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Author |
Berson, D.M.; Dunn, F.A.; Takao, M. |
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Title |
Phototransduction by retinal ganglion cells that set the circadian clock |
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Journal Article |
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Year |
2002 |
Publication |
Science (New York, N.Y.) |
Abbreviated Journal |
Science |
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Volume |
295 |
Issue |
5557 |
Pages |
1070-1073 |
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Keywords |
Human Health; Animals; Axons/ultrastructure; *Biological Clocks; *Circadian Rhythm; Dendrites/ultrastructure; Isoquinolines; Kinetics; Light; *Light Signal Transduction; Patch-Clamp Techniques; Rats; Rats, Sprague-Dawley; Retinal Ganglion Cells/chemistry/cytology/*physiology; Rod Opsins/analysis/physiology; Suprachiasmatic Nucleus/cytology/*physiology |
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Abstract |
Light synchronizes mammalian circadian rhythms with environmental time by modulating retinal input to the circadian pacemaker-the suprachiasmatic nucleus (SCN) of the hypothalamus. Such photic entrainment requires neither rods nor cones, the only known retinal photoreceptors. Here, we show that retinal ganglion cells innervating the SCN are intrinsically photosensitive. Unlike other ganglion cells, they depolarized in response to light even when all synaptic input from rods and cones was blocked. The sensitivity, spectral tuning, and slow kinetics of this light response matched those of the photic entrainment mechanism, suggesting that these ganglion cells may be the primary photoreceptors for this system. |
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Department of Neuroscience, Brown University, Providence, RI, 02912 USA. David_Berson@brown.edu |
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0036-8075 |
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PMID:11834835 |
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LoNNe @ kagoburian @ |
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720 |
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Author |
Blask, D.E.; Brainard, G.C.; Dauchy, R.T.; Hanifin, J.P.; Davidson, L.K.; Krause, J.A.; Sauer, L.A.; Rivera-Bermudez, M.A.; Dubocovich, M.L.; Jasser, S.A.; Lynch, D.T.; Rollag, M.D.; Zalatan, F. |
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Title |
Melatonin-depleted blood from premenopausal women exposed to light at night stimulates growth of human breast cancer xenografts in nude rats |
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Journal Article |
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Year |
2005 |
Publication |
Cancer Research |
Abbreviated Journal |
Cancer Res |
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Volume |
65 |
Issue |
23 |
Pages |
11174-11184 |
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Keywords |
Human Health; Animals; Breast Neoplasms/*blood/genetics/pathology; Cell Growth Processes/physiology; Circadian Rhythm/*physiology; Female; Humans; Light; Liver Neoplasms, Experimental/metabolism; Male; Melatonin/blood/*deficiency; Premenopause/blood; RNA, Messenger/biosynthesis/genetics; Rats; Rats, Nude; Receptors, Melatonin/biosynthesis/genetics; Transplantation, Heterologous |
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The increased breast cancer risk in female night shift workers has been postulated to result from the suppression of pineal melatonin production by exposure to light at night. Exposure of rats bearing rat hepatomas or human breast cancer xenografts to increasing intensities of white fluorescent light during each 12-hour dark phase (0-345 microW/cm2) resulted in a dose-dependent suppression of nocturnal melatonin blood levels and a stimulation of tumor growth and linoleic acid uptake/metabolism to the mitogenic molecule 13-hydroxyoctadecadienoic acid. Venous blood samples were collected from healthy, premenopausal female volunteers during either the daytime, nighttime, or nighttime following 90 minutes of ocular bright, white fluorescent light exposure at 580 microW/cm2 (i.e., 2,800 lx). Compared with tumors perfused with daytime-collected melatonin-deficient blood, human breast cancer xenografts and rat hepatomas perfused in situ, with nocturnal, physiologically melatonin-rich blood collected during the night, exhibited markedly suppressed proliferative activity and linoleic acid uptake/metabolism. Tumors perfused with melatonin-deficient blood collected following ocular exposure to light at night exhibited the daytime pattern of high tumor proliferative activity. These results are the first to show that the tumor growth response to exposure to light during darkness is intensity dependent and that the human nocturnal, circadian melatonin signal not only inhibits human breast cancer growth but that this effect is extinguished by short-term ocular exposure to bright, white light at night. These mechanistic studies are the first to provide a rational biological explanation for the increased breast cancer risk in female night shift workers. |
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Laboratory of Chrono-Neuroendocrine Oncology, Bassett Research Institute, The Mary Imogene Bassett Hospital, Cooperstown, New York 13326, USA. david.blask@bassett.org |
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0008-5472 |
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PMID:16322268 |
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LoNNe @ kagoburian @ |
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721 |
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Bukalev, A.V.; Vinogradova, I.A.; Zabezhinskii, M.A.; Semenchenko, A.V.; Anisimov, V.N. |
