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Drought stress inducing pollen sterility can reduce crop yield worldwide. The regulatory crosstalk associated with the effects of drought on pollen formation at the cellular level has not been explored in detail so far. In this study, we performed morphological and cytoembryological analysis of anther perturbations and examined pollen development in two spring barley genotypes that differ in earliness and drought tolerance. The Syrian breeding line CamB (drought-tolerant) and the European cultivar Lubuski (drought-sensitive) were used as experimental materials to analyze the drought-induced changes in yield performance, chlorophyll fluorescence kinetics, the pollen grain micromorphology and ultrastructure during critical stages of plant development. In addition, fluctuations in HvGAMYB expression were studied, as this transcription factor is closely associated with the development of the anther. In the experiments, the studied plants were affected by drought, as was confirmed by the analyses of yield performance and chlorophyll fluorescence kinetics. However, contrary to our expectations, the pollen development of plants grown under specific conditions was not severely affected. The results also suggest that growth modification, as well as the perturbation in light distribution, can affect the HvGAMYB expression. This study demonstrated that the duration of the vegetation period can influence plant drought responses and, as a consequence, the processes associated with pollen development as every growth modification changes the dynamics of drought effects as well as the duration of plant exposition to drought.

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In 1755 in Bergemoletto, Italy, an avalanche buried 4 people (2 women, a girl, and a boy) and several animals in a stable. After 37 d in a pitch-dark confined space, 3 of the 4 people were rescued alive. The 3 survivors had only goat milk, a few chestnuts, a few kg of raw kid meat, and meltwater for nutrition. We describe the longest-known survival in an avalanche burial and discuss the medical and psychological problems of the survivors. The boy died. When they were extricated, all 3 survivors were exhausted, cachectic, and unable to stand or walk. They were severely malnourished and were experiencing tingling, tremors, and weakness in the legs; constipation; changes in taste; and amenorrhea. One of the women had persistent eye problems and developed symptoms consistent with post-traumatic stress disorder. The survivors were given slow refeeding. It took from 1 to 6 wk before they could walk. We compare this case to other long-duration burials, especially mining accidents, and describe the rescue and patient care after long-duration burials. This case demonstrates that people can overcome extremely adverse conditions and survive.

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It was well documented that both the size of the dendritic field and receptive field of retinal ganglion cells (RGCs) are developmentally regulated in the mammalian retina, and visual stimulation is required for the maturation of the dendritic and receptive fields of mouse RGCs. However, it is not clear whether the developmental changes of the RGC receptive field correlate with the dendritic field and whether visual stimulation regulates the maturation of the dendritic field and receptive field of RGCs in a correlated manner. The present work demonstrated that both the dendritic and receptive fields of RGCs continuously develop after eye opening. However, the correlation between the developmental changes in the receptive field size and the dendritic field varies among different RGC types. These results suggest a continuous change of synaptic converging of RGC synaptic inputs in an RGC type-dependent manner. Besides, light deprivation impairs both the development of dendritic and receptive fields.

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We studied the effect of long-term light deprivation which began at different stages of ontogeny on the content of α-tocopherol in rats during the first 3 months of postnatal development. In the offspring postnatally exposed to constant darkness, the level of α-tocopherol in the liver, kidneys, heart, skeletal muscles, and lungs was significantly decreased at the early stages of postnatal ontogeny (2 weeks and 1 month). In rats kept under constant darkness after birth, the content of α-tocopherol in the lungs was also reduced at the age of 1 month. The modulating effect of light deprivation on the level of α-tocopherol can be associated both with the impact of disturbed circadian rhythms and with increased content of melatonin in the body.

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Mutation of the α-thalassemia/mental retardation syndrome X-linked protein, ATRX, causes intellectual disability and is associated with pleiotropic defects including ophthalmological abnormalities. We have previously demonstrated that Atrx deficiency in the mouse retina leads to the selective loss of inhibitory interneurons and inner retinal dysfunction. Onset of the amacrine cell neurodegenerative phenotype in Atrx-deficient retinas occurs postnatally after neuronal specification, and coincides with eye opening. Given this timing, we sought to interrogate the influence of light-dependent visual signaling on Atrx-mediated neuronal survival and function in the mouse retina. Retina-specific Atrx conditional knockout (cKO) mice were subjected to light deprivation using two different paradigms: (1) a dark-rearing regime, and (2) genetic deficiency of metabotropic glutamate receptor 6 (mGluR6) to block the ON retinal signaling pathway. Scotopic electroretinography was performed for adult dark-reared Atrx cKO mice and controls to measure retinal neuron function in vivo. Retinal immunohistochemistry and enumeration of amacrine cells were performed for both light deprivation paradigms. We observed milder normalized a-wave, b-wave and oscillatory potential (OP) deficits in electroretinograms of dark-reared Atrx cKO mice compared to light-exposed counterparts. In addition, amacrine cell loss was partially limited by genetic restriction of retinal signaling through the ON pathway. Our results suggest that the temporal features of the Atrx cKO phenotype are likely due to a combined effect of light exposure upon eye opening and coincident developmental processes impacting the retinal circuitry. In addition, this study reveals a novel activity-dependent role for Atrx in mediating post-replicative neuronal integrity in the CNS.

