Nitric oxide release is induced by dopamine during illumination of the carp retina: serial neurochemical control of light adaptation.
Several lines of indirect evidence have suggested that nitric oxide may play an important role during light adaptation of the vertebrate retina. We aimed to verify directly the effect of light on nitric oxide release in the isolated carp retina and to investigate the relationship between nitric oxide and dopamine, an established neuromodulator of retinal light adaptation. Using a biochemical nitric oxide assay, we found that steady or flicker light stimulation enhanced retinal nitric oxide production from a basal level. The metabotropic glutamate receptor agonist L-amino-4-phosphonobutyric acid, inhibited the light adaptation-induced nitric oxide production suggesting that the underlying cellular pathway involved centre-depolarizing bipolar cell activity. Application of exogenous dopamine to retinas in the dark significantly enhanced the basal production of nitric oxide and importantly, inhibition of endogenous dopaminergic activity completely suppressed the light-evoked nitric oxide release. The effect of dopamine was mediated through the D1 receptor subtype. Imaging of the nitric oxide-sensitive fluorescent indicator 4,5-diaminofluorescein di-acetate in retinal slices revealed that activation of D1 receptors resulted in nitric oxide production from two main spatial sources corresponding to the photoreceptor inner segment region and the inner nuclear layer. The results taken together would suggest that during the progression of retinal light adaptation there is a switch from dopaminergic to nitrergic control, probably to induce further neuromodulatory effects at higher levels of illumination and to enable more efficient spreading of the light adaptive signal.
Sekaran
S
S
Department of Visual Neuroscience, Faculty of Medicine, Imperial College London, Charing Cross Campus, W6 8RF, UK. s.sekaran@ic.ac.uk
Cunningham
J
J
Neal
M J
MJ
Hartell
N A
NA
Djamgoz
M B A
MB
D000221:Adaptation, Ocular / Q000502:physiology*; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002347:Carps; D003624:Darkness; D004298:Dopamine / Q000494:pharmacology*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004563:Electrochemistry / Q000379:methods; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019793:Fluorescein / Q000378:metabolism; D016257:Fura-2 / Q000378:metabolism; D007191:Indazoles / Q000494:pharmacology; D008029:Lighting; D016014:Linear Models; D009569:Nitric Oxide / Q000378:metabolism*; D010775:Photic Stimulation / Q000379:methods; D012160:Retina / Q000187:drug effects* / Q000378:metabolism / Q000528:radiation effects; D013997:Time Factors
C111205:4,5-diaminofluorescein; D002121:Calcium Channel Blockers; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D004791:Enzyme Inhibitors; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D007191:Indazoles; D009569:Nitric Oxide; D019793:Fluorescein; D016257:Fura-2; C080122:7-nitroindazole; D004298:Dopamine