Photoreceptor damage and eye pigmentation: Influence on the sensitivity of rat pineal n-acetyltransferase activity and melatonin levels to light at night

Susan M. Webb, Thomas H. Champney, Andrzej K. Lewiński, Russel J. Reiter

Research output: Contribution to journalArticle

44 Scopus citations


The threshold of light irradiance capable of inhibiting nighttime pineal serotonin N-acetyltransferase (NAT) activity and melatonin content, and the importance of intact photoreceptors and eye pigmentation on these changes, were investigated in the rat. Groups of intact albino and black-eyed rats and albino animals with light-induced photoreceptor damage were studied in the dark period before, and after 15 and 30 min of exposure to either 0.0005, 0.175 or 3.33 µW/cm2 irradiance of light. In animals with photoreceptor damage, the sensitivity of the pineal gland to light decreased so that only the highest irradiance tested (3.33 µW/cm2) was capable of totally inhibiting pineal NAT activity and melatonin levels. In one study, pineal NAT and melatonin levels in intact albino rats were inhibited by all three irradiances studied. In a second experiment, albino and black-eyed animals behaved identically, only responding with a depression in pineal NAT and melatonin after exposure to light irradiances of either 0.175 or 3.33 µW/cm2. In conclusion, the lowest irradiance of cool white light capable of inhibiting pineal NAT and melatonin in albino rats is around 0.0005 µW/cm2. At the irradiances studied, photoreceptor damage influences the response of pineal NAT and melatonin to acute light exposure at night. On the other hand, eye pigmentation does not seem to have a major effect on the nighttime inhibition of the pineal by light.

Original languageEnglish (US)
Pages (from-to)205-209
Number of pages5
Issue number3
StatePublished - Jan 1 1985



  • Eye pigmentation
  • Melatonin
  • N-Acetyltransferase
  • Photoreceptor damage
  • Pineal gland
  • Rats
  • Sensitivity to light

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

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