Adrenal-mediated depression of N-acetyltransferase activity and melatonin levels in the rat pineal gland |
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| Authors: | B N Joshi M E Troiani J Milin F Nürnburger R J Reiter |
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| Affiliation: | 3. Welbio and the Laboratory of Physiological Chemistry, Université Catholique de Louvain, 1200 Brussels, Belgium;4. Ludwig Institute for Cancer Research, Université Catholique de Louvain, 1200 Brussels, Belgium;5. Protein Phosphorylation Unit, de Duve Institute, Université Catholique de Louvain, 1200 Brussels, Belgium;1. Meyer Cancer Center, Department of Medicine, Weill Cornell Medical College, New York City, NY 10065, USA;1. Human Genetics Center, University of Texas Health Science Center, Houston, TX 77030, USA;2. Center for Precision Health, School of Biomedical Informatics, University of Texas Health Science Center at Houston, Houston, TX 77030, USA;3. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, USA;4. Institute for Minority Health Research, University of Illinois College of Medicine, Chicago, IL 60612, USA;5. Department of Biostatistics, University of North Carolina Gilling School of Global Public Health, Chapel Hill, NC 27599, USA;6. Department of Epidemiology, University of North Carolina Gilling School of Global Public Health, Chapel Hill, NC 27599, USA;7. Carolina Center of Genome Sciences, University of North Carolina, Chapel Hill, NC 27514, USA;8. Department of Biostatistics, University of Washington, Seattle, WA 98195, USA;9. Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA |
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| Abstract: | N-acetyltransferase (NAT) is believed to be the rate-limiting enzyme in the synthesis of melatonin from serotonin in the pineal gland. Norepinephrine released from sympathetic nerve endings within the pineal gland stimulates NAT activity and, therefore, melatonin synthesis. When an animal is subjected to a stressful stimulus, it would be expected that the increase in plasma stimulus, it would be expected that the increase in plasma catecholamines originating from the adrenal medulla and/or the sympathetic nervous system would result in a stimulation of pineal NAT activity. Adult male rats were given a 1.5cc injection of physiological saline subcutaneously into the back leg. Compared to non-injected controls, animals stressed in this manner were shown to have significantly lower pineal melatonin content 10 min after the saline injection late in the light phase of the light/dark cycle (at 18.30 h-lights on at 07.00 h). To test this more thoroughly, a time course study was conducted during the dark phase (at 02.00 h-5 hours after lights out) when pineal NAT activity and melatonin levels are either increasing or elevated. NAT activity and melatonin levels in the pineal were significantly depressed in stressed animals as compared to controls by 10 min after the saline injection, and remained so until 60 min after injection. By 90 min they had returned to control values. In the next study the nighttime response of the pineal to stress was compared in intact and adrenalectomized rats. Adrenalectomy prevented the changes in NAT activity and melatonin content associated with the saline injection. Some factor, such as a catecholamine or corticosterone from the adrenal, seems to be eliciting the response in the pineal to the saline injection. It is not known if the factor is acting centrally or directly on the pineal gland. |
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