Interaction Of Red- And Green-sensitive Cone Signals In Luminosity-type Horizontal Cell Of Carp Retina

The role of presynaptic metabotropic glutamate receptor (mGluRs) on theinteraction of red- and green-cone signals was investigated in luminosity-typehorizontal cell (LHC) of isolated carp retina. In addition, confocal calcium imagingtechnique was used to examine the L-AP4 sensitive mGluRs related calcium signal insynaptic terminals of freshly dissociated cone photoreceptors. It was found that a dim red background could enhance LHC's light response togreen stimulus, and a dim green background was also able to increase the cell'sresponse to red flash. Such mutual color enhancement was eliminated by applicationof group II and group III mGluRs antagonist (S)-methyl-4-carboxyphenyl-glycine(MCPG). Furthermore, inhibition of glutamate uptake by using D-aspartate (D-Asp)or DL-threo-β-hydroxy-aspartic acid (THA) completely blocked the mutualenhancement of color signals in LHC. However, the GABAergic feedback pathway inthe outer retina was unnecessarily involved. Additionally, either destroyingdopaminergic interplexiform cells with 6-OHDA or superfusing the retina withdopamine had little effect on the interaction of red- and green-sensitive cone signals iii红绿敏视锥信号的相互作用in LHC. We hypothesize that glutamate spilt over from synaptic cleft may depress thetransmitter release through activation of mGluRs, presumably at the perisynapticregion of the cone terminals. This process provides a mechanism for sensingneighboring activity in neural circuits and fine adjustment of the efficacy of synaptictransmission, and for signaling the context of stimulation imposed on. The latter maybe responsible for the interaction of red- and green-cone signals in LHC. The calcium imaging experiments showed that application of glutamateeffectively decreased the [Ca2+]i of cone terminals. Also, the group III mGluRsspecific agonist L-AP4 remarkably reduced [Ca2+]i. The results suggested theexistence of L-AP4 sensitive mGluRs on cone terminals, the activation of whichcaused a drop of terminal [Ca2+]i and thus depressed the glutamate release from conephotoreceptors.