Melatonin enhances horizontal cell sensitivity in salamander retina

Wiechmann, Allan F.; Yang, Xiaolong; Wu, Samuel M.; Hollyfield, Joe G.

doi:10.1016/0006-8993(88)90182-5

Cited by 90 publications

(54 citation statements)

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“…The impact of melatonin on tectal functioning is thus mediated in part by GABA C receptors, and the circadian periods when melatonin levels are high are predicted to be periods of high GABA C -mediated disinhibition within the tectum. However, melatonin also affects other components of the visual system that influence tectal function; as noted above, melatonin receptors directly affect retinal functioning (Brzezinski 1997;Wiechmann et al 1988), and our work in progress also shows that melatonin influences the responses of retinotectal axons (Prada and Udin, unpublished observations). Moreover, melatonin also affects calcium levels in the nucleus isthmi, a midbrain structure with reciprocal connections to the tectum (Gruberg and Udin 1978;R.…”

Section: Melatonin Modulation Of Gaba C -Receptor Function and Possibmentioning

confidence: 58%

“…Binding and molecular studies indicate that melatonin receptors undergo a daily rhythm of expression, increasing late during the light period and decreasing late during the dark period (Brooks and Cassone 1992;Wiechmann et al 1999). Melatonin is synthesized at night by retinal photoreceptors where it is involved in photoreceptor outer disc shedding and phagocytosis (White and Fisher 1989), photomechanical movements (Pierce and Besharse 1987), increases in sensitivity of horizontal cells (Wiechmann et al 1988), and changes in photoreceptor conductance (Brzezinski 1997). Melatonin also is synthesized at night in the pineal gland (Borjigin et al 1999;Reiter 1991), from which it is released into the cerebrospinal fluid and blood; it modulates functions such as circadian rhythms, sleep, seasonal reproduction, neuroimmunological activities, and avian seasonal neuroplasticity (Arendt 2000;Brzezinski 1997;Guerrero and Reiter 2002).…”

Section: Introductionmentioning

confidence: 99%

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Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABA_C Receptors

Prada

Udin²,

Wiechmann³

et al. 2005

Journal of Neurophysiology

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. To investigate the physiological effects of melatonin receptors in the Xenopus tectum, we have used the fluorescent indicator Fluo-4 AM to monitor calcium dynamics of cells in tectal slices. Bath application of KCl elicited fluorescence increases that were reduced by melatonin. This effect was stronger at the end of the light period than at the end of the dark period. Melatonin increased ␥-aminobutyric acid-C (GABA C )-receptor activity, as demonstrated by the ability of the GABA C -receptor antagonists, picrotoxin and TPMPA, to abolish the effects of melatonin. In contrast, neither the GABA A -receptor antagonist bicuculline nor the GABA B -receptor antagonist CGP 35348 diminished the effects of melatonin. RT-PCR analyses revealed expression of the 3 known melatonin receptors, MT1 (Mel1 a ), MT2 (Mel1 b ), and Mel1 c . Because the effect of melatonin on tectal calcium increases was antagonized by an MT2-selective antagonist, 4-P-PDOT, we performed Western blot analyses with an antibody to the MT2 receptor; the data indicate that the MT2 receptor is expressed primarily as a dimeric complex and is glycosylated. The receptor is present in higher amounts at the end of the light period than at the end of the dark period, in a pattern complementary to the changes in melatonin levels, which are higher during the night than during the day. These results imply that melatonin, acting by MT2 receptors, modulates GABA C receptor activity in the optic tectum and that this effect is influenced by the light-dark cycle.

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Section: Melatonin Modulation Of Gaba C -Receptor Function and Possibmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABA_C Receptors

Prada

Udin²,

Wiechmann³

et al. 2005

Journal of Neurophysiology

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“…Melatonin inhibits electrically stimulated and light-evoked release of ACh (Mitchell and Redburn, 1991), while dopamine stimulates ACh release (Hensler and Dubocovich, 1986). Melatonin enhances the sensitivity of horizontal cells (Wiechmann et al, 1988), and decreases the trans-epithelial potential of retinal pigment epithelial (RPE) cells and the c-wave of the electroretinogram (ERG) (Nao-I et al, 1989;Rudolf et al, 1992). Dopamine decreases the response of horizontal cells to full-field stimulation (Mange1 and Dowling, 1987) and increases the transepithelial potential of RPE cells and the c-wave amplitude (Gallemore and Steinberg, 1990;Rudolf et al, 1992).…”

mentioning

confidence: 99%

Functional interaction of melatonin receptors and D1 dopamine receptors in cultured chick retinal neurons

