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Author (up) Bedrosian, T.A.; Vaughn, C.A.; Galan, A.; Daye, G.; Weil, Z.M.; Nelson, R.J.
Title Nocturnal light exposure impairs affective responses in a wavelength-dependent manner Type Journal Article
Year 2013 Publication The Journal of Neuroscience : the Official Journal of the Society for Neuroscience Abbreviated Journal J Neurosci
Volume 33 Issue 32 Pages 13081-13087
Keywords Analysis of Variance; Animals; Circadian Rhythm/*physiology; Cricetinae; Dose-Response Relationship, Radiation; Female; Food Deprivation/physiology; Food Preferences/physiology/radiation effects; Fourier Analysis; Gene Expression Regulation/radiation effects; Hippocampus/pathology/radiation effects; Immobility Response, Tonic/radiation effects; Light/*adverse effects; Mood Disorders/*etiology/pathology; Motor Activity/physiology/radiation effects; Phodopus; Proto-Oncogene Proteins c-fos/metabolism; Social Behavior; Suprachiasmatic Nucleus/metabolism; Time Factors
Abstract Life on earth is entrained to a 24 h solar cycle that synchronizes circadian rhythms in physiology and behavior; light is the most potent entraining cue. In mammals, light is detected by (1) rods and cones, which mediate visual function, and (2) intrinsically photosensitive retinal ganglion cells (ipRGCs), which primarily project to the suprachiasmatic nucleus (SCN) in the hypothalamus to regulate circadian rhythms. Recent evidence, however, demonstrates that ipRGCs also project to limbic brain regions, suggesting that, through this pathway, light may have a role in cognition and mood. Therefore, it follows that unnatural exposure to light may have negative consequences for mood or behavior. Modern environmental lighting conditions have led to excessive exposure to light at night (LAN), and particularly to blue wavelength lights. We hypothesized that nocturnal light exposure (i.e., dim LAN) would induce depressive responses and alter neuronal structure in hamsters (Phodopus sungorus). If this effect is mediated by ipRGCs, which have reduced sensitivity to red wavelength light, then we predicted that red LAN would have limited effects on brain and behavior compared with shorter wavelengths. Additionally, red LAN would not induce c-Fos activation in the SCN. Our results demonstrate that exposure to LAN influences behavior and neuronal plasticity and that this effect is likely mediated by ipRGCs. Modern sources of LAN that contain blue wavelengths may be particularly disruptive to the circadian system, potentially contributing to altered mood regulation.
Address Department of Neuroscience, Ohio State University Wexner Medical Center, Columbus, Ohio 43210, USA. Bedrosian.2@osu.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0270-6474 ISBN Medium
Area Expedition Conference
Notes PMID:23926261 Approved no
Call Number IDA @ john @ Serial 27
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Author (up) Bedrosian, T.A.; Weil, Z.M.; Nelson, R.J.
Title Chronic dim light at night provokes reversible depression-like phenotype: possible role for TNF Type Journal Article
Year 2013 Publication Molecular Psychiatry Abbreviated Journal
Volume 18 Issue Pages 930-936
Keywords Animals
Abstract The prevalence of major depression has increased in recent decades and women are twice as likely as men to develop the disorder. Recent environmental changes almost certainly have a role in this phenomenon, but a complete set of contributors remains unspecified. Exposure to artificial light at night (LAN) has surged in prevalence during the past 50 years, coinciding with rising rates of depression. Chronic exposure to LAN is linked to increased risk of breast cancer, obesity and mood disorders, although the relationship to mood is not well characterized. In this study, we investigated the effects of chronic exposure to 5 lux LAN on depression-like behaviors in female hamsters. Using this model, we also characterized hippocampal brain-derived neurotrophic factor expression and hippocampal dendritic morphology, and investigated the reversibility of these changes 1, 2 or 4 weeks following elimination of LAN. Furthermore, we explored the mechanism of action, focusing on hippocampal proinflammatory cytokines given their dual role in synaptic plasticity and the pathogenesis of depression. Using reverse transcription-quantitative PCR, we identified a reversible increase in hippocampal tumor necrosis factor (TNF), but not interleukin-1β, mRNA expression in hamsters exposed to LAN. Direct intracerebroventricular infusion of a dominant-negative inhibitor of soluble TNF, XPro1595, prevented the development of depression-like behavior under LAN, but had no effect on dendritic spine density in the hippocampus. These results indicate a partial role for TNF in the reversible depression-like phenotype observed under chronic dim LAN. Recent environmental changes, such as LAN exposure, may warrant more attention as possible contributors to rising rates of mood disorders.
