Journal of Neuroendocrinology
1365-2826
0953-8194
Anh Quốc
Cơ quản chủ quản: Wiley-Blackwell Publishing Ltd , WILEY
Lĩnh vực:
Endocrinology, Diabetes and MetabolismEndocrinologyEndocrine and Autonomic SystemsCellular and Molecular Neuroscience
Các bài báo tiêu biểu
Neurodevelopmental and Neurophysiological Actions of Thyroid Hormone For over 100 years, thyroid hormones have been known to be essential for neonatal neurodevelopment but whether they are required by the foetal brain remains a matter of controversy. For decades, the prevailing view was that thyroid hormones are not necessary until after birth because circulating levels in the foetus are very low and the placenta forms an efficient barrier to their transfer from the mother. Clinical observations of good neurological outcome following early treatment of congenital hypothyroidism were used to support the view that thyroid hormones are not required early in neurodevelopment. Nevertheless, the issue remained contentious because of findings that the severity of foetal neurological deficit due to maternal iodine deficiency correlated with the degree of maternal thyroxine (T4) deficiency. Furthermore, neurological damage in these cases could be prevented by correction of maternal T4 deficiency before mid‐gestation. This observation led to the opposing view, supported by epidemiological studies of neurological cretinism, that maternal thyroid hormones are important and necessary for early foetal neurodevelopment. It is now clear that thyroid hormones are essential for both foetal and post‐natal neurodevelopment and for the regulation of neuropsychological function in children and adults. In recent years, this controversial subject has progressed very rapidly following remarkable progress in understanding of the molecular mechanisms of thyroid hormone action. This article reviews the contributions of molecular biology and genetics to our new understanding of the physiological effects of thyroid hormones on neurodevelopment and in the adult brain.
Tập 20 Số 6 - Trang 784-794 - 2008
Coexpression of Leptin Receptor and Preproneuropeptide Y mRNA in Arcuate Nucleus of Mouse Hypothalamus
Tập 8 Số 10 - Trang 733-735 - 1996
Endocrine Disrupters: A Review of Some Sources, Effects, and Mechanisms of Actions on Behaviour and Neuroendocrine Systems Some environmental contaminants interact with hormones and may exert adverse consequences as a result of their actions as endocrine disrupting chemicals (EDCs). Exposure in people is typically a result of contamination of the food chain, inhalation of contaminated house dust or occupational exposure. EDCs include pesticides and herbicides (such as dichlorodiphenyl trichloroethane or its metabolites), methoxychlor, biocides, heat stabilisers and chemical catalysts (such as tributyltin), plastic contaminants (e.g. bisphenol A), pharmaceuticals (i.e. diethylstilbestrol; 17α‐ethinylestradiol) or dietary components (such as phytoestrogens). The goal of this review is to address the sources, effects and actions of EDCs, with an emphasis on topics discussed at the International Congress on Steroids and the Nervous System. EDCs may alter reproductively‐relevant or nonreproductive, sexually‐dimorphic behaviours. In addition, EDCs may have significant effects on neurodevelopmental processes, influencing the morphology of sexually‐dimorphic cerebral circuits. Exposure to EDCs is more dangerous if it occurs during specific ‘critical periods’ of life, such as intrauterine, perinatal, juvenile or puberty periods, when organisms are more sensitive to hormonal disruption, compared to other periods. However, exposure to EDCs in adulthood can also alter physiology. Several EDCs are xenoestrogens, which can alter serum lipid concentrations or metabolism enzymes that are necessary for converting cholesterol to steroid hormones. This can ultimately alter the production of oestradiol and/or other steroids. Finally, many EDCs may have actions via (or independent of) classic actions at cognate steroid receptors. EDCs may have effects through numerous other substrates, such as the aryl hydrocarbon receptor, the peroxisome proliferator‐activated receptor and the retinoid X receptor, signal transduction pathways, calcium influx and/or neurotransmitter receptors. Thus, EDCs, from varied sources, may have organisational effects during development and/or activational effects in adulthood that influence sexually‐dimorphic, reproductively‐relevant processes or other functions, by mimicking, antagonising or altering steroidal actions.