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Blue light has been previously reported to play a salient role in the treatment of seasonal affective disorder. The present study aimed to investigate whether blue light had antidepressant effect on light-deprivation-induced depression model, and the underlying visual neural mechanism. Blue light mitigated depression-like behaviors induced by light deprivation as measured by elevated sucrose preference and reduced immobility time. Blue light enhanced melanopsin expression and light responses in the retina. We also found the upregulation of serotonin and brain derived neurotrophic factor expression in the c-fos-positive areas of rats treated with blue light compared with those maintained in darkness. The species gap between nocturnal albino (Sprague-Dawley rat) and diurnal pigmented animals (human) might have influenced extrapolating data to humans. Blue light has antidepressant effect on light-deprived Sprague-Dawley rats, which might be related to activating the serotonergic system and neurotrophic activity via the retinoraphe and retinoamygdala pathways. Blue light is the effective component of light therapy for treatment of depression.

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Vision loss, among the most feared complications of diabetes, is primarily caused by diabetic retinopathy, a disease that manifests in well-recognized, characteristic microvascular lesions. The reasons for retinal susceptibility to damage in diabetes are unclear, especially considering that microvascular networks are found in all tissues. However, the unique metabolic demands of retinal neurons could account for their vulnerability in diabetes. Photoreceptors are the first neurons in the visual circuit and are also the most energy-demanding cells of the retina. Here, we review experimental and clinical evidence linking photoreceptors to the development of diabetic retinopathy. We then describe the influence of retinal illumination on photoreceptor metabolism, effects of light modulation on the severity of diabetic retinopathy, and recent clinical trials testing the treatment of diabetic retinopathy with interventions that impact photoreceptor metabolism. Finally, we introduce several possible mechanisms that could link photoreceptor responses to light and the development of retinal vascular disease in diabetes. Collectively, these concepts form the basis for a growing body of investigative efforts aimed at developing novel pharmacologic and nonpharmacologic tools that target photoreceptor physiology to treat a very common cause of blindness across the world.

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Illumination of the retina is a major determinant of energy expenditure by its neurons. However, it remains unclear whether light exposure significantly contributes to the pathophysiology of common retinal disease. Driven by the premise that light exposure reduces the metabolic demand of the retina, recent clinical trials failed to demonstrate a benefit for constant illumination in the treatment of diabetic retinopathy. Here, we instead ask whether light deprivation or blockade of visual transduction could modulate the severity of this common cause of blindness. We randomized adult mice with two different models of diabetic retinopathy to 1-3 months of complete dark housing. Unexpectedly, we find that diabetic mice exposed to short or prolonged light deprivation have reduced diabetes-induced retinal pathology, using measures of visual function, compared to control animals in standard lighting conditions. To corroborate these results, we performed assays of retinal vascular health in diabetic Gnat1-/- and Rpe65-/- mice, which lack phototransduction. Both mutants displayed less diabetes-associated retinal vascular disease compared to respective wild-type controls. Collectively, these results suggest that light-induced visual transduction promotes the development of diabetic retinopathy and implicate photoreceptors as an early source of visual pathology in diabetes.