Address
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Notes Approved no
Call Number LoNNe @ christopher.kyba @ Serial 386
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Author (up) Fonken, L.K.; Aubrecht, T.G.; Melendez-Fernandez, O.H.; Weil, Z.M.; Nelson, R.J.
Title Dim light at night disrupts molecular circadian rhythms and increases body weight Type Journal Article
Year 2013 Publication Journal of Biological Rhythms Abbreviated Journal J Biol Rhythms
Volume 28 Issue 4 Pages 262-271
Keywords Animals; Blood Glucose/metabolism; Body Weight/*physiology; CLOCK Proteins/biosynthesis/genetics; Circadian Rhythm/*physiology; Corticosterone/metabolism; Feeding Behavior/physiology; Immunohistochemistry; Light; *Lighting; Male; Mice; Motor Activity; Polymerase Chain Reaction; Suprachiasmatic Nucleus/metabolism/physiology; clock genes; feeding rhythm; light pollution; obesity
Abstract With the exception of high latitudes, life has evolved under bright days and dark nights. Most organisms have developed endogenously driven circadian rhythms that are synchronized to this daily light/dark cycle. In recent years, humans have shifted away from the naturally occurring solar light cycle in favor of artificial and sometimes irregular light schedules produced by electric lighting. Exposure to unnatural light cycles is increasingly associated with obesity and metabolic syndrome; however, the means by which environmental lighting alters metabolism are poorly understood. Thus, we exposed mice to dim light at night and investigated changes in the circadian system and metabolism. Here we report that exposure to ecologically relevant levels of dim (5 lux) light at night altered core circadian clock rhythms in the hypothalamus at both the gene and protein level. Circadian rhythms in clock expression persisted during light at night; however, the amplitude of Per1 and Per2 rhythms was attenuated in the hypothalamus. Circadian oscillations were also altered in peripheral tissues critical for metabolic regulation. Exposure to dimly illuminated, as compared to dark, nights decreased the rhythmic expression in all but one of the core circadian clock genes assessed in the liver. Additionally, mice exposed to dim light at night attenuated Rev-Erb expression in the liver and adipose tissue. Changes in the circadian clock were associated with temporal alterations in feeding behavior and increased weight gain. These results are significant because they provide evidence that mild changes in environmental lighting can alter circadian and metabolic function. Detailed analysis of temporal changes induced by nighttime light exposure may provide insight into the onset and progression of obesity and metabolic syndrome, as well as other disorders involving sleep and circadian rhythm disruption.
Address Department of Neuroscience and Institute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA. fonken.1@osu.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0748-7304 ISBN Medium
Area Expedition Conference
Notes PMID:23929553; PMCID:PMC4033305 Approved no
Call Number IDA @ john @ Serial 28
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Author (up) Fonken, L.K.; Bedrosian, T.A.; Zhang, N.; Weil, Z.M.; DeVries, A.C.; Nelson, R.J.