Tập 24 Số 1 - Trang 144-159 - 2012
Anxiolytic Effect of Progesterone is Mediated by the Neurosteroid Allopregnanolone at Brain GABA<sub>A</sub> Receptors Abstract Previous studies from this laboratory have shown that progesterone (PROG) treatment in ovariectomized rats produces an anti‐anxiety response similar to that observed after the administration of prototypical anxiolytic benzodiazepine (BDZ) compounds. The PROG‐induced anxiolytic response was highly correlated with an increased level of 3α‐hydroxy‐5α‐pregnan‐20‐one (allopregnanolone) in the blood and brain, and was also associated with a facilitation of GABA‐stimulated chloride ion (Cl− ) influx in cortical synaptoneurosomes. This correlative evidence suggested that the anxiolytic effect of PROG was a result of its in vivo reduction to the neuroactive steroid, allopregnanolone. In this report, a series of studies was conducted to determine the mechanism(s) by which PROG alters behavior in animal models of anxiety. In the first experiment, ovariectomized rats were injected with PROG (1 mg/0.2 ml, SC) 4 h prior to a test in the elevated plus‐maze. Some animals also received an injection of picrotoxin (0.75 mg/kg, IP), a GABAA receptor‐gated Cl− channel antagonist, whereas other animals were pretreated with RU 38486 (5 mg/0.2 ml, SC), a progestin receptor antagonist. PROG elicited anxiolytic behavior in the plus‐maze, an effect that was blocked by picrotoxin administration. Pretreatment with RU 38486 was not effective in altering PROG‐induced anxiolytic behavior in the plus‐maze. In a second experiment, the effect of PROG on behavior in the plus‐maze was determined in the presence of N,N‐diethyl‐4‐methyl‐3‐oxo‐4‐aza‐5α‐androstane‐17β‐carboxamide (4‐MA; 10 mg/0.2 ml, SC), a 5α‐reductase inhibitor. The enzyme inhibitor was potent in preventing the anxiolytic effect observed in the plus‐maze after PROG administration. In the defensive burying paradigm, PROG treatment also produced anxiolysis by reducing the duration of burying behavior, and this effect was prevented by 4‐MA pretreatment, but not by RU 38486 administration. After the completion of the behavioral assays, analysis of blood allopregnanolone levels revealed a marked increase in PROG‐treated females. The PROG‐induced elevation in circulating allopregnanolone was blocked by pretreatment with 4‐MA. In cortical synaptoneurosomes, the sensitivity (inverse of the EC50 ) and the maximal response (Emax) in GABA‐stimulated 36 Cl− uptake were increased in PROG‐treated females. The potentiation of PROG on both of these neurochemical measures was not observed in animals pretreated with 4‐MA. Together, these studies provide evidence that the anxiolytic effect of PROG is not associated with an intracellular steroid receptor that initiates genomic‐mediated responses. The evidence is consistent with a nongenomic mechanism whereby PROG is metabolized to allopregnanolone, a neuroactive steroid that potentiates GABAA receptor‐mediated responses.
