Critical Period Of Sensitivity Research Articles

Association between prenatal exposure to bisphenol a and birth outcomes: A systematic review with meta-analysis.

Background:Previous studies investigated the relation of prenatal exposure to bisphenol A (BPA) and birth outcomes, but these results were inconsistent. The aim of this study was to investigate the relation of prenatal exposure to BPA and birth outcomes, provide comprehensive results based on current studies.Methods:The PubMed, Cochrane databases, and Web of Science databases were searched systematically by two researchers respectively from their inceptions to Oct. 2018, using the following keywords “bisphenol A, birth weight, birth length, head circumference, gestational age, birth outcomes”. We extracted β coefficient and 95% confidence interval (CI) or β coefficient and standard deviation (SD) from included study. The subgroup analysis was performed to evaluate the potential heterogeneity between studies. We conducted sensitivity analysis by excluding the each individual study to assess the results whether were stable. Finally, the publication bias was performed by accumulative forest plot.Results:Seven studies with 3004 participants met the inclusion criteria. BPA had significant positively association with birth weight (β = 21.92, 95%CI: 1.50–42.35, P = .04). No significant associations were found between BPA and birth length, head circumference and gestational age (All of P > .05).Conclusion:This meta-analysis demonstrated that the BPA was positively associated with birth weight. Therefore, further studies are needed to investigate the critical sensitive period of influencing fetal development and to investigate the difference on gender.

Midlife reversibility of early-established biobehavioral risk factors: A research agenda.

Epidemiological evidence links exposure to early life adversities-such as childhood maltreatment-with impaired health and well-being in adulthood. Since these effects are usually unrecognized or untreated in childhood, preventive and remediating interventions in adults are needed. Our focus on adulthood prompted three major questions. First, does our increased understanding of mechanisms accounting for the long-term effects of early life adversities help delineate underlying dimensions that underscore key similarities and differences among these adversities? Second, can adults accurately report on adversities they experienced in childhood? Third, can we identify malleable risk processes in adulthood that might be targets for preventive intervention? Supported by the National Institute on Aging, the U.K. Economic and Social and the Biotechnology and Biological Sciences Research Councils, a network of researchers in human and animal development addressed these questions through meetings and literature review. A small number of dimensions may adequately distinguish among a range of co-occurring childhood adversities. Widely used adult ascertainments of childhood adversity are poorly related to prospective ascertainment. Strategies for preventive interventions should be aimed both at adults who were actually exposed to adversity as well as those who recall adversity, but the targeted risk processes may be different. Now is an opportune time to support research on adult interventions based on unfolding research on critical periods of sensitivity to adversity in fetal and child development, on improved understanding of risk mechanisms that may persist across the life span, and on new insights on enhancing neuroplasticity in adults. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Adolescent but not adult ethanol binge drinking modulates ethanol behavioral effects in mice later in life

BackgroundAlcohol use disorder is a serious illness marked by uncontrollable drinking and a negative withdrawal state when not using. Alcohol is one of the most commonly used drugs among adolescent populations. Given that adolescence is a unique developmental stage during which alcohol has long-term effects on future drug-taking behavior; it is essential to understand how early exposure to ethanol during adolescence may affect the abuse liability of the drug later in life. Our studies focused on characterizing how exposure to alcohol in adolescence alters later adult alcohol dependence behaviors, by using well-established mouse models of ethanol drinking. We hypothesized that early exposure to ethanol leads to increased ethanol intake in adults and other behavioral phenotypes that may lead to dependence. MethodsWe investigated the impact of ethanol drinking in early adolescent C57BL/6J mice using a modified Drinking in the Dark (DID) model. ResultsOur results showed that exposure to ethanol during adolescence enhanced ethanol intake in adulthood in the DID, and the 2-bottle choice drinking paradigms. In contrast, adult exposure of alcohol did not enhance later alcohol intake. We also conducted tests for ethanol behavioral sensitivity such as loss of righting reflex and anxiety-related behaviors to further elucidate the relationship between adolescent ethanol exposure and enhanced ethanol intake in adult mice. ConclusionsOverall, our results suggest that adolescence is a critical period of sensitivity and binge drinking that can lead to lasting changes in ethanol intake in adulthood. Further research will be required in order to more fully examine the neurochemical mechanisms underlying the lasting changes in adulthood.