Title Dim light at night impairs recovery from global cerebral ischemia Type Journal Article
Year 2019 Publication Experimental Neurology Abbreviated Journal Exp Neurol
Volume 317 Issue Pages 100-109
Keywords Animals; mouse models; cerebral ischemia
Abstract Nighttime lighting is one of the great conveniences of modernization; however, there is mounting evidence that inopportune light exposure can disrupt physiological and behavioral functions. Hospital patients may be particularly vulnerable to the consequences of light at night due to their compromised physiological state. Cardiac arrest/cardiopulmonary resuscitation (CA) was used to test the hypothesis in mice that exposure to dim light at night impairs central nervous system (CNS) recovery from a major pathological insult. Mice exposed to dim light at night (5lx) had higher mortality in the week following cardiac arrest compared to mice housed in dark nights (0lx). Neuronal damage was significantly greater in surviving mice exposed to dim light at night after CA versus those housed in dark nights. Dim light at night may have elevated neuronal damage by amplifying pro-inflammatory pathways in the CNS; Iba1 immunoreactivity (an indication of microglia activation) and pro-inflammatory cytokine expression were elevated in mice exposed to dim light at night post-CA. Furthermore, selective inhibition of IL-1beta or TNFalpha ameliorated damage in mice exposed to dim light at night. The effects of light at night on CA outcomes were also prevented by using a wavelength of nighttime light that has minimal impact on the endogenous circadian clock, suggesting that replacing broad-spectrum nighttime light with specific circadian-inert wavelengths could be protective. Together, these data indicate that exposure to dim light at night after global cerebral ischemia increases neuroinflammation, in turn exacerbating neurological damage and potential for mortality.
Address Department of Neuroscience, Wexner Medical Center, The Ohio State University, Columbus, OH 43210, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0014-4886 ISBN Medium
Area Expedition Conference
Notes PMID:30822422 Approved no
Call Number GFZ @ kyba @ Serial 2235
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Author (up) Fonken, L.K.; Finy, M.S.; Walton, J.C.; Weil, Z.M.; Workman, J.L.; Ross, J.; Nelson, R.J.
Title Influence of light at night on murine anxiety- and depressive-like responses Type Journal Article
Year 2009 Publication Behavioural Brain Research Abbreviated Journal Behav Brain Res
Volume 205 Issue 2 Pages 349-354
Keywords Human Health; Animals; Anxiety/*physiopathology; Corticosterone/blood; Depression/*physiopathology; Dietary Sucrose/administration & dosage; Drinking Behavior/physiology; Light/*adverse effects; Lighting; Locomotion/physiology; Male; Maze Learning; Mice; Neuropsychological Tests; Organ Size; Photic Stimulation; *Photoperiod; Random Allocation; Swimming; Testis/pathology
Abstract Individuals are increasingly exposed to light at night. Exposure to constant light (LL) disrupts circadian rhythms of locomotor activity, body temperature, hormones, and the sleep-wake cycle in animals. Other behavioural responses to LL have been reported, but are inconsistent. The present experiment sought to determine whether LL produces changes in affective responses and whether behavioural changes are mediated by alterations in glucocorticoid concentrations. Relative to conspecifics maintained in a light/dark cycle (LD, 16:8 light/dark), male Swiss-Webster mice exposed to LL for three weeks increased depressive-like behavioural responses as evaluated by the forced swim test and sucrose anhedonia. Furthermore, providing a light escape tube reversed the effects of LL in the forced swim test. LL mice displayed reduced anxiety as evaluated by the open field and elevated-plus maze. Glucocorticoid concentrations were reduced in the LL group suggesting that the affective behavioural responses to LL are not the result of elevated corticosterone. Additionally, mice housed in LD with a clear tube displayed increased paired testes mass as compared to LL mice. Taken together, these data provide evidence that exposure to unnatural lighting can induce significant changes in affect, increasing depressive-like and decreasing anxiety-like responses.
Address Department of Psychology, The Ohio State University, Columbus, OH 43210, USA. Fonken.1@osu.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0166-4328 ISBN Medium
Area Expedition Conference
Notes PMID:19591880 Approved no
Call Number LoNNe @ kagoburian @ Serial 749
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Author (up) Fonken, L.K.; Lieberman, R.A.; Weil, Z.M.; Nelson, R.J.
