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PubMed1998

Sexual behaviour in Drosophila is irreversibly programmed during a critical period.

Sexual differentiation in Drosophila is controlled by a short cascade of regulatory genes, the expression pattern of which determines all aspects of maleness and femaleness, including complex behaviours displayed by males and females [1-3]. One sex-determining gene is transformer (tra), the activity of which is needed for female development. Flies with a female karyotype (XX) but which are mutant for tra develop and behave as males. In such flies, a female phenotype can be restored by a transgene that carries the female-specific cDNA of tra under the control of a heat-shock promoter. This transgene, called hs[trafem], also transforms XY animals into sterile females [4]. When we raised these XX and XY 'females' at 25 degreesC, however, they displayed vigorous male courtship while at the same time, as a result of their female pheromone pattern, they were attractive to males. Intriguingly, their male courtship behaviour was indiscriminately directed towards both females and males. When we forced expression of tra by heat shock, applied during a limited period around puparium formation, male behaviour was abolished and replaced by female behaviour. We conclude that sexual behaviour is irreversibly programmed during a critical period as a result of the activity or inactivity of a single control gene.

Animals↗
PubMed1990

Post-critical period plasticity of callosal transfer to visual cortex cells of cats following early conditioning of monocular deprivation and late optic chiasm transection.

We studied whether plasticity-induced callosal transfer exists after the critical period for sensitivity of visual cortex cells in kittens postnatally monocularly deprived and in which interocular competition was cancelled by chiasm transection during adulthood. Callosal transfer was studied acutely (n = 3 cats) and chronically (n = 7) following the chiasm transection (OCAMD). For comparison, adult cats in which chiasm transection only was performed (OCA) were also studied acutely (n = 3) and chronically (n = 9). The results were also compared to cats in which monocular deprivation and chiasm transection were simultaneously performed (OCKMD) during development (n = 6) and to normal control cats (n = 18). Unit recording was extracellularly carried out in visual cortex areas 17 and 18 and their boundary region, where the corpus callosum is represented. When no interocular competition was allowed between the non-deprived and the deprived eye via the thalamocortical direct visual pathways on cortical cells, such as in the OCKMD cats, the absolute majority of the cells were ipsilaterally driven, regardless of which hemisphere was studied. Only a minor proportion (4.1%) of the cells had some contralateral input from the non-deprived eye in the hemisphere ipsilateral to the deprived eye, indicating almost no interhemispheric callosal transfer. A slight increase in the proportion of cells callosally driven from the non-deprived eye (9.8%), was found in this hemisphere in cats in which interocular competition was allowed via the direct visual pathways prior to its cancellation by chiasm transection (OCAMD), if studied acutely after the chiasm transection. A remarkable increase in callosal transfer was found in this hemisphere under chronic conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Critical periods associated with stressor effects on antibody titers and on the plaque-forming cell response to sheep red blood cells.

A series of experiments assessed the effects of stressors on the antibody response in mice. A critical period existed (72 h following antigen administration; sheep red blood cells 10(6) cells, ip) at which footshock reduced the plaque-forming cell (PFC) response in CD-1 mice. When shock was applied at other intervals following immunization (0, 24, 48, or 95 h) the PFC response was unaffected. The immunosuppression was unrelated to the time between stressor application and sacrifice, in that the reduced PFC response was evident both 24 and 48 h after stressor application, and reduced serum antibody titers (IgG) were evident 1 week after stressor exposure. The reduction of the PFC response was dependent on the severity of the stressor, but was not related to stressor controllability, being evident after both escapable and inescapable shock. It appears that stressful events may profoundly influence the immune response but the time between antigen administration and subsequent exposure to a stressor is critical in determining whether such an effect will be evident.

Animals↗
PubMed2006

A review of critical periods for opportunistic infection in the new transplantation era.