Facultative Adjustments in Future Planning Tendencies: Insights on Life History Plasticity from the Flint Water Crisis

Life history theory (LHT) is a powerful explanatory framework examining how developmental environments and life experiences shape allocations of effort to fitness-promoting domains in nested sets of trade-offs. Time orientation is a central psychological aspect of human life history variation, representing the degree to which behaviors are oriented towards immediate versus future goals. Identifying critical sensitive periods for shaping life history variation and verifying the scope of life history plasticity are important issues for both theory and practical application. Many LHT frameworks propose sensitive periods from gestational development through middle childhood, though recent research suggests facultative adjustments may occur much later in the lifespan. The current study examines how experiences of poor tap water quality during the Flint water crisis, associated with toxic contamination and adverse health effects, may have affected time orientations. Degraded expectations for health and longevity may have affected psychological aspects of life history variation, with important consequences for health-related behaviors. Controlling for socio-demographics and other environmental factors associated with life history variation, those who experienced worse tap water quality had lower general tendencies for future planning. Tap water quality experiences predicted several health-related behaviors, independent of socio-demographics, some relationships were mediated through tendencies for future planning.

Temporal, Diagnostic, and Tissue-Specific Regulation of NRG3 Isoform Expression in Human Brain Development and Affective Disorders.

Genes implicated in schizophrenia are enriched in networks differentially regulated during human CNS development. Neuregulin 3 (NRG3), a brain-enriched neurotrophin, undergoes alternative splicing and is implicated in several neurological disorders with developmental origins. Isoform-specific increases in NRG3 are observed in schizophrenia and associated with rs10748842, a NRG3 risk polymorphism, suggesting NRG3 transcriptional dysregulation as a molecular mechanism of risk. The authors quantitatively mapped the temporal trajectories of NRG3 isoforms (classes I-IV) in the neocortex throughout the human lifespan, examined whether tissue-specific regulation of NRG3 occurs in humans, and determined if abnormalities in NRG3 transcriptomics occur in mood disorders and are genetically determined. NRG3 isoform classes I-IV were quantified using quantitative real-time polymerase chain reaction in human postmortem dorsolateral prefrontal cortex from 286 nonpsychiatric control individuals, from gestational week 14 to 85 years old, and individuals diagnosed with either bipolar disorder (N=34) or major depressive disorder (N=69). Tissue-specific mapping was investigated in several human tissues. rs10748842 was genotyped in individuals with mood disorders, and association with NRG3 isoform expression examined. NRG3 classes displayed individually specific expression trajectories across human neocortical development and aging; classes I, II, and IV were significantly associated with developmental stage. NRG3 class I was increased in bipolar and major depressive disorder, consistent with observations in schizophrenia. NRG3 class II was increased in bipolar disorder, and class III was increased in major depression. The rs10748842 risk genotype predicted elevated class II and III expression, consistent with previous reports in the brain, with tissue-specific analyses suggesting that classes II and III are brain-specific isoforms of NRG3. Mapping the temporal expression of genes during human brain development provides vital insight into gene function and identifies critical sensitive periods whereby genetic factors may influence risk for psychiatric disease. Here the authors provide comprehensive insight into the transcriptional landscape of the psychiatric risk gene, NRG3, in human neocortical development and expand on previous findings in schizophrenia to identify increased expression of developmentally and genetically regulated isoforms in the brain of patients with mood disorders. Principally, the finding that NRG3 classes II and III are brain-specific isoforms predicted by rs10748842 risk genotype and are increased in mood disorders further implicates a molecular mechanism of psychiatric risk at the NRG3 locus and identifies a potential developmental role for NRG3 in bipolar disorder and major depression. These observations encourage investigation of the neurobiology of NRG3 isoforms and highlight inhibition of NRG3 signaling as a potential target for psychiatric treatment development.

The influence of low-dose cadmium on the laryngeal microstructure and ultrastructure of Pelophylax nigromaculata.

