Red-light-induced suppression of melatonin synthesis is mediated by N- methyl-D-aspartate receptor activation in retinally normal and retinally degenerate rats

B. H. Poeggeler, L. R. Barlow-Walden, Russel J Reiter, S. Saarela, A. Menendez-Pelaez, K. Yaga, L. C. Manchester, L. D. Chen, D. X. Tan

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Pineal gland N-acetyltransferase (NAT) activity and pineal and serum levels of melatonin declined linearly in albino rats acutely exposed to different intensities of red light (600 nm or higher; low, 140 Ω/cm2; moderate, 690 μW/cm2; high, 1200 μW/cm2) during the middle of the night. The high intensity red light was as effective as white light (780 μW/cm2) in suppressing NAT activity and pineal and circulating melatonin. Red-light- inhibited nighttime NAT activity and suppressed nocturnal melatonin levels in both retinally degenerate and normal rats. Pretreatment with the N-methyl-D- aspartate (NMDA) receptor antagonist MK-801 (10 mg/kg intraperitoneally) completely prevented the red-light-induced inhibition of nighttime melatonin synthesis. Magnesium chloride (300 mg/kg intraperitoneally) reduced the inhibitory effects of low and moderate intensities of red light but was ineffective when high red-light intensity was used. However, both agents failed to antagonize the suppression of nighttime melatonin synthesis elicited by the exposure to white light. Since retinally degenerate and retinally normal animals respond in the same way to both red-light and pharmacological intervention with the NMDA receptor blocker MK-801, the findings indicate that the activation of central hypothalamic NMDA receptors might mediate the photic inhibition of nocturnal melatonin synthesis in the pineal gland elicited by the exposure to red light at night. Red-light- induced suppression of nocturnal melatonin synthesis possibly can be used to investigate the biochemical mechanisms by which light entrains melatonin synthesis and to study the pharmacological and physiological effects of endogenous and synthetic agents that antagonize the NMDA receptor response.

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalJournal of Neurobiology
Volume28
Issue number1
DOIs
StatePublished - 1995

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Melatonin
N-Methyl-D-Aspartate Receptors
Light
Acetyltransferases
Pineal Gland
Dizocilpine Maleate
Pharmacology
Magnesium Chloride

Keywords

  • melatonin
  • N-acetyltransferase activity
  • NMDA receptor
  • pineal gland
  • retina

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Red-light-induced suppression of melatonin synthesis is mediated by N- methyl-D-aspartate receptor activation in retinally normal and retinally degenerate rats. / Poeggeler, B. H.; Barlow-Walden, L. R.; Reiter, Russel J; Saarela, S.; Menendez-Pelaez, A.; Yaga, K.; Manchester, L. C.; Chen, L. D.; Tan, D. X.

In: Journal of Neurobiology, Vol. 28, No. 1, 1995, p. 1-8.

Research output: Contribution to journalArticle

Poeggeler, B. H. ; Barlow-Walden, L. R. ; Reiter, Russel J ; Saarela, S. ; Menendez-Pelaez, A. ; Yaga, K. ; Manchester, L. C. ; Chen, L. D. ; Tan, D. X. / Red-light-induced suppression of melatonin synthesis is mediated by N- methyl-D-aspartate receptor activation in retinally normal and retinally degenerate rats. In: Journal of Neurobiology. 1995 ; Vol. 28, No. 1. pp. 1-8.
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abstract = "Pineal gland N-acetyltransferase (NAT) activity and pineal and serum levels of melatonin declined linearly in albino rats acutely exposed to different intensities of red light (600 nm or higher; low, 140 Ω/cm2; moderate, 690 μW/cm2; high, 1200 μW/cm2) during the middle of the night. The high intensity red light was as effective as white light (780 μW/cm2) in suppressing NAT activity and pineal and circulating melatonin. Red-light- inhibited nighttime NAT activity and suppressed nocturnal melatonin levels in both retinally degenerate and normal rats. Pretreatment with the N-methyl-D- aspartate (NMDA) receptor antagonist MK-801 (10 mg/kg intraperitoneally) completely prevented the red-light-induced inhibition of nighttime melatonin synthesis. Magnesium chloride (300 mg/kg intraperitoneally) reduced the inhibitory effects of low and moderate intensities of red light but was ineffective when high red-light intensity was used. However, both agents failed to antagonize the suppression of nighttime melatonin synthesis elicited by the exposure to white light. Since retinally degenerate and retinally normal animals respond in the same way to both red-light and pharmacological intervention with the NMDA receptor blocker MK-801, the findings indicate that the activation of central hypothalamic NMDA receptors might mediate the photic inhibition of nocturnal melatonin synthesis in the pineal gland elicited by the exposure to red light at night. Red-light- induced suppression of nocturnal melatonin synthesis possibly can be used to investigate the biochemical mechanisms by which light entrains melatonin synthesis and to study the pharmacological and physiological effects of endogenous and synthetic agents that antagonize the NMDA receptor response.",
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AB - Pineal gland N-acetyltransferase (NAT) activity and pineal and serum levels of melatonin declined linearly in albino rats acutely exposed to different intensities of red light (600 nm or higher; low, 140 Ω/cm2; moderate, 690 μW/cm2; high, 1200 μW/cm2) during the middle of the night. The high intensity red light was as effective as white light (780 μW/cm2) in suppressing NAT activity and pineal and circulating melatonin. Red-light- inhibited nighttime NAT activity and suppressed nocturnal melatonin levels in both retinally degenerate and normal rats. Pretreatment with the N-methyl-D- aspartate (NMDA) receptor antagonist MK-801 (10 mg/kg intraperitoneally) completely prevented the red-light-induced inhibition of nighttime melatonin synthesis. Magnesium chloride (300 mg/kg intraperitoneally) reduced the inhibitory effects of low and moderate intensities of red light but was ineffective when high red-light intensity was used. However, both agents failed to antagonize the suppression of nighttime melatonin synthesis elicited by the exposure to white light. Since retinally degenerate and retinally normal animals respond in the same way to both red-light and pharmacological intervention with the NMDA receptor blocker MK-801, the findings indicate that the activation of central hypothalamic NMDA receptors might mediate the photic inhibition of nocturnal melatonin synthesis in the pineal gland elicited by the exposure to red light at night. Red-light- induced suppression of nocturnal melatonin synthesis possibly can be used to investigate the biochemical mechanisms by which light entrains melatonin synthesis and to study the pharmacological and physiological effects of endogenous and synthetic agents that antagonize the NMDA receptor response.

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