BACKGROUND: The risk of opportunistic infection (OI) is considered to be maximum during the first six months after solid organ transplantation. The aim of this study was to know the incidence and risk factors for OI in the late period (>6 months) compared with the early period (<6 months) after solid organ transplantation. METHODS: We used the online database of the Spanish Network of Infection in Transplantation (RESITRA), which prospectively analyzed 2,702 solid organ transplantation recipients from August 2003 to February 2005. Univariate and multivariate analyses were performed to calculate the risk factors associated with the development of late OI. RESULTS: A total of 131 patients (6%) developed 176 infectious episodes in the late period. Although the incidence of infection and cytomegalovirus disease (0.4 per 1000 transplant days and 0.05 per 1000 transplant days, respectively) was lower than in the early period (3.5 per 1000 transplant days and 0.8 per 1000 transplant days; P<0.0001), the incidence of other OIs was similar in both periods (0.05 per 1000 transplant days versus 0.03 per 1000 transplant-days, P=0.5). Patients with the higher risk for developing late OI were those receiving early cytomegalovirus prophylaxis, patients who developed two or more episodes of acute rejection during the early period, patients with recurrent bacterial infection during the early period, patients with renal failure requiring dialysis, and patients with chronic graft malfunction. CONCLUSIONS: Our data suggest that in some high-risk patients, the critical period of risk for OI must be expanded beyond the first six months after transplant.

Adult↗
PubMedDate not supplied

Psychological stress and antibody response to influenza vaccination: when is the critical period for stress, and how does it get inside the body?

OBJECTIVES: This study attempted to determine whether stress of moderate intensity could modulate the antibody response to an influenza vaccination in healthy young adults, identify critical periods during which stress could influence antibody response, and delineate behavioral and biological pathways that might explain relations between stress and antibody. METHODS: A cohort of 83 healthy young adults underwent 13 days of ambulatory monitoring before, during, and after vaccination. Four times daily, subjects reported the extent to which they felt stressed and overwhelmed and collected a saliva sample that was later used to measure cortisol. A battery of health practices (cigarette smoking, alcohol use, physical activity, sleep hygiene) was assessed daily. Antibody titers to the vaccine components were measured at baseline and at 1-month and 4-month follow-up assessments. RESULTS AND CONCLUSIONS: To the extent that they reported higher levels of stress across the monitoring period, subjects exhibited poorer antibody responses to the New Caledonia strain of the vaccine. Stress ratings on the 2 days before the vaccine and the day it was given were not associated with antibody response. However, the 10 days afterward appeared to be a window of opportunity during which stress could shape the long-term antibody response to varying degrees. With respect to potential mediating pathways, little evidence emerged in favor of cortisol secretion, alcohol consumption, physical activity, or cigarette smoking. However, analyses were consistent with a pattern in which feelings of stress and loss of sleep become locked into a feed-forward circuit that ultimately diminishes the humoral immune response. These findings may shed light on the mechanisms through which stress increase vulnerability to infectious disease.

Adolescent↗
PubMed1959

Critical period for effects of infantile experience on maturation of stress response.

Manipulated infant rats respond to cold with depletion of adrenal ascorbic acid (AAA) significantly earlier than nonmanipulated infants. The study discussed in this report examined the critical period for infantile manipulation on the depletion of AAA. It was found that infant rats manipulated immediately following birth exhibited significant AAA depletion, whereas infants manipulated later did not exhibit depletion.

Adrenal Cortex↗
PubMed2003

A critical period for gravitational effects on otolith formation.

The otoliths of adult animals do not change significantly during space flight. However, during the period when otoliths are first developing, rearing in space produces significantly larger otoliths. Conversely, animals reared on a centrifuge have smaller than normal otoliths. To identify a critical period during development for gravitational effects on otolith growth, fertilized zebrafish (Danio rerio) eggs were reared on a centrifuge for 1 week. The fine structure of their inner ear during development was studied by both light- and transmission electron microscopy. By 16 hours after fertilization (1-g, at 28.5 degrees C), precursors of the otoliths are seen but no sign of a sensory epithelium is present. Mature hair cells, appearing capable of mechanotransduction, are not seen until between 48 and 72 hours after fertilization. Zebrafish reared at 3-g from 1 to 7 days after fertilization exhibit significantly slower otolith growth than did 1-g controls. Fish exposed to 3-g only from 12-36 h after fertilization had slightly smaller otoliths than 1-g controls, but this difference was not significant. Animals exposed to 3-g from 36 h to 7d after fertilization did have significantly smaller otoliths. If the fish use their hair cells to assess otolith weight in a regulatory role, the hair cells would have to be functional. Thus the earliest stage zebrafish, which were not significantly affected by centrifugation, probably did not have an adequate means of sensing otolith weight to "correct" for the excess weight.