Cadmium (Cd) is one of the common heavy metals dispersed throughout the modern environment that disrupts the development of aquatic organisms. Amphibians appear to be particularly vulnerable to this heavy metal contaminant since their eggs and aquatic larvae live in aquatic habitats and have permeable skin. During this critical sensitive period, amphibians live primarily in the water and are thus susceptible to the effects of environmental pollutants in water. Pelophylax nigromaculata completes their laryngeal development from Gosner stage 19 (GS 19, embryonic stage) to GS 46 (metamorphosis stage). To study whether long-term (from GS 19 to GS 46) exposure to low Cd concentrations (0, 4, 8, 16, 32, 64, and 128μg/L) affects the development of the larynx in P. nigromaculata, a comparative study of microstructures and ultrastructures of female and male P. nigromaculata larynges was carried out. In histological structure, the larynx was composed of epithelial tissue, skeletal muscle, and hyaline cartilage, and there were no differences between male and female frogs except that males had a larger cross-section area than females. In contrast to controls, 64 and 128μg/L Cd treatments caused a significant decrease in cross-sectional area, while other treatments showed no significant differences. Under the scanning electron microscope, the surface of the larynx could be seen to be attached to developed and evenly distributed cilia, with no significant differences between young male and female frogs, even among the Cd treatments. Under transmission electron microscopy, developed laryngeal epithelial cells could be observed, with obvious cross striations of skeletal muscle cells and mitochondria distributed around the muscle and skeletal muscle satellite cells. Compared with the control group, mitochondria around the skeletal muscle grew in size and decreased in number in the high-concentration treatment.

Long-Lasting Consequences of Testosterone Exposure.

Evidence of reciprocal regulation of androgen signaling and obesity has been well documented (1, 2); it is clear that late gestational and early postnatal periods are most vulnerable to perturbation of these signaling pathways (3). Exposure to high caloric nutrition early in life causes significant changes in reproductive physiology which cannot be reversed by resumption of the normal diet. A maternal highfat diet produces prostatic hyperplasia in adult male and ovarian failure in adult female offspring (4, 5). Importantly, the embryo exposure to high caloric diet does not immediately activate androgen signaling and postnatal androgen surge in females does not immediately affect the weight; the effects of these stimuli are delayed until the organism is mature. Similarly, extensive experimental data indicate that the perturbations of hormonal balance during this developmental period have long-lasting effects not only on reproductive characteristics, including ovarian and neuroendocrine changes (6), but also changes in metabolic functions (7). The phenotype resembling human polycystic ovarian syndrome often associated with impaired insulin sensitivity and increased weight is observed in rodent females subjected to transient neonatal or prepubertal androgen treatment (8). The study published in this issue of Endocrinology by Jang et al (9) narrows down the critical period of sensitivity to exogenous androgen treatment in mice (9). Three temporal windows were used: within 24 hours after birth and at 3 or 6 weeks of age. A single injection of testosterone enanthate (TE) was used at every time point. Reproductive abnormalities were detected in adult females treated with androgens 24 hours after birth. No abnormalities were detected in females treated with TE at 3 or 6 weeks, suggesting that the developmental program at that stage was fully determined. An increase in blood testosterone concentration in newborn female pups partially mimicked the surge of testosterone in late neonatal/early postnatal period in male rodents (10). In males, the increase of testosterone at the end of pregnancy is required for completion of the full masculinization program (11), including scrotum development, testicular descent, and the substitution of fetal with adult Leydig cells (12). In females, the oocyte nest breakdown occurs, and the primordial follicle pool is established the early postnatal period (13). In this report, neonatal TE treatment caused reproductive abnormalities in adult females such as irregular cycling, anovulatory phenotype and increased ovarian weight. Surprisingly, despite clearly abnormal cystic ovaries and theabsenceof corpora lutea in treated females, no changes in estradiol, LH, or FSH levels and expression of estrogen receptors and and androgen receptor genes were detected. This distinguishes the results of these experiments from previous reports on androgen treatment in the prenatal or neonatal rodent females (14). It is possible that the much lower dose and significantly more stable derivative of testosterone used in the Jang et al study was responsible for these differences and that the signaling pathways in the target cells downstream from steroid receptors were affected. Additionally, metabolic parameters were changed in TE-treated females when compared with the vehicle-treated controls such as a greater body weight, including lean body and fat mass. When insulin resistance was compared in 30-week-old females injected with oil or TE 24 hours after birth, TE-treated females displayed significantly lower blood glucose levels in response to insulin injections as compared with controls. Increases in lipoprotein lipase and resistin mRNA levels, the key genes in lipogenic and lipolytic pathways in adipose tissues, were

Visceral pain and gastrointestinal microbiome.