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BACKGROUND: Color directly affects fruit quality and consumer preference. In fig syconia, the female flower tissue is contained in a receptacle. Anthocyanin pigmentation of this tissue and the peel differs temporally and spatially. A transcriptome study was carried out to elucidate key genes and transcription factors regulating differences in fig coloring. RESULTS: Anthocyanins in the female flower tissue were identified mainly as pelargonidin-3-glucoside and cyanidin-3-rutinoside; in the peel, the major anthocyanins were cyanidin 3-O-glucoside and cyanidin-3-rutinoside. Anthocyanin content was significantly higher in the female flower tissue vs. peel before fig ripening, whereas at ripening, the anthocyanin content in the peel was 5.39 times higher than that in the female flower tissue. Light-deprivation treatment strongly inhibited peel, but not female flower tissue, anthocyanin pigmentation. RNA-Seq revealed 522 differentially expressed genes (recruited with criteria log2 ≥ 2 and P < 0.05) at fig ripening, with 50 upregulated and 472 downregulated genes in the female flower tissue. Light deprivation upregulated 1180 and downregulated 856 genes in the peel, and upregulated 909 and downregulated 817 genes in the female flower tissue. KEGG enrichment revealed significantly changed expression in the phenylpropanoid-biosynthesis and flavonoid-biosynthesis pathways in the peel, but not in the female flower tissue, with significant repression of FcCHS, FcCHI, FcF3H, FcF3'H, FcDFR and FcUFGT transcripts. Light deprivation led to differential expression of 71 and 80 transcription factor genes in the peel and female flower tissue, respectively. Yeast one-hybrid screen revealed that FcHY5 and FcMYB114 bind the promoter regions of FcCHS and FcDFR, respectively in the flavonoid-biosynthesis pathway. CONCLUSIONS: Phenylpropanoid- and flavonoid-biosynthesis pathways were differentially expressed spatially and temporally in the peel and female flower tissue of fig syconia; pathway expression in the peel was strongly regulated by light signal. Differentially expressed transcription factors were recruited as candidates to screen important expression regulators in the light-dependent and light-independent anthocyanin-synthesis pathway. Our study lays the groundwork for further elucidation of crucial players in fig pigmentation.

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We studied the age-related features of circadian rhythms of superoxide dismutase (SOD) and catalase activity in the liver of rats under light deprivation. In standard light conditions (LD), significant daily fluctuations in SOD activity with a maximum at 07:00 am was detected only in young animals (1,5 months) but catalase activity was observed in young (1,5 months) and in adults (7,5 months) with peak at 04:00 am. The daily dynamics of total and specific activity of SOD and catalase in the liver in young and adult rats differed depending on the period of ontogeny in which the impact of light deprivation began. When the females and offspring were moved to darkness after birth (group LD/DD), the circadian rhythms of SOD and catalase activitys were observed in young and were absent in adult rats. However, circadian rhythms of the antioxidant enzymes (AOE) activities were inherent only adult rats when light deprivation impacted on pregnant females (group DD/DD). Changes in circadian rhythms under light deprivation were characterized either by a phase shift of the enzymes activity (in the LD/DD group) or by a violation of their develpoment in ontogeny (in the DD/DD group). During aging significant decreasing of catalase activity was compensated by an increase in the amplitude of circadian rhythms of activity of this enzyme in animals of all groups. A distinctive feature of daily fluctuations in AOЕ activity in young rats in LD and LD/DD groups can be considered the presence of an ultradian rhythm in the general circadian cycle, which had a second peak with a smaller amplitude and shorter period.

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Retinal ganglion cells (RGCs) have a wide variety of dendritic architectures, which are critical for the formation of their function-specific synaptic circuitry. The developmental regulation of the dendrites of RGCs is thought to be subtype dependent. The purpose of this study is to characterize the dendritic development of a genetically identified RGC subtype, JamB RGCs (J-RGCs), and the roles of glutamate receptor activity on the dendritic development of these cells. We show that the dendrites of J-RGCs are strictly ramified in the outer portion of the inner plexiform layer (IPL) of the retina at the age of postnatal day 8 (P8), mimicking the ramification pattern of adults. However, several other important features of dendrites undergo substantial developmental refinement after P8. From P8 to P13, the dendritic development of J-RGCs is characterized by a dramatic increase of dendritic length and the size of the dendritic field. After eye opening, the dendritic development of J-RGCs is characterized by a tremendous decrease of the number of dendritic protrusions (spine-like structures) and a consolidation of the size of the dendritic field. To determine whether the dendritic development of J-RGCs is regulated by glutamatergic activity, we conditionally knocked out the expression of an obligatory subunit of N-methyl-D-aspartate receptors (NMDARs), NR1 (Grin1), in J-RGCs. We found that J-RGCs with the NMDAR mutation have decreased dendrite outgrowth and dendritic field expansion but increased number of dendritic protrusions before eye opening. To determine if visual experience regulates the development of J-RGC dendrites, we raised the mice in complete darkness after birth. Light deprivation prevented the decrease in the number of dendritic protrusions and the consolidation of the dendritic field of wild type (WT) mice after eye opening. However, light deprivation has no additional effect on the number of dendritic protrusions or the size of the dendritic field of J-RGCs with NMDAR mutation. Together, these results revealed the roles of light stimulation and NMDAR activity on the dendritic development of J-RGCs.