Animals↗
PubMed1993

Abnormal upregulation of myelin genes underlies the critical period of myelination in undernourished developing rat brain.

Since myelin gene expression is suppressed during active myelination of the undernourished brain, this study was designed to determine the effects of undernourishment on the upregulation of myelin genes and the relationship between upregulation and the 'critical period' associated with permanent hypomyelination of the brain. Long-Evans rat dams were given either ad libitum or restricted access to rat chow to produce two populations of developing offsprings. The food deprivation schedule was designed to produce a degree of growth retardation comparable to our earlier studies of hypomyelination in undernourished brain. The expression of myelin genes, at various developmental ages, was determined in the forebrains from undernourished and normal, well fed controls by Northern analysis. In well nourished forebrain, proteolipid protein (PLP), myelin associated glycoprotein (MAG), and basic protein (BP) messages began to increase polynomially after day 8 post partum, leading to a rapid accumulation of message during the following several days. In undernourished forebrain, PLP, MAG, and BP messages did not show any increase until day 10, and then increased at a diminished rate as compared to well nourished forebrain. Additionally, the two PLP messages (1.6 kb and 3.2 kb) showed different vulnerabilities to protein-calorie undernourishment, which explains the abnormal ratio of the 3.2 and 1.6 kb forms we previously found in undernourished brain. This study shows a pattern of temporal specificity when the myelin PLP, MAG, and BP genes are synchronously upregulated in the normal forebrain to a high rate of transcription between day 7 to 9, which is several days before the onset of rapid myelination of the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Cocaine's lethality increases during late gestation in the rat: a study of "critical periods" of exposure.

OBJECTIVE: Cocaine-associated morbidities in pregnant women (e.g., abruptio placentae, hypertension, seizures) occur mostly during the final stages of gestation. The purpose of our study was to determine whether cocaine's toxicity and blood levels varied as a function of "critical periods" of exposure during gestation. STUDY DESIGN: To evaluate mortality rates, pregnant Long-Evans rats received subcutaneously 30, 40, or 50 mg/kg cocaine hydrochloride twice daily (C30, C40, and C50 groups) either during gestational days 7 to 13 (midgestation) or gestational days 14 to 20 (late gestation) (n 9 to 20 per group). Serum levels of the cocaine metabolite benzoylecgonine were examined in other groups of rats on either gestational day 13 (mid) or day 20 (late) in the C30 treatment condition (n = 5 and 10 per group). RESULTS: There were no maternal mortalities in the midgestation groups at any dose. In contrast, the late-gestation groups showed a dramatic dose-dependent effect, with maternal mortality rates of 0%, 40%, and 72% in the C30, C40, and C50 groups. The late-gestation group had higher benzoylecgonine levels than the midgestation groups did. CONCLUSIONS: Late gestation was associated with higher maternal mortality rates and higher benzoylecgonine levels, indicating that some underlying physiologic change enhanced cocaine's toxicity as pregnancy progressed. This increased sensitivity to cocaine may be mediated by estrogen or progesterone, suggesting that the cocaine-abusing woman is at increased risk for cocaine-induced morbidities whenever levels of these hormones are elevated, such as during the final stages of pregnancy or possibly when taking oral contraceptives.

Animals↗
PubMed1989

Critical period of phenytoin teratogenic action in the sea urchin, Arbacia punctulata embryo.