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Title |
Light pollution increases morbidity and mortality rate from different causes in female rats |
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Journal Article |
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2013 |
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Advances in Gerontology |
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Adv Gerontol |
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3 |
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3 |
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180-188 |
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light-at-night; spontaneous tumors; nontumor pathology epiphysis; rats; animals; mammals |
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The influence of different light regimes (constant light, LL; constant darkness, DD; standard light regime, LD, 12 hours light/12 hours darkness; and natural lighting of the northwest of Russia (NL) on non-tumor pathology revealed in the post-mortem examination of female rats has been studied. It was found that keeping 25-days-old animals under LL and NL conditions led to an increase in the number of infectious diseases and the substantially faster development of spontaneous tumors (2.9 and 3.3 diseases per one rat, respectively), variety of nontumor pathology found in dead rats, compared with the animals in standard (standard light) regime (1.72 diseases per one rat). Light deprivation (DD) led to a substantial reduction in the development of new growth, as well as nontumor and infectious diseases (1.06 diseases per one rat), compared to the same parameters in a standard light regime. |
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2079-0570 |
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IDA @ john @ |
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89 |
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Dauchy, Robert T; Dauchy, Erin M; Tirrell, Robert P; Hill, Cody R; Davidson, Leslie K; Greene, Michael W; Tirrell, Paul C; Wu, Jinghai; Sauer, Leonard A; Blask, David E |
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Title |
Dark-phase light contamination disrupts circadian rhythms in plasma measures of endocrine physiology and metabolism in rats |
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Journal Article |
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Year |
2010 |
Publication |
Comparative Medicine |
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60 |
Issue |
5 |
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348-356 |
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Keywords |
Animals; Chronobiology Disorders; Rats |
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Dark-phase light contamination can significantly disrupt chronobiologic rhythms, thereby potentially altering the endocrine physiology and metabolism of experimental animals and influencing the outcome of scientific investigations. We sought to determine whether exposure to low-level light contamination during the dark phase influenced the normally entrained circadian rhythms of various substances in plasma. Male Sprague-Dawley rats (n = 6 per group) were housed in photobiologic light-exposure chambers configured to create 1) a 12:12-h light:dark cycle without dark-phase light contamination (control condition; 123 μW/cm(2), lights on at 0600), 2) experimental exposure to a low level of light during the 12-h dark phase (with 0.02, 0.05, 0.06, or 0.08 μW/cm(2) light at night), or 3) constant bright light (123 μW/cm(2)). Dietary and water intakes were recorded daily. After 2 wk, rats underwent 6 low-volume blood draws at 4-h intervals (beginning at 0400) during both the light and dark phases. Circadian rhythms in dietary and water intake and levels of plasma total fatty acids and lipid fractions remained entrained during exposure to either control conditions or low-intensity light during the dark phase. However, these patterns were disrupted in rats exposed to constant bright light. Circadian patterns of plasma melatonin, glucose, lactic acid, and corticosterone were maintained in all rats except those exposed to constant bright light or the highest level of light during the dark phase. Therefore even minimal light contamination during the dark phase can disrupt normal circadian rhythms of endocrine metabolism and physiology and may alter the outcome of scientific investigations. |
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LoNNe @ schroer @ |
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1582 |
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Author |
Foster, R.G.; Hankins, M.W. |
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Title |
Circadian vision |
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Journal Article |
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Year |
2007 |
Publication |
Current Biology : CB |
Abbreviated Journal |
Curr Biol |
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17 |
Issue |
17 |
Pages |
R746-51 |
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Keywords |
Human Health; Animals; Circadian Rhythm/*physiology; Mice; Photoreceptor Cells, Vertebrate/*physiology; Rats; Rod Opsins/physiology; Vision, Ocular/*physiology |
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Department of Ophthalmology, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK. russell.foster@eye.ox.ac.uk |
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0960-9822 |
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PMID:17803920 |
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LoNNe @ kagoburian @ |
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751 |
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