Tập 7 Số 3 - Trang 171-177 - 1995
Gonadectomy Reverses The Sexually Diergic Patterns Of Circadian and Stress‐Induced Hypothalamic‐Pituitary‐Adrenal Axis Activity In Male and Female Rats Abstract Enhanced corticosterone release by female compared to male rats under basal and stress conditions is well documented. The demonstration that gonadectomy enhances stress‐induced corticosterone secretion in male rats, but reduces such levels in female rats, suggests a causal association between gonadal steroids and corticosterone release. The present study examined the corticosterone profile of sham gonadectomized and gonadectomized female and male rats under basal and stress conditions. An automated sampling system collected blood from each freely moving, unanaesthetized rat every 10 min (i) over a 24‐h period; (ii) following noise stress; and (iii) following an immune‐mediated stress (lipopolysaccharide, LPS). Plasma was analysed for corticosterone content using radioimmunoassay. Castration resulted in a significant increase in basal corticosterone release compared to the sham‐castrated male rats. Pulsar analysis revealed a significant two‐fold increase in the number of corticosterone pulses over 24 h. Corticosterone increases in response to noise stress and to LPS injection were enhanced following castration. Conversely, ovariectomy resulted in a two‐fold reduction in the number of corticosterone pulses as well as the stress response compared to sham‐ovariectomized female rats. Arginine vasopressin (AVP), corticotrophin‐releasing hormone (CRH) and glucocorticoid receptor mRNAs in the paraventricular nucleus and pro‐opiomelanocortin (POMC) mRNA in the anterior pituitary were analysed post‐LPS administration by in situ hybridization. Significantly higher values were found for AVP, CRH and POMC mRNAs examined for sham females and castrated males compared to sham males and ovariectomized females. This study confirms previous reports concerning the influence of gonadal factors in regulating HPA axis activity and stress responsiveness. The present results extend these observations to the regulation of the dynamic pattern of corticosterone release under basal conditions and suggests that this alteration in pulsatility is important for the differences in stress responsiveness when comparing males and females.
Tập 16 Số 6 - Trang 516-524 - 2004
Gonadal Steroid Replacement Reverses Gonadectomy‐Induced Changes in the Corticosterone Pulse Profile and Stress‐Induced Hypothalamic‐Pituitary‐Adrenal Axis Activity of Male and Female Rats Abstract We investigated the effects of gonadal hormone replacement on the pulsatile parameters underlying basal circadian corticosterone secretion in castrated male and ovariectomized female rats using an automated sampling system. Blood was collected from freely moving, unanaesthetized rats every 10 min over a 24‐h period and sampling was continued during a noise stress and after lipopolysaccharide (LPS) administration. Castrated male rats had markedly higher corticosterone levels than intact controls. This was reflected by increased number and frequency of pulses in addition to an increase in the pulse height and amplitude under both basal circadian and stress conditions. Hormone replacement with either testosterone or dihydrotestosterone returned these corticosterone levels and circadian profile to those found in intact males, confirming an androgen‐mediated effect. Ovariectomized females had significantly lower basal and stress‐induced corticosterone levels with lower frequency and amplitude of corticosterone pulses than intact females. 17β‐oestradiol replacement returned basal levels, pulsatile measurements and stress‐induced corticosterone levels to those found in intact females. Three hours post‐LPS administration, castrated males demonstrated significantly higher values of parvocellular paraventricular nucleus (PVN) arginine vasopressin and corticotrophin‐releasing factor and anterior pituitary pro‐opiomelanocortin mRNA while ovariectomized females showed significantly lower levels of all three transcripts compared to intact controls. PVN glucocorticoid receptor mRNA levels 3 h post‐LPS administration were significantly decreased in castrated males and significantly increased in ovariectomized female rats. Replacement of gonadal steroids resulted in a return to the levels found in intact controls after LPS. Gonadal steroid replacement is sufficient to reverse changes in the pulsatile characteristics of corticosterone release after gonadectomy. In addition, gonadal steroid replacement reverses stress‐induced alterations in hypothalamic‐pituitary‐adrenal (HPA) activity. These data demonstrate a major contribution of gonadal steroids to the regulation of HPA axis activity and to the pulsatile characteristics of corticosterone release.