We characterized the susceptibility of sea urchin embryogenesis to phenytoin developmental toxicity. Concentration-dependent effects were assessed by exposing embryos from fertilization through the late gastrula/prism stage and scoring abnormal development via light microscopy. Malformations were observed as early as the first cleavage, when asymmetric, incomplete and arrested cleavage were noted, and also at the prism stage. These effects were concentration-dependent with an EC50 value of approximately 40 microM at both the cleavage and prism stages. Several phenytoin analogs of varying toxicity were identified. Comparison of zygote uptake of phenytoin and one nonteratogenic analog found that toxicity was not limited by uptake as the analog achieved intracellular concentrations which would have been sufficient to induce abnormal development if it had an intracellular potency equal to that of phenytoin. Periods in sea urchin embryogenesis susceptible to phenytoin actions were identified by exposing embryos to phenytoin (120 microM) for discrete intervals after fertilization and scoring development at the prism stage. A critical period of unique susceptibility coincided with the cleavage and morula stages (0- approximately 64 cells/embryo, 0-5 hr after fertilization). Drug exposure after this period did not alter development. Studies examining phases of the cell cycle for susceptibility to phenytoin effects on cleavage found that drug exposure confined to M phase was necessary and sufficient to manifest developmental toxicity. Drug uptake was similar during the sensitive and insensitive developmental stages and cell cycle phases and thus was not responsible for the variations in susceptibility observed. We conclude that the direct effects of phenytoin on sea urchin embryogenesis are confined to the cleavage and morula stages.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Critical periods of sensitivity to the developmental toxicity of inhaled methanol in the CD-1 mouse.

Exposure of pregnant CD-1 mice to methanol (MeOH) by inhalation on gestation days (gd) 6-15 results in dose-related increases in fetal cleft palate, exencephaly, and skeletal defects. Here, critical periods for the developmental toxicity of MeOH were assessed in pregnant CD-1 mice exposed to 10,000 ppm MeOH or filtered air for 7 hr/day on 2 consecutive days during gd 6-13, or to single day (7 hr) exposures to 10,000 ppm MeOH during gd 5-9. Mice received water but not food during exposure. Maternal blood MeOH was determined at times during, at the end of, and subsequent to a single 7 hr exposure on gd 7. On gd 17, remaining mice were weighed, killed, and gravid uteri removed. Live, dead, and resorbed fetuses were counted, and live fetuses were examined, weighed, and preserved in 70% ethanol. All fetuses were examined externally and for cleft palate, eviscerated, and stained with Alizarin red for skeletal examination. Pregnant mice lost an average of 0.3-2.9 g during 7 hr exposure to either filtered air or MeOH, but a MeOH treatment effect was evident only with 2-day exposure on gd 7-8. Peak maternal blood MeOH concentration (at the end of exposure) was approximately 4 mg/ml, and MeOH was cleared from maternal blood within 24 hr. Some fully resorbed litters were observed with 2-day MeOH exposures on gd 6-7 or 7-8, or 1-day exposure on gd 7. With 1-day MeOH exposure on gd 7, the number live was lower than with exposure on any other day. As previously reported, cleft palate, exencephaly, and skeletal defects were the fetal anomalies observed in this mouse strain. Cleft palate occurred with 2-day exposures on gd 6-7 through gd 11-12 (peak on gd 7-8), and with 1-day exposure on gd 5 through gd 9 (peak on gd 7). Exencephaly occurred with 2-day exposures on gd 6-7 through gd 8-9 (peak gd 6-7) or 1-day exposure on gd 5 through gd 8 (peak on gd 7). Skeletal elements malformed included the exoccipital (peak gd 6-7, gd 5), atlas (peak gd 6-7, gd 5,6), axis (peak gd 6-7, gd 7), cervical vertebra 7 with a rib (peak gd 6-7, gd 7), and lumbar vertebra 1 with a rib (peak gd 7-8, gd 7). An increased incidence of fetuses with 25 presacral vertebrae (normal = 26) was observed with methanol exposure on gd 5, whereas an increased incidence of fetuses with 27 presacral vertebrae was observed with MeOH exposure on gd 7. These results indicate that gastrulation and early organogenesis represent a period of increased embryonal sensitivity to methanol.

Abnormalities, Drug-Induced↗
PubMed1980

Regenerative critical periods for locus coeruleus in postnatal rat pups following intracisternal 6-hydroxydopamine: a model of noradrenergic development.