A complex set of interactions between the microbiome, gut and brain modulate responses to visceral pain. These interactions occur at the level of the gastrointestinal mucosa, and via local neural, endocrine or immune activity; as well as by the production of factors transported through the circulatory system, like bacterial metabolites or hormones. Various psychological, infectious and other stressors can disrupt this harmonious relationship and alter both the microbiome and visceral pain responses. There are critical sensitive periods that can impact visceral pain responses in adulthood. In this review we provide a brief background of the intestinal microbiome and emerging concepts of the bidirectional interactions between the microbiome, gut and brain. We also discuss recent work in animal models, and human clinical trials using prebiotics and probiotics that alter the microbiome with resultant alterations in visceral pain responses.

Life course epidemiology in nutrition and chronic disease research: a timely discussion.

Humans are exposed to a complex and changing combination of nutritional factors during the life course, necessitating their investigation over time to capture "critical periods of sensitivity." A life course approach provides a framework to examine trajectories and long-term effects of nutritional and other risk factors, particularly the role of timing, accumulation, and temporal relationships of these exposures in relation to chronic disease development. Currently, most epidemiologic research does not sufficiently address this issue in relation to disease etiology. Although applying a life course approach would augment our knowledge about disease development, this approach presents major challenges in designing, conducting, and analyzing studies. A scientific symposium was held that reviewed emerging research and discussed methodological concerns in applying the life course approach. The research presented at this session focused on the role of timing, with the pre- and postnatal and pubertal periods as critical windows of exposure for chronic conditions. Methodological issues and complexities in analyzing and selecting datasets were highlighted. This symposium elucidated unique study designs and statistical strategies to demonstrate the strengths of this methodology, and served as a catalyst for new research in the area of nutrition and chronic disease epidemiology.

L’impact du cannabis à l’adolescence sur la transition psychotique de l’adulte

It is now well known that cannabis can precipitate the onset of psychosis. The epidemiological studies have shown that the increased risk is significant from ‘recreational’ consumptions (ten times exposure at the age of 18), but the effect is more important with higher doses (dose-dependent effect) and more marked in adolescent (with a two-fold increase of exposure at the age of 15 compared to 18). The effect is also dependent on the composition in cannabinoids: delta-9-tetrahydrocannabinol have psychotomimetic effects while cannabidiol has anxiolytic and possibly antipsychotic. This question is timely since some production of cannabis includes genetic modifications that tend to decrease the level of cannabidiol. Cannabis interferes with endogeneous cannabinoides systems, involved in the maturation processes at adolescence, and adolescence seems a critical period of sensitivity to the deleterious effects of cannabis. The recent literature in human and animal have demonstrated that exposure to cannabis at adolescence can result in chronic deleterious effect on cognition in adulthood. While the reliable data are compelling, we now need to disseminate these informations in an appropriate way, without militant excess but without complaisance. It is also needed to identify the markers that shall alert the environment of the adolescent or young adults and identify subjects at risk of complications when exposed to cannabis. It is already established that exposure at adolescence should not be minimized since adolescence per se appears as a risk factor for chronic cognitive deleterious effect and sometimes psychotic complications, even after relatively minor exposure.

Differential Effects of Bisphenol A and Diethylstilbestrol on Human, Rat and Mouse Fetal Leydig Cell Function