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Emerging technologies are now giving us unprecedented access to manipulate brain circuits, shedding new light on treatments for amblyopia. This research is identifying key circuit elements that control brain plasticity and highlight potential therapeutic targets to promote rewiring in the visual system during and beyond early life. Here, we explore how such recent advancements may guide future pharmacological, genetic, and behavioral approaches to treat amblyopia. We will discuss how animal research, which allows us to probe and tap into the underlying circuit and synaptic mechanisms, should best be used to guide therapeutic strategies. Uncovering cellular and molecular pathways that can be safely targeted to promote recovery may pave the way for effective new amblyopia treatments across the lifespan.

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Recent evidence suggests that the glutamate system plays an important role in the pathogenesis of major depressive disorder (MDD). The aim of this study was to investigate the effects of light deprivation (LD) in the prefrontal cortex (PFC) of animals with depression-like behavior, targeting the glutamate system, using in vivo proton magnetic resonance spectroscopy (1H MRS). Male Sprague-Dawley rats were housed in constant darkness for six weeks (n = 12; LD group), while controls (n = 8) were housed under normal light cycles. The animals were assessed with forced swim tests. Point-resolved spectroscopy was used to quantify metabolite levels in the PFC. To substantiate the validity of the use of in vivo1H MRS in this study, the spectra obtained in the in vivo1H MRS, parametrically matched spectral simulation, and in vitro experiments were analyzed. The results of the spectral analyses showed that the quantification of glutamate and glutamine was not significantly affected by spectral overlaps. Thus, these results suggested that in vivo1H MRS can be used to reliably investigate the glutamate system. The results of the forced swim test showed LD-induced behavioral despairs in the animals. The levels of glutamate, myo-inositol, phosphocreatine, and total creatine were found significantly (p < 0.010) increased in the PFC of the LD animals compared with the controls. These results suggested that the LD-induced metabolic changes were consistent with the previous findings in patients with MDD and that short-echo-time in vivo1H MRS can be used to effectively measure depression-induced alterations in glutamate systems.

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Neural physiological functions and synaptic changes underlying the pathogenesis of depression have obtained great achievements. However, neuronal morphological changes under a depressive state have not been well understood yet. Here a depressive-like YFP-H transgenic mouse model was produced by light deprivation (LD), and morphological changes of retinal ganglion cells (RGCs) and primary visual and auditory cortical layer 5 pyramidal cells (L5PCs) were investigated. Three distinct RGC subtypes were identified based on soma- and dendritic field (DF) size. RGA cells were highlighted by large soma and medium-sized to large DF. RGB cells were characterized by small- to medium-sized soma and small- to medium-sized DF. RGC cells were typical of small- to medium-sized soma and large DF. LD showed cell-type-specific morphological orchestrations on RGCs and predominantly promoted the dendritic growth of RGA cells, leaving no significant effect on RGB and RGC cells. LD produced a consistently suppressed effect on the morphology of primary visual and auditory cortical L5PCs. LD enhanced the dendritic spine density of primary visual cortical L5PCs, implying a compensation mechanism underlying morphological changes in individual cortical L5PCs. The increased morphological complexity of RGA cells and the simplified morphology of cortical L5PCs suggest a broad range of neuronal morphological "cross-modal plasticity" among different brain areas. Our observations in morphological changes of RGCs and cortical L5PCs under a depressive-like state will provide some insights into the pathogenesis of depression at a single neuronal morphological level.

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PURPOSE: To assess whether the early light deprivation induced by congenital cataract may influence the cone-driven retinal function in humans. METHODS: Forty-one patients affected by congenital cataract (CC) who had undergone uncomplicated cataract extraction surgery and intraocular lens implant, and 14 healthy subjects (HS) were enrolled. All patients underwent complete ophthalmological and orthoptic evaluations and best-corrected visual acuity (BCVA) measurement; light-adapted full-field electroretinograms (ERG) and photopic negative responses (PhNR) were recorded to obtain a reliable measurement of the outer/inner retinal function and of the retinal ganglion cells' function respectively. RESULTS: Mean values of light-adapted ERG a- and b-wave and PhNR amplitude of CC eyes were significantly reduced and photopic ERG b-wave implicit time mean values were significantly delayed when compared to HS ones. When studying photopic ERG mean amplitudes at 5 ms, significant differences were found when comparing CC and control eyes. In CC eyes, statistically significant correlations were found between a- and b- wave amplitudes and PhNR amplitudes. No significant correlations were found between ERG parameters and BCVA, as well as between the age of CC patients at surgery and the time elapsed from lens extraction. No significant differences were found when functional parameters of bilateral and unilateral congenital cataract (uCC) eyes were compared, however uCC eyes showed significant differences when compared with contralateral healthy eyes. CONCLUSION: We found a significant impairment of cone-driven retinal responses in patients with a history of congenital cataract. These changes might result from the long-lasting effects of early light deprivation on the cone retinal pathways. Our findings support the relevance of retinal involvement in deficits induced by early light deprivation.