Rat pups were injected intracisternally with 20, 40 or 80 microgram of 6-hydroxydopamine (6-OHDA) at various ages over the first 12 postnatal days in order to determine the critical period of the noradrenergic regenerative-sprouting response in the cerebellum. Twenty-four hours after the treatment NE fibers in the cerebellum had become extensively degenerated. NE levels were reduced by greater than 90-95% and histofluorescence microscopy revealed an absence of innervation except for lesioned axon stumps in the basal white matter and peduncles. The 80 microgram dose produced considerable cellular degeneration in the locus coeruleus and no regenerative growth was seen to follow this treatment. Following the two lower doses, however, regenerative growth did occur. This was maximal in those rats treated closest to birth and declined progressively to become insignificant in rats which were treated on postnatal days 5-12, depending upon the cerebellar subregion. This decline in regenerative potential paralleled the time course for development of NE levels in control cerebella. For this reason the mechanism(s) controlling noradrenergic developmental and regenerative growth in the cerebellum appear to be similar. Such regenerative growth may thus be a useful model for the study of developmental growth of locus coeruleus axons. Contrary to the cerebellar projection, regenerative growth of the forebrain noradrenergic projection was not detected until the rats were between 7 and 12 days old at the time of treatment. This regeneration in the cerebral cortex was preceded by incomplete initial destruction of NE fibers there, in apparent similarity to regenerative growth described to occur in the adult rat forebrain.

Adrenergic Fibers↗
PubMed2002

Co-existence of thrombocytopenia and hyperleukocytosis ('critical period') as a risk factor of haemorrhage into the central nervous system in patients with acute leukaemias.

The aim of this work was to examine whether the risk of death i.a. due to haemorrhage into the central nervous system (CNS) is higher during some phases of acute myeloblastic leukaemia (AML), lymphoblastic leukaemia (ALL), and the blastic phase of chronic myelogenous leukaemia (BP) when two important risk factors that worsen the prognosis are simultaneously present: low thrombocytopenia and hyperleukocytosis. Clinical and post-mortem neuropathological examination was performed in 143 patients, aged 17-76 years, who died from AML (80 cases), BP (38), and ALL (25). Periods with co-existence of thrombocytopenia below 25 x 10(9) per l and hyperleukocytosis above 100 x 10(9) per l were identified after plotting the results and were termed the 'critical period' (CP). The study showed that the risk of death was disproportionately high during the CP. This finding was obtained in all patient groups, although it involved mainly patients with AML and BP, i.e. leukaemias with the highest frequency of hyperleukocytosis in peripheral blood. It is suggested that the risk of death during the CP is so high because leukaemic cells are a potent synergistic factor to thrombocytopenia in causing CNS haemorrhage. When a CP is detected, hyperleukocytosis and thrombocytopenia should be controlled and treated aggressively: leukapheresis and platelet concentrates should be administered. Patients with CP should not be given packed red blood cells, in order to avoid a further increase in blood viscosity, which is already high due to hyperleukocytosis. In fact, anaemia during the CP should be regarded as a potentially life-saving factor.

Acute Disease↗
PubMed1991

Critical period of rat development when sidedness of asymmetric body structures is determined.

We recently reported that rat embryos cultured from the presomite stage in a medium containing the alpha-1 adrenergic agonist, phenylephrine, have a high incidence of situs inversus. In the present study, we have determined more precisely the critical period of development when situs inversus is induced. Rat embryos were harvested at 8 AM on Day 9 of gestation (plug day = Day 0), and divided into different stages of development, namely, early, mid, and late primitive streak stages and early, mid, and late neural plate stages. They then were cultured in rotating bottles to which phenylephrine, 0.5 mM, was added for various durations. After 49 hr of culture, embryos were examined for general morphology including sidedness of the bulboventricular loop, tail, and chorioallantoic placenta. Phenylephrine increased the incidence of situs inversus above control when administered throughout culture from either the early neural plate stage or before, and when administered for 4 hr or more from the early neural plate stage. This increase was significant even at the mid and late primitive streak stages when the control incidence was high. Our results suggest that sidedness of asymmetric body structures is determined during the early neural plate stage. This period is well before the 6-8-somite stage when morphological signs of body asymmetry first appear.

Animals↗
PubMed2003

Lack of maternal dietary exposure effects of bisphenol A and nonylphenol during the critical period for brain sexual differentiation on the reproductive/endocrine systems in later life.