Title Dim light at night exaggerates weight gain and inflammation associated with a high-fat diet in male mice Type Journal Article
Year 2013 Publication Endocrinology Abbreviated Journal Endocrinology
Volume 154 Issue 10 Pages 3817-3825
Keywords Adipose Tissue, White/*immunology/metabolism/pathology; Animals; Antigens, CD11b/biosynthesis/genetics/metabolism; Appetite Regulation/*radiation effects; Arcuate Nucleus/*immunology/metabolism/pathology; Behavior, Animal/radiation effects; Circadian Rhythm; Cytokines/biosynthesis/genetics/metabolism; Diet, High-Fat/*adverse effects; Feeding Behavior/radiation effects; Gene Expression Regulation; Glucose Intolerance/etiology/immunology/metabolism/pathology; I-kappa B Kinase/biosynthesis/genetics/metabolism; Insulin Resistance; Lighting/*adverse effects; Male; Mice; Microglia/immunology/metabolism/pathology; Nerve Tissue Proteins/biosynthesis/genetics/metabolism; Obesity/*etiology/immunology/metabolism/pathology; Random Allocation; *Weight Gain
Abstract Elevated nighttime light exposure is associated with symptoms of metabolic syndrome. In industrialized societies, high-fat diet (HFD) and exposure to light at night (LAN) often cooccur and may contribute to the increasing obesity epidemic. Thus, we hypothesized that dim LAN (dLAN) would provoke additional and sustained body mass gain in mice on a HFD. Male mice were housed in either a standard light/dark cycle or dLAN and fed either chow or HFD. Exposure to dLAN and HFD increase weight gain, reduce glucose tolerance, and alter insulin secretion as compared with light/dark cycle and chow, respectively. The effects of dLAN and HFD appear additive, because mice exposed to dLAN that were fed HFD display the greatest increases in body mass. Exposure to both dLAN and HFD also change the timing of food intake and increase TNFalpha and MAC1 gene expression in white adipose tissue after 4 experimental weeks. Changes in MAC1 gene expression occur more rapidly due to HFD as compared with dLAN; after 5 days of experimental conditions, mice fed HFD already increase MAC1 gene expression in white adipose tissue. HFD also elevates microglia activation in the arcuate nucleus of the hypothalamus and hypothalamic TNFalpha, IL-6, and Ikbkb gene expression. Microglia activation is increased by dLAN, but only among chow-fed mice and dLAN does not affect inflammatory gene expression. These results suggest that dLAN exaggerates weight gain and peripheral inflammation associated with HFD.
Address Department of Neuroscience, Wexner Medical Center, The Ohio State University, 636 Biomedical Research Tower, 460 West 12th Avenue, Columbus, Ohio 43210. fonken.1@osu.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0013-7227 ISBN Medium
Area Expedition Conference
Notes PMID:23861373 Approved no
Call Number IDA @ john @ Serial 93
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Author (up) Fonken, L.K.; Weil, Z.M.; Nelson, R.J.