Endocrine disruptors (ED) have been incriminated in the current increase of male reproductive alterations. Bisphenol A (BPA) is a widely used weak estrogenic environmental ED and it is debated whether BPA concentrations within the average internal exposure are toxic. In the present study we investigated the effects of 10−12 to 10−5 M BPA concentrations on fetal Leydig cell function, as fetal life is a critical period of sensitivity to ED effects on male reproductive function. To this aim, fetal testes from human at 6.5–10.5 gestational weeks (GW) or from rat and mouse at a comparable critical period of development (14.5 days post-coitum (dpc) for rat and 12.5 dpc for mouse) were explanted and cultured using our validated organotypic culture system in the presence or absence of BPA for 1–3 days. BPA concentrations as low as 10−8 M reduced testosterone secretion by human testes from day 1 of culture onwards, but not by mouse and rat testes where concentrations equal to 10−5 M BPA were required. Similarly, 10−8 M BPA reduced INSL3 mRNA levels only in human cultured testes. On the contrary, 10−5 and 10−6 M diethylstilbestrol (DES), a classical estrogenic compound, affected testosterone secretion only in rat and mouse testis cultures, but not in human testis cultures. Lastly, contrarily to the DES effect, the negative effect of BPA on testosterone produced by the mouse fetal testis was maintained after invalidation of estrogen receptor α (ERα). In conclusion, these results evidenced i) a deleterious effect of BPA on fetal Leydig cells function in human for concentrations from 10−8 M upwards, ii) species-specific differences raising concerns about extrapolation of data from rodent studies to human risk assessment, iii) a specific signaling pathway for BPA which differs from the DES one and which does not involve ERα.

Losing sleep over the caffeination of prematurity

Losing sleep over the caffeination of prematurity

Germ Cell Degeneration in High-Temperature Treated Pufferfish, Takifugu rubripes

Exogenous factors such as temperature, social behavior, and salinity play a crucial role during the critical sensitive period of sex differentiation in many vertebrates. In fishes, amphibians, and reptiles temperature treatment is known to induce all-male (or female) individuals, and genes related to sex differentiation have been studied. The Japanese pufferfish, Takifugu rubripes, possesses the most compact genome among vertebrates and has immense potential for studies focusing on comparative genome analysis. In this study, we describe gonadal morphology and vasa (germ cell marker) and dmrt1 (Sertoli cell marker) expression on a molecular level in relation to the development of temperature-treated pufferfish. To investigate the relationship between temperature and gonadal development, pufferfish were exposed to high-temperature conditions (32°C) during early gonadal development. Morphological observations showed that this high-temperature treatment did not influence sexual differentiation as determined by ovarian cavity characteristics; however, high-temperature treatment induces gonadal degeneration that is devoid of germ cells. RT-PCR results revealed no vasa expression within germ cell-degenerated gonads. In situ hybridization results showed that dmrt1 was expressed in somatic cells of germ cell-degenerated ovaries. These results suggest that high-temperature treatment during early gonadal development induces germ cell degeneration and masculinization of ovarian somatic cells in pufferfish.

CRITICAL PERIOD OF SENSITIVITY FOR EFFECTS OF CADMIUM ON FROG GROWTH AND DEVELOPMENT

Cadmium is a ubiquitous pollutant in aquatic environments that can alter organismal physiology and ecology. Previous experiments found that ecological Cd exposures increased the growth and development of two North American anurans. However, the generality of these effects among species, the time period over which they occur, and the mechanisms responsible remain conjectural. The goal of the present study was to determine the critical period of sensitivity of Rana pipiens exposed to ecologically relevant levels of Cd. We exposed tadpoles to Cd (0 [control], 1.0, and 10.0 microg/L) from Gosner stage (GS) 25 to metamorphic climax. We assessed effects of Cd on amphibian length, survival, and development during premetamorphosis (GS 25-30) and prometamorphosis (GS 31-42). After 14 d of exposure, we staged tadpoles and recorded snout-vent length. Tadpoles were then pooled according to treatment and stage (GS < or =29 or GS > or =30) and allowed to undergo metamorphic development. Tadpoles exposed to 10 microg/L were significantly larger and more advanced in development by 14 d. Survival to forelimb emergence exceeded 90% in all treatments, and time to metamorphic climax was not different from that in controls. Body burdens of Cd were positively correlated with increasing treatment. Early amphibian development (premetamorphosis) was shown to be the critical period of sensitivity for growth and development. Whereas the freshwater criterion for Cd appears to be protective for survival, a lack of knowledge remains about the sublethal effects of chronic exposures of metal pollutants, especially as they relate to tissue concentrations at various stages of amphibian life history.