Two potential endocrine-disrupting chemicals, bisphenol A (BPA) and nonylphenol (NP), were assessed for their long-lasting effects on endocrine/reproductive systems following transplacental and lactational exposure to rat offspring during a time-window that included the critical period for brain sexual differentiation. Each chemical was mixed with diet at concentrations of 60, 600 and 3000 ppm and was provided to maternal Sprague-Dawley rats from gestational day (GD) 15 to postnatal day (PND) 10. Ethinylestradiol (EE) at 0.5 ppm was used as an estrogenic reference drug. During pregnancy and lactation, including the exposure period, a soy-free rodent diet was provided to eliminate possible modification of the study results by plant-derived phytoestrogens. Effects on endocrine/reproductive systems were evaluated by examining the anogenital distance, organ weights before puberty, onset of puberty, estrous cyclicity, and organ weights and histopathology of adult endocrine organs (at 11 weeks of age), as well as the volume of the sexually dimorphic nucleus of preoptic area. Both NP and BPA, at high doses, caused decreases in maternal body weights and retardation of offspring growth, but neither affected any of the endocrine/reproductive endpoints of offspring, whereas EE induced irreversible changes in estrous cyclicity and histopathology of ovaries and uterus of adult females. The results indicated that maternal dietary exposure to NP or BPA at concentrations up to 3000 ppm from GD 15 through PND 10 do not exert any apparent adverse effects on the endocrine/reproductive systems of offspring.

Administration, Oral↗
PubMed2005

Synapse-specific downregulation of NMDA receptors by early experience: a critical period for plasticity of sensory input to olfactory cortex.

Olfaction is required at birth for survival; however, little is known about the maturation of olfactory cortical circuits. Here we show that in vivo sensory experience mediates the development of excitatory transmission in pyramidal neurons of rat olfactory cortex. We find a postnatal critical period during which there is an experience-dependent increase in the contribution of AMPARs versus NMDARs to transmission at primary sensory synapses but not associational inputs. The shift in receptors underlying transmission is mediated by a strong activity-dependent downregulation of NMDARs and modest increase in AMPARs. Sensory activity leads to a loss of "silent" NMDAR-only synapses and an increase in threshold for inducing long-term plasticity. These results indicate the importance of early olfactory experience in the establishment of cortical circuits and could reflect mechanisms governing early olfactory "imprinting."

Aging↗
PubMed1986

Meningeal cells influence cerebellar development over a critical period.

We have investigated the influence of meningeal cells on the development of the cerebellum by destroying these cells with 6-hydroxydopamine in hamsters of different ages. The ensuing foliation and lamination disruption in the cerebellar vermis is attributed to a disintegration of the cerebellar surface and a disorganization of the glial scaffold of the cerebellar cortex due to a loss of meningeal-glial interaction in stabilizing the extracellular matrix at the glia limitans superficialis (v. Knebel Doeberitz et al. 1986, Neuroscience 17:409-426). The severity of these cerebellar defects is correlated with the ontogenetic stage at which meningeal cells are destroyed, being greatest after treatment at postnatal day 1 and decreasing thereafter until day 5 and beyond, when no abnormalities occur, although all meningeal cells are destroyed throughout. The absence of cerebellar defects after destruction of meningeal cells at day 5 or later is associated firstly with the end of the period of branching morphogenesis of the cerebellum when all folial primordia are established, and, secondly, with the maturation of the glia limitans superficialis. These findings indicate that meningeal cells stabilize the cerebellar surface and glial scaffold over a critical period that ends, when the pattern of cerebellar foliation is established, and when the glia limitans superficialis has reached a mature state. Beyond this stage glial end-feet alone are sufficient to maintain the epithelial integrity of the cerebellum.

Aging↗
PubMed1984

Critical period for the marked loss of retinal X-cells following visual cortex damage in cats.

Visual cortex damage in newborn kittens produces a 78% loss of retinal X-cells whereas damage in adult cats produces only a 22% loss. Retinal Y- and W-cells are unaffected. The present experiment showed that the critical period for the severe loss of retinal X-cells ends between birth and 2 weeks of age. These results have implications for understanding the neural mechanisms of recovery from early visual cortex damage.

Age Factors↗