Iuvone

Gan

1995

J. Neurosci.

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The possible interaction of melatonin receptors and D1 dopamine receptors was investigated in neural cells prepared from embryonic day 8 chick retinas and cultured for 6 d. Dopamine stimulated cAMP accumulation in cultured retinal cells. This effect of dopamine was antagonized by addition of dopamine receptor antagonists (haloperidol and SCH23390) or melatonin receptor agonists (melatonin, 2- iodomelatonin, and 6-chloromelatonin). The inhibition of dopamine- stimulated cAMP accumulation by melatonin was concentration dependent, with half-maximal inhibition at approximately 160 pM. Melatonin inhibited the effect of dopamine at all dopamine concentrations, suppressing the maximal response to the neurotransmitter by approximately 70%. Melatonin also inhibited the stimulation of cAMP accumulation by SKF 82958, a selective D1 dopamine receptor agonist. Pretreatment of cultures with pertussis toxin had no significant effect on dopamine-stimulated cAMP accumulation, but inhibited the response to melatonin. In contrast to its effect on cAMP accumulation, melatonin had no effect on dopamine-stimulated inositol phosphate accumulation. These results suggest that melatonin receptors are coupled to dopamine receptor-regulated adenylate cyclase via an inhibitory G protein, and demonstrate another mechanism, in addition to inhibition of dopamine release, through which melatonin can modulate dopaminergic neurotransmission.

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“…Melatonin administration increases the degree of photoreceptor cell death in response to environmental light exposure, but is also involved in the regulation of necessary circadian events that occur in the retina, such as photoreceptor outer segment disk shedding and phagocytosis (Besharse and Dunis, 1983;White and Fisher, 1989), modulation of dopamine release (Dubocovich, 1983;Dubocovich and Takahashi, 1987), and increased sensitivity of the retina to light (Wiechmann et al, 1988(Wiechmann et al, , 2003. Melatonin also delays photoreceptor degeneration in a dystrophic animal model (Liang et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Melatonin may play an important role in dark adaptation; it alters the sensitivity of the central visual system to light (Reuss and Kiefer, 1989;Semm and Vollrath, 1982), and increases the sensitivity of horizontal cells to light in the salamander retina (Wiechmann et al, 1988). Melatonin, synthesized at night, may bind to receptors in the retina to increase the sensitivity of the visual system when photic input is low, and thus facilitate retinal dark adaptation by increasing horizontal cell coupling through inhibition of dopamine release (Krizaj and Witkovsky, 1993) and perhaps by stimulating the photoreceptors directly (Cosci et al, 1997, Wiechmann et al, 2003.…”

Section: Introductionmentioning

confidence: 99%

Influence of dietary melatonin on photoreceptor survival in the rat retina: An ocular toxicity study

Wiechmann

Chignell

Roberts

2008

Experimental Eye Research

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Previous studies have shown that melatonin treatment increases the susceptibility of retinal photoreceptors to light-induced cell death. The purpose of this study was to evaluate under various conditions the potential toxicity of dietary melatonin on retinal photoreceptors. Male and female Fischer 344 (non-pigmented) and Long-Evans (pigmented) rats were treated with daily single doses of melatonin by gavage for a period of 14 days early in the light period or early in the dark period. In another group, rats were treated 3 times per week with melatonin early in the light period, and then exposed to high intensity illumination (1,000 −1,500 lux; HII) for two hours, and then returned to the normal cyclic lighting regime. At the end of the treatment periods, morphometric measurements of outer nuclear layer thickness (ONL; the layer containing the photoreceptors cell nuclei) were made at specific loci throughout the retinas. In male and female non-pigmented Fischer rats, melatonin administration increased the degree of photoreceptor cell death when administered during the nighttime and during the day when followed by exposure to HII. There were some modest effects of melatonin on photoreceptor cell death when administered to Fisher rats during the day or night without exposure to HII. Melatonin treatment caused increases in the degree of photoreceptor cell death when administered in the night to male pigmented Long-Evans rats, but melatonin administration during the day, either with or without exposure to HII, had little if any effect on photoreceptor cell survival. In pigmented female Long Evans rats, melatonin administration did not appear to have significant effects on photoreceptor cell death in any treatment group. The results of this study confirm and extend previous reports that melatonin increases the susceptibility of photoreceptors to light-induced cell death in non-pigmented rats. It further suggests that during the dark period, melatonin administration alone (i.e., no HII exposure) to pigmented male rats may have a toxic effect on retinal cells. These results suggest that dietary melatonin, in combination with a brief exposure to high intensity illumination, induces cellular disruption in a small number of photoreceptors. Chronic exposure to natural or artificial light and simultaneous intake of melatonin may potentially contribute to a significant loss of photoreceptor cells in the aging retina.

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Melatonin enhances horizontal cell sensitivity in salamander retina

Cited by 90 publications

References 11 publications

Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABA_C Receptors

Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABA_C Receptors

Functional interaction of melatonin receptors and D1 dopamine receptors in cultured chick retinal neurons

Influence of dietary melatonin on photoreceptor survival in the rat retina: An ocular toxicity study

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Melatonin enhances horizontal cell sensitivity in salamander retina

Cited by 90 publications

References 11 publications

Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABAC Receptors

Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABAC Receptors

Functional interaction of melatonin receptors and D1 dopamine receptors in cultured chick retinal neurons

Influence of dietary melatonin on photoreceptor survival in the rat retina: An ocular toxicity study

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Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABA_C Receptors

Stimulation of Melatonin Receptors Decreases Calcium Levels in Xenopus Tectal Cells by Activating GABA_C Receptors