Critical Prenatal and Postnatal Periods for Persistent Effects of Dexamethasone on Serotonergic and Dopaminergic Systems

Glucocorticoid administration to preterm infants is associated with neurodevelopmental disorders. We treated developing rats with dexamethasone (Dex) at 0.05, 0.2, or 0.8 mg/kg, doses below or spanning the range in clinical use, testing the effects of administration during three different stages: gestational days 17-19, postnatal days 1-3 or postnatal days 7-9. In adulthood, we assessed the impact on synaptic biomarkers for serotonin (5-hydroxytryptamine (5HT)) systems. Across all three regimens, Dex administration evoked upregulation of cerebrocortical 5HT1A and 5HT2 receptors and the presynaptic 5HT transporter, greatest for 5HT1A receptors. The effects were fully evident even at the lowest dose. In contrast, 5HT levels in the cerebral cortex and hippocampus showed disparate patterns of temporal sensitivity, with no change after gestational treatment, an increase with the early postnatal regimen, and a decrease with the later postnatal exposure. None of the changes in 5HT concentrations were offset by adaptive changes in the fractional 5HT turnover rate. Furthermore, the critical period of sensitivity seen for 5HT levels differed from that of dopamine even within the same brain region. These findings suggest that developmental exposure to Dex during the critical neurodevelopmental period corresponding to its use in preterm infants, elicits selective changes in 5HT and dopaminergic synaptic function over and above its effects on general aspects of neural cell development, below the threshold for somatic growth impairment, and even at doses below those used clinically. Accordingly, adverse neurobehavioral consequences may be inescapable in glucocorticoid therapy of preterm infants.

Postnatal haloperidol eliminates the deficit in circling behavior produced by prenatal exposure to the same drug

Up to 35% of pregnant women take psychotropic drugs at least once during gestation [Austin and Mitchell, 1998]. From concurrent animal and human evidence, it has been proposed that exposure to several psychoactive medications in utero or during lactation increases the risk for permanent brain disorders . Present preventive or therapy practices applied on humans for this type of long-lasting behavioral alterations are mainly based on empirical results. Here, we test an experimental approach designed to counteract a circling performance deficit that appears in Sprague–Dawley rats at puberty on exposure to the dopaminergic blocker haloperidol (HAL) during gestation [J.L. Brusés, J.M. Azcurra, The circling training: A behavioral paradigm for functional teratology testing, in: P.M. Conn (Ed.), Paradigms for the study of behavior, Acad. Press, New York, 1993, pp. 166–179. Method Neurosci. 14]. Gestational exposure to HAL (GD 5–18, 2.5 mg/kg/day ip) induced the expected circling activity decrease in the offspring at the fifth week of life. When prenatal exposure to HAL was continued through lactation (PD5–21, 1.5 mg/kg/day ip), rats otherwise showed a control-like circling performance. No difference was yet found between lactation-only, HAL-exposed pups and saline (SAL)-treated controls ( n=8 each group). We further performed saturating ( 3H)-spiroperidol (SPI) binding assays on striatal P2 membrane fractions 2 months later. The dopamine-type D2-specific binding results suggested that above circling behavior findings could be partially explained by enduring HAL-induced neurochemical changes. The role of critical periods of sensitivity as transient windows for opportunistic therapies for behavioral teratology is discussed.

The effect of irrigation and sowing date on crop yield and yield components of Kabuli chickpea (Cicer arietinum L.) in a cool-temperate subhumid climate

The canopy development, radiation absorption and its utilization for biomass production in response to irrigation at different growth stages of three Kabuli chickpea (Cicer arietinum L.) cultivars was studied on a Wakanui silt loam soil in Canterbury, New Zealand (43°38S, 172°30E). The study also aimed at quantifying the yield potential of the crop under varying irrigation regimes and sowing dates. Green area duration (GAD), intercepted radiation (Fi), radiation use efficiency (U) and total intercepted PAR were significantly (P&lt;0·001) increased by irrigation. Total dry matter (TDM) yield was more strongly correlated (R2=0·69–0·83) with GAD than seed yield (R2=0·60–0·69). Accumulation of TDM was highly related to intercepted PAR. Fully irrigated November-sown crops had a final U of 1·46 g DM/MJ PAR. The unirrigated crop had a U of only 0·92 g DM/MJ PAR. The U tended to decrease with delayed sowing.Averaged over the 2 years, irrigation increased seed yield by 74–124% and trends were similar for TDM yield. Seed yield was doubled in November-sown chickpeas (4·6 t/ha) and cv. Sanford produced 14 and 16% more seed than cvs Dwelley and B-90 respectively. Full irrigation from emergence to physiological maturity always gave the highest seed yield (&gt;4·7 t/ha), and there was no indication of a critical period of sensitivity to water stress. Based on results collected in the first growing season a simple model relating seed yield to radiation interception, U and HI was made. Results from the second growing season were then used as a simple verification to test the accuracy of predictions. The results suggest that these varieties have the potential to yield more than 4·5 t/ha of seed in Canterbury.

