Effects of a constant light environment on hippocampal neurogenesis and memory in mice

Department of Emergency and Critical Care Medicine, Yamaguchi University Graduate School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan.
Neuroscience Letters (Impact Factor: 2.03). 11/2010; 488(1):41-4. DOI: 10.1016/j.neulet.2010.11.001
Source: PubMed


Because the environmental light-dark cycle is a key factor involved in modulating circadian rhythm in mammals, disruption of cyclic light conditions has a variety of effects on physiology and behavior. In the hippocampus, neurogenesis, which continues to occur throughout life, has been reported to exhibit circadian variation under cyclic light-dark conditions. In the present study, we examined whether a constant light environment affected hippocampal neurogenesis in mice. Half of the animals were exposed to continuous light conditions (L/L group), while the other half remained under normal cyclic light-dark conditions (L/D group). In the L/L group, the number of BrdU-labeled cells (proliferating cells) and that of BrdU and class III β-tubulin double-labeled cells (newborn neurons) in the granule cell layer were significantly decreased compared with the L/D group. Because hippocampal neurogenesis is involved in memory and learning, we also investigated the effects on performance in water maze tasks to assess spatial learning. Exposure to L/L treatment for 3 weeks impaired spatial learning task performance, although there was no difference in the open field behaviors between the groups. These findings demonstrate that the constant light conditions impaired hippocampal neurogenesis as well as cognitive performance, and suggest an important role for the cyclic light-dark environment in appropriate maintenance of the hippocampal system.

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    • "Constant light exposure was applied in animal models studying circadian disruption-induced memory defect (Eckel- Mahan et al., 2008; Fujioka et al., 2011; Ma et al., 2007). Our previous work and other studies had demonstrated that the hippocampus-dependent long-term memory but not shortterm memory in Morris water maze was impaired by circadian disruption (Devan et al., 2001; Ma et al., 2007; Zelinski et al., 2013; Zelinski et al., 2014b). "
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    ABSTRACT: Previous study reported that chronic constant light exposure caused hippocampus-dependent long-term memory deficit. However, the underlying cellular mechanism of this impairment is still unclear. Multiple lines of evidence indicated that long-term potentiation (LTP) is a cellular model for memory formation. Here we found that, by recording of field excitatory postsynaptic potential (fEPSP) in vitro, chronic constant light (CCL, 3 weeks) exposure impaired the late long-term potentiation (L-LTP), but not early long-term potentiation (E-LTP) and basal transmission in Schaffer collateral (SC)-CA1 synapses of hippocampal slices from rats. Because L-LTP depends on D1/D5 receptors, we examined whether interference of D1/D5 receptors can modulate L-LTP of CCL rats. Bath application of D1/D5 receptors antagonist SCH23390 (1μM) blocked L-LTP in control rats and attenuated the impaired L-LTP in CCL rats. In contrast, pre-incubation of D1/D5 receptors agonist SKF38393 (25μM) occluded further L-LTP in control rats while exacerbated the L-LTP impairment in CCL rats. These results suggested that CCL-induced L-LTP impairment can be modulated by D1/D5 receptors. Our findings may contribute to the further understanding of synaptic plasticity mechanism underlying hippocampal long-term memory impairment induced by circadian rhythm disruption. Copyright © 2015. Published by Elsevier B.V.
    Brain research 06/2015; 1622. DOI:10.1016/j.brainres.2015.06.023 · 2.84 Impact Factor
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    • "Constant light (i.e., conditions of a 12 h/12 h light/light [LL] cycle, in contrast to the usual light/dark [LD] cycle) has been shown to induce depressive-like behavior [9] [19] and reduce hippocampal neurogenesis in animal models [12]. Prolonged exposure to LL also induces arrhythmicity in circadian locomotor activity [7]. "
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    ABSTRACT: Circadian rhythm disruptions are often observed in depressed patients, and changes in the light/dark cycle promote depressive-like behavior in animal models. Prolonged exposure to constant light (LL) is known to lead to arrhythmicity of circadian locomotor activity and depressive-like behavior in rats. Interestingly, neonatal exposure to LL prevents both arrhythmicity and depressive behavior in adulthood. Arrhythmic rats under LL conditions that cohabitate with a rhythmic rat exhibit improvement in circadian rhythms. We tested whether such cohabitation also protects against LL-induced depressive-like behavior. Wistar rats were assigned to conditions of either neonatal constant light (neonatal-LL) on postnatal days 10-22 or a regular light/dark cycle (neonatal-LD). On day 45, the animals were assigned to three possible pair combinations. After a baseline sucrose preference test, half of the pairs were placed under LL conditions. Weekly sucrose preference tests were conducted to evaluate depressive-like behavior. The animals were isolated by an aluminum wall on the test day. At week 2 of LL, sucrose preference was reduced in neonatal-LD/neonatal-LD pairs of animals. At week 5, neonatal-LD/neonatal-LD pairs exhibited anhedonic-like behavior, but the pairs with at least one neonatal-LL rat did not. The LL cycle was returned to an LD cycle, and the neonatal-LD/neonatal-LD pairs exhibited a restoration of sucrose preference 2 weeks later. We conclude that social interaction can prevent depressive-like behavior induced by circadian rhythm disruption as long as one of the animals is more prone to present a strong rhythm. Copyright © 2014. Published by Elsevier Ireland Ltd.
    Neuroscience Letters 12/2014; 588. DOI:10.1016/j.neulet.2014.12.042 · 2.03 Impact Factor
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    • "dLAN decreased the percentage of time spent investigating the target hole, indicating decreased memory reten- tion. These results confirm and extend previous findings (Ma et al., 2007; Ling et al., 2009; Fujioka et al., 2011), indicating that housing nocturnal rodents under light at night impairs spatial learning and memory. Our results demonstrate that nighttime light exposure also impairs spatial learning and memory in diurnal rodents. "
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    ABSTRACT: Circadian disruption is a common by-product of modern life. Although jet lag and shift work are well-documented challenges to circadian organization, many more subtle environmental changes cause circadian disruption. For example, frequent fluctuations in the timing of the sleep/wake schedule, as well as exposure to nighttime lighting, likely affect the circadian system. Most studies of these effects have focused on nocturnal rodents, which are very different from diurnal species with respect to their patterns of light exposure and the effects that light can have on their activity. Thus, the authors investigated the effect of nighttime light on behavior and the brain of a diurnal rodent, the Nile grass rat. Following 3 weeks of exposure to standard light/dark (LD; 14:10 light [~150 lux] /dark [0 lux]) or dim light at night (dLAN; 14:10 light [~150 lux] /dim [5 lux]), rats underwent behavioral testing, and hippocampal neurons within CA1, CA3, and the dentate gyrus (DG) were examined. Three behavioral effects of dLAN were observed: (1) decreased preference for a sucrose solution, (2) increased latency to float in a forced swim test, and (3) impaired learning and memory in the Barnes maze. Light at night also reduced dendritic length in DG and basilar CA1 dendrites. Dendritic length in the DG positively correlated with sucrose consumption in the sucrose anhedonia task. Nighttime light exposure did not disrupt the pattern of circadian locomotor activity, and all grass rats maintained a diurnal activity pattern. Together, these data suggest that exposure to dLAN can alter affective responses and impair cognition in a diurnal animal.
    Journal of Biological Rhythms 08/2012; 27(4):319-27. DOI:10.1177/0748730412448324 · 2.77 Impact Factor
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