Title Dark nights reverse metabolic disruption caused by dim light at night Type Journal Article
Year 2013 Publication Obesity (Silver Spring, Md.) Abbreviated Journal Obesity (Silver Spring)
Volume 21 Issue 6 Pages 1159-1164
Keywords Animals; Body Mass Index; Energy Intake; Gene Expression; Glucose Tolerance Test; *Light; Male; Mice; Obesity/*epidemiology/etiology; *Photoperiod; Weight Gain
Abstract OBJECTIVE: The increasing prevalence of obesity and related metabolic disorders coincides with increasing exposure to light at night. Previous studies report that mice exposed to dim light at night (dLAN) develop symptoms of metabolic syndrome. This study investigated whether mice returned to dark nights after dLAN exposure recover metabolic function. DESIGN AND METHODS: Male Swiss-Webster mice were assigned to either: standard light-dark (LD) conditions for 8 weeks (LD/LD), dLAN for 8 weeks (dLAN/dLAN), LD for 4 weeks followed by 4 weeks of dLAN (LD/dLAN), and dLAN for 4 weeks followed by 4 weeks of LD (dLAN/LD). RESULTS: After 4 weeks in their respective lighting conditions both groups initially placed in dLAN increased body mass gain compared to LD mice. Half of the dLAN mice (dLAN/LD) were then transferred to LD and vice versa (LD/dLAN). Following the transfer dLAN/dLAN and LD/dLAN mice gained more weight than LD/LD and dLAN/LD mice. At the conclusion of the study dLAN/LD mice did not differ from LD/LD mice with respect to weight gain and had lower fat pad mass compared to dLAN/dLAN mice. Compared to all other groups dLAN/dLAN mice decreased glucose tolerance as indicated by an intraperitoneal glucose tolerance test at week 7, indicating that dLAN/LD mice recovered glucose metabolism. dLAN/dLAN mice also increased MAC1 mRNA expression in peripheral fat as compared to both LD/LD and dLAN/LD mice, suggesting peripheral inflammation is induced by dLAN, but not sustained after return to LD. CONCLUSION: These results suggest that re-exposure to dark nights ameliorates metabolic disruption caused by dLAN exposure.
Address Department of Neuroscience and Institute for Behavioral Medicine Research, Wexner Medical Center, Ohio State University, Columbus, Ohio 43210, USA. fonken.1@osu.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1930-7381 ISBN Medium
Area Expedition Conference
Notes PMID:23666854 Approved no
Call Number IDA @ john @ Serial 167
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Author (up) Fonken, L.K.; Workman, J.L.; Walton, J.C.; Weil, Z.M.; Morris, J.S.; Haim, A.; Nelson, R.J.
Title Light at night increases body mass by shifting the time of food intake Type Journal Article
Year 2010 Publication Proceedings of the National Academy of Sciences of the United States of America Abbreviated Journal Proc Natl Acad Sci U S A
Volume 107 Issue 43 Pages 18664-18669
Keywords Animals; Body Mass Index; *Circadian Rhythm; Disease Models, Animal; Eating/*physiology/psychology/*radiation effects; Energy Intake; Feeding Behavior/physiology/psychology/radiation effects; Glucose Tolerance Test; Humans; Male; Metabolic Syndrome X/etiology; Mice; Motor Activity; Obesity/*etiology/pathology/physiopathology/psychology; *Photoperiod
Abstract The global increase in the prevalence of obesity and metabolic disorders coincides with the increase of exposure to light at night (LAN) and shift work. Circadian regulation of energy homeostasis is controlled by an endogenous biological clock that is synchronized by light information. To promote optimal adaptive functioning, the circadian clock prepares individuals for predictable events such as food availability and sleep, and disruption of clock function causes circadian and metabolic disturbances. To determine whether a causal relationship exists between nighttime light exposure and obesity, we examined the effects of LAN on body mass in male mice. Mice housed in either bright (LL) or dim (DM) LAN have significantly increased body mass and reduced glucose tolerance compared with mice in a standard (LD) light/dark cycle, despite equivalent levels of caloric intake and total daily activity output. Furthermore, the timing of food consumption by DM and LL mice differs from that in LD mice. Nocturnal rodents typically eat substantially more food at night; however, DM mice consume 55.5% of their food during the light phase, as compared with 36.5% in LD mice. Restricting food consumption to the active phase in DM mice prevents body mass gain. These results suggest that low levels of light at night disrupt the timing of food intake and other metabolic signals, leading to excess weight gain. These data are relevant to the coincidence between increasing use of light at night and obesity in humans.
Address Department of Neuroscience, Ohio State University, Columbus, OH 43210, USA. fonken.1@osu.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0027-8424 ISBN Medium
Area Expedition Conference
Notes PMID:20937863; PMCID:PMC2972983 Approved no
Call Number IDA @ john @ Serial 169
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Author (up) Ikeno, T.; Weil, Z.M.; Nelson, R.J.