Tập 16 Số 12 - Trang 989-998 - 2004
Maternal Deprivation in Rats is Associated with Corticotrophin‐Releasing Hormone (CRH) Promoter Hypomethylation and Enhances CRH Transcriptional Responses to Stress in Adulthood Exposure to stress during early development causes long‐lasting alterations in behaviour and hypothalamic pituitary adrenal (HPA) axis activity, including increased expression of corticotrophin‐releasing hormone (CRH). To determine whether early‐life stress causes epigenetic changes in the CRH promoter leading to increased CRH transcription, 8‐week old female and male rats, subjected to maternal deprivation (MD) between days 2 and 13 post‐birth, were studied for HPA axis responses to stress and CRH promoter methylation in the hypothalamic paraventricular nucleus (PVN) and central nucleus of the amygdala (CeA). Plasma corticosterone and PVN CRH heteronuclear (hn)RNA responses to acute restraint stress were higher in MD rats of both sexes. DNA methylation analysis of the CRH promoter revealed a significantly lower percentage of methylation in two CpGs preceding (CpG1) and inside (CpG2) the cyclic AMP‐response element (CRE) at −230 bp in the CRH promoter in the PVN but not the CeA of MD rats. Gel‐shift assays, using nuclear proteins from forskolin‐treated hypothalamic 4B cells and CRH promoter CRE oligonucleotides, unmethylated or methylated at CpG1, revealed a strong band that was supershifted by phospho‐cAMP response element‐binding antibody. This band was 50% weaker using oligonucleotides methylated at CpG2 (intra‐CRE), or methylated at both CpG1 and CpG2. These findings demonstrate that HPA axis hypersensitivity caused by neonatal stress causes long‐lasting enhanced CRH transcriptional activity in the PVN of both sexes. Hypomethylation of the CRH promoter CRE, a region critical for CRH transcriptional activation, could serve as a mechanism for the increased transcriptional responses to stress observed in MD rats.
Tập 24 Số 7 - Trang 1055-1064 - 2012
Effect of Intraseptal Vasotocin and Vasoactive Intestinal Polypeptide Infusions on Courtship Song and Aggression in the Male Zebra Finch (<i>Taeniopygia guttata</i>) The present experiments were conducted to test the hypothesis that septal arginine vasotocin (AVT) and vasoactive intestinal polypeptide (VIP) modulate directed song (a courtship behaviour) and aggression in male zebra finches (Taeniopygia guttata ). Subjects were surgically fitted with a guide cannula directed at the septum. Following recovery they were tested for aggression and directed song following infusions of AVT, its antagonist (anti‐vasopressin, AVP), and saline volume control. Infusion of the AVT antagonist significantly reduced all three aggressive behaviours measured (pecks, beak fences and chases); and AVT infusion significantly facilitated beak fencing. Vasoactive intestinal polypeptide treatment significantly reduced pecking. No treatment produced a change in directed song. Comparison with findings in mammals suggests that modulation of aggression by septal AVT (or AVP) is evolutionarily conserved in vertebrates, but modulation of aggression by VIP has not previously been reported for any vertebrate.
Tập 11 Số 1 - Trang 19-25 - 1999
Projection Sites of Medial Preoptic Area and Ventral Bed Nucleus of the Stria Terminalis Neurons that Express Fos during Maternal Behavior in Female Rats Medial preoptic area (MPOA) and ventral bed nucleus of the stria terminalis (VBST) neurons are involved in maternal behavior, but the neural sites to which the maternally relevant neurons project have not been determined. Since MPOA and VBST neurons express Fos during maternal behavior, we used a double‐labeling immunocytochemical procedure to detect both Fos and a retrograde tracer, wheat germ agglutinin (WGA), in order to determine where these Fos neurons project. On Day 4 postpartum, fully maternal females were separated from their litters. On Day 5, WGA was iontophoretically injected into one of the following regions known to receive MPOA and/or VBST input: Lateral septum, medial hypothalamus at the level of the ventromedial nucleus, lateral habenula, ventral tegmental area, retrorubral field, or periaqueductal gray. On Day 7, females received a 2‐h test with either pups or candy, after which they were perfused and their brains were processed for the detection of Fos and WGA. As expected, females tested with pups had more Fos‐containing neurons in the MPOA and VBST than did females tested with candy. After WGA injections into several brain sites, the number of double‐labeled cells observed in the MPOA and VBST was greater for the maternal females when compared to the non‐maternal females. Therefore, these results pinpointed neural circuits that were activated during maternal behavior. For the maternal females, Fos‐containing neurons in the MPOA projected most strongly to the medial hypothalamus at the level of the ventromedial nucleus and to the lateral septum, while Fos‐containing neurons in the VBST projected most strongly to the retrorubral field, ventral tegmental area, and medial hypothalamus. Although relatively few MPOA and VBST neurons which expressed Fos during maternal behavior projected to the periaqueductal gray, these Fos