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OBJECTIVES: There are few reports have demonstrated the effect of a change-in-light experience on the structure and function of hippocampus. A change-in-light experience also affects the circadian pattern of melatonin secretion. This study aimed to investigate developmental effect of exogenous melatonin on synaptic plasticity of hippocampus of light deprived rats. MATERIALS AND METHODS: The effects of intracerebroventricular (ICV) injection of 2µg/5µl melatonin was evaluated on the basic and tetanized field excitatory post-synaptic potentials (fEPSPs) recorded in the hippocampal CA3-CA1 pathway of normal light-reared (LR) and dark-reared (DR) rats at 2, 4, and 6 weeks of age. Using RT-PCR and western blotting, developmental changes in the expression of melatonin receptors, MT1 and MT2, in the hippocampus were also evaluated. RESULTS: The amplitude of basic responses decreased across age in the LR rats. While light deprivation increased the amplitude of baseline fEPSPs, it decreased the degree of potentiation in post-tetanus responses. Melatonin injection also increased the amplitude of fEPSPs and suppressed the induction of long-term potentiation in both LR and DR rats. The expression of melatonin receptors increased in the hippocampus during brain development, and dark rearing reversed the expression patterns of both receptors. CONCLUSION: Although melatonin changed basic and tetanized responses of CA1 neurons across age during critical period of brain development, the pattern of its effects did not match the expression pattern of melatonin receptors in the hippocampus. Thus, the effects of melatonin on hippocampal neuronal responses may be exerted through other ways, like intercellular molecules and nuclear hormone receptors.

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Our previous investigation found that Ginkgo extract EGb761 could attenuate the depressive-like behaviours induced by a single injection of lipopolysaccharide in mice. However, it has not been investigated whether EGb761 is effective on depressive-like behaviours induced by long-term light deprivation and whether its effects are associated with the inhibition of NF-κB-IL-6 signalling pathway. In this study, three groups (vehicle group, EGb761 low-dose group, and EGb761 high-dose group) of C57BL/6J male mice were exposed to constant darkness for four weeks. The control mice remained on a 12 : 12 light-dark cycle. Depressive-like behaviours were evaluated by tail suspension test (TST), forced swim test (FST), and sucrose preference test (SPT). Spontaneous locomotor activity was evaluated by open field test (OFT). Levels of IL-6, IL-6 mRNA, NF-κB p65, phospho-NF-κB p65, IκBα, and phospho-IκBα were measured using Elisa, western blotting, or PCR assays. NF-κB p65 DNA binding activity was evaluated using Chemi Transcription Factor Assay Kit. Results showed long-term light deprivation prolonged the immobile time in TST and FST, shortened the latency to immobility in FST, reduced spontaneous locomotor activity in OFT, decreased sucrose preference in SPT, and increased levels of IL-6, IL-6 mRNA, NF-κB p65, phospho-NF-κB p65, and phospho-IκBα in hippocampal tissue. EGb761 dose-dependently reversed the changes of the above parameters induced by long-term light deprivation, without affecting spontaneous locomotor activity. We conclude that EGb761 could attenuate the depressive-like behaviours and inhibit the NF-κB-IL-6 signalling pathway in a light-deprivation-induced mouse model of depression.

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Retinal light responsiveness measured via electroretinography undergoes developmental modulation, and is thought to be critically regulated by both visual experience and dopamine. The primary goal of this study was to determine whether dopamine D2 receptors regulate the visual experience-dependent functional development of the retina. Accordingly, we recorded electroretinograms from wild-type mice and mice with a genetic deletion of the gene that encodes the D2 receptor raised under normal cyclic light conditions and constant darkness. Our results demonstrate that D2 receptor mutation preferentially increases the amplitude of the inner retinal light responses evoked by high-intensity light measured as oscillatory potentials in adult mice. During postnatal development, all three major components of electroretinograms, i.e. a-waves, b-waves, and oscillatory potentials, increase with age. Comparatively, D2 receptor mutation preferentially reduces the age-dependent increase in b-waves evoked by low-intensity light. Light deprivation from birth reduces b-wave amplitudes and completely abolishes the increased amplitude of oscillatory potentials of D2 receptor mutants. Taken together, these results demonstrate that D2 receptors play an important role in the activity-dependent functional development of the mouse retina.

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