Title Dim light at night disrupts the short-day response in Siberian hamsters Type Journal Article
Year 2014 Publication General and Comparative Endocrinology Abbreviated Journal Gen Comp Endocrinol
Volume 197 Issue Pages 56-64
Keywords 2,4-dinitro-1-flourobenzene; Dnfb; Dth; Eya3; Eyes absent 3; GnIH; GnRH; Immune function; Ld; Lps; Light pollution; Pt; Pelage; Per1; Period1; Photoperiodism; Rfrp; RFamide-related peptide; Scn; Sd; Seasonality; Tsh; TSH receptor; Tshr; dLAN; delayed-type hypersensitivity; dim light at night; gonadotropin-inhibiting hormone; gonadotropin-releasing hormone; lipopolysaccharide; long days; pars tuberalis; short days; suprachiasmatic nuclei; thyroid-stimulating hormone
Abstract Photoperiodic regulation of physiology, morphology, and behavior is crucial for many animals to survive seasonally variable conditions unfavorable for reproduction and survival. The photoperiodic response in mammals is mediated by nocturnal secretion of melatonin under the control of a circadian clock. However, artificial light at night caused by recent urbanization may disrupt the circadian clock, as well as the photoperiodic response by blunting melatonin secretion. Here we examined the effect of dim light at night (dLAN) (5lux of light during the dark phase) on locomotor activity rhythms and short-day regulation of reproduction, body mass, pelage properties, and immune responses of male Siberian hamsters. Short-day animals reduced gonadal and body mass, decreased spermatid nuclei and sperm numbers, molted to a whiter pelage, and increased pelage density compared to long-day animals. However, animals that experienced short days with dLAN did not show these short-day responses. Moreover, short-day specific immune responses were altered in dLAN conditions. The nocturnal activity pattern was blunted in dLAN hamsters, consistent with the observation that dLAN changed expression of the circadian clock gene, Period1. In addition, we demonstrated that expression levels of genes implicated in the photoperiodic response, Mel-1a melatonin receptor, Eyes absent 3, thyroid stimulating hormone receptor, gonadotropin-releasing hormone, and gonadotropin-inhibitory hormone, were higher in dLAN animals than those in short-day animals. These results suggest that dLAN disturbs the circadian clock function and affects the molecular mechanisms of the photoperiodic response.
Address Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. Electronic address: randy.nelson@osumc.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0016-6480 ISBN Medium
Area Expedition Conference
Notes PMID:24362257 Approved no
Call Number IDA @ john @ Serial 82
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Author (up) Weil, Z.M.; Borniger, J.C.; Cisse, Y.M.; Abi Salloum, B.A.; Nelson, R.J.
Title Neuroendocrine control of photoperiodic changes in immune function Type Journal Article
Year 2014 Publication Frontiers in Neuroendocrinology Abbreviated Journal Frontiers in Neuroendocrinology
Volume 37 Issue Pages 108-118
Keywords Animals; Photoperiod; Melatonin day length; Seasonality immune function; Neuroendocrine
Abstract Seasonal variation in immune function putatively maximizes survival and reproductive success. Day length (photoperiod) is the most potent signal for time of year. Animals typically organize breeding, growth, and behavior to adapt to spatial and temporal niches. Outside the tropics individuals monitor photoperiod to support adaptations favoring survival and reproductive success. Changes in day length allow anticipation of seasonal changes in temperature and food availability that are critical for reproductive success. Immune function is typically bolstered during winter, whereas reproduction and growth are favored during summer. We provide an overview of how photoperiod influences neuronal function and melatonin secretion, how melatonin acts directly and indirectly to govern seasonal changes in immune function, and the manner by which other neuroendocrine effectors such as glucocorticoids, prolactin, thyroid, and sex steroid hormones modulate seasonal variations in immune function. Potential future research avenues include commensal gut microbiota and light pollution influences on photoperiodic responses.
Address Department of Neuroscience, Ohio State University, Biomedical Research Tower #618, 460 West 12th Avenue, Columbus, OH, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0091-3022 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ john @ Serial 1062
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