Hormonal control of male horn length dimorphism in Onthophagus taurus (Coleoptera: Scarabaeidae): a second critical period of sensitivity to juvenile hormone

Male dung beetles ( Onthophagus taurus) facultatively produce a pair of horns that extend from the base of the head: males larger than a threshold body size develop long horns, whereas males that do not achieve this size develop only rudimentary horns or no horns at all. Using topical applications of methoprene, we identified a sensitive period during the feeding stage of third (final) instar larvae when application of methoprene shifted the threshold body size for horn expression. Male larvae that received methoprene at this time delayed horn production until they attained a larger threshold body size than acetone-treated control larvae. This new sensitive period occurs earlier than a sensitive period previously reported for male horn regulation, and it coincides with a morph-specific pulse of ecdysteroid secretion described for this species. It appears that male horn expression is influenced by endocrine events at two different periods of larval development. We incorporate these results into an expanded model for the endocrine regulation of male horn expression.

Functioning of the rat circadian system is modified by light applied in critical postnatal days.

Lighting conditions influence biological clocks. The present experiment was designed to test the presence of a critical window of days during the lactation stage of the rat in which light has a decisive role on the development of the circadian system. Rats were exposed to 4, 8, or 12 days of constant light (LL) during the first days of life. Their circadian rhythm was later studied under LL and constant darkness. The response to a light pulse was also examined. Results show that the greater the number of LL days during lactation, the stronger the rhythm under LL and the smaller the phase shift due to the light pulse. These responses are enhanced when rats are exposed to LL days around postnatal day 12. A mathematical model was built to explain the responses of the circadian system with respect to the timing of LL during lactation, and we deduced that between postnatal days 10 to 20 there is a critical period of sensitivity to light; consequently, exposure to LL during this time modifies the circadian organization of the motor activity.

Environment and sex determination in farmed fish

A certain plasticity of gonadal sex differentiation was reported in the 1930s following exogenous steroid treatments in fish, but demonstration that some environmental factors (temperature, pH, density and social interactions) can influence the sex ratio in gonochoristic species, is relatively recent. In fish, as in reptiles and amphibians displaying environmental sex determination the main environmental factor influencing sex seems to be temperature (TSD = Temperature Sex Determination). In most of the thermosensitive species (some Atherinids, Poecilids, Cichlids, the tilapias, the goldfish, a Siluriform, a flatfish,...) the male to female ratio increases with temperature, and/or ovarian differentiation is induced by low temperatures. Conversely, in some rare species (Dicentrarchus labrax, Ictalurus punctatus), high temperatures may produce female-biased sex ratios and/or low temperatures promote male-biased sex ratios. In the case of the hirame Paralichthys olivaceus, both high and low temperatures induce monosex inale populations while intermediate temperatures yield a 1 :I sex ratio (U-shape curve). Fish show particularities in their TSD patterns since monosex populations are generally not produced at extreme temperatures, suggesting the existence of strong temperature/genotype interactions. In reptiles, amphibians as well as fish displaying TSD, temperature treatments must be applied at a critical sensitive period which is relatively similar to the hormone-sensitive period. In gonochoristic fish, steroid hormones with estrogens in females and II-oxygenated androgens in males, are probably key physiological steps in the regulation of the gonadal sex differentiation. Cytochrome P450-aromatase, an enzyme which catalyses the conversion of androgens to estrogens, seems to be a critical enzyme for ovarian differentiation. The molecular mechanisms of thermosensitivity have been addressed in only two species. In both the tilapia, Oreochromis niloticus and the hirame, aromatase gene expression is down-regulated by masculinizing-temperature treatments. Furthermore, in tilapia the gene expression of II [beta]-hydroxylase (a key enzyme involved in the synthesis of II-oxygenated androgens) does not appear to be affected by temperature treatments. (Texte integral)