to all-trans and 13-cis RA but not to the 9-cis isomer and photoisomerized all-trans RA. Modulation of receptive field size occurred independently of the dopaminergic system. Furthermore, RA affected the light responsiveness of cone horizontal cells. Compared to the dark-adapted condition, responsiveness to intense light stimulation was enhanced but decreased when low intensities were used. Moreover, following RA treatment H2-type horizontal cells of dark-adapted retinae which do not give rise to colour-opponent light properties became colour-opponent and performed depolarizing responses to long-wavelength stimulation. In all these cases RA perfectly matched the effects of light adaptation, supporting the notion that RA acts as an endogenous neuromodulator.
Pottek
M
M
Neurobiology FB 7, University of Oldenburg, 26111 Oldenburg, Germany.
Weiler
R
R
D000080462:Acyclic Monoterpenes; D000222:Adaptation, Physiological / Q000187:drug effects*; D000445:Aldehyde Oxidoreductases / Q000037:antagonists & inhibitors; D000077556:Alitretinoin; D000818:Animals; D004298:Dopamine / Q000502:physiology; D005136:Eye Proteins / Q000037:antagonists & inhibitors; D017629:Gap Junctions / Q000502:physiology; D006054:Goldfish; D008027:Light; D039821:Monoterpenes; D009473:Neuronal Plasticity / Q000187:drug effects* / Q000528:radiation effects; D012160:Retina / Q000166:cytology / Q000187:drug effects* / Q000528:radiation effects; D050697:Retinal Dehydrogenase; D012243:Rhodopsin / Q000378:metabolism; D013729:Terpenes / Q000494:pharmacology; D014212:Tretinoin / Q000378:metabolism / Q000494:pharmacology*
D000080462:Acyclic Monoterpenes; D005136:Eye Proteins; D039821:Monoterpenes; D013729:Terpenes; D000077556:Alitretinoin; D014212:Tretinoin; D012243:Rhodopsin; D000445:Aldehyde Oxidoreductases; D050697:Retinal Dehydrogenase; C007076:citral; D004298:Dopamine