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J Physiol Volume 569, Number 3, 857-871, December 15, 2005 DOI: 10.1113/jphysiol.2005.098798
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Modulation by melatonin of glutamatergic synaptic transmission in the carp retina

Hai Huang1,2, Shu-Chen Lee1 and Xiong-Li Yang1

1 Institute of Neurobiology, Institutes of Brain Science, Fudan University, 220 Handan Road, Shanghai, 200433, China
2 Shanghai Institutes for Biological Sciences and Graduate School, Chinese Academy of Sciences, 320 Yueyang Road, Shanghai, 200031, China

Melatonin is involved in a variety of physiological functions through activating specific receptors coupled to GTP-binding protein. Melatonin and its receptors are abundant in the retina. Here we show for the first time that melatonin modulates glutamatergic synaptic transmission from cones to horizontal cells (HCs) in carp retina. Immunocytochemical data revealed the expression of the MT1 receptor on carp HCs. Whole-cell recordings further showed that melatonin of physiological concentrations potentiated glutamate-induced currents from isolated cone-driven HCs (H1 cells) in a dose-dependent manner, by increasing the efficacy and apparent affinity of the glutamate receptor. The effects of melatonin were reversed by luzindole, but not by K 185, indicating the involvement of the MT1 receptor. Like melatonin, methylene blue (MB), a guanylate cyclase inhibitor, also potentiated the glutamate currents, but internal infusion of cGMP suppressed them. The effects of melatonin were not observed in cGMP-filled and MB-incubated HCs. These results suggest that the melatonin effects may be mediated by decreasing the intracellular concentration of cGMP. Consistent with these observations, melatonin depolarized the membrane potential of H1 cells and reduced their light responses, which could also be blocked by luzindole. These effects of melatonin persisted in the presence of the antagonists of receptors for dopamine, GABA and glycine, indicating a direct action of melatonin on H1 cells. Such modulation by melatonin of glutamatergic transmission from cones to HCs is thought to be in part responsible for circadian changes in light responsiveness of cone HCs in teleost retina.

(Received 14 September 2005; accepted after revision 18 October 2005; first published online 20 October 2005)
Corresponding author X.-L. Yang: Institute of Neurobiology, Fudan University, 220 Handan Road, Shanghai, 200433, China. Email: xlyang{at}fudan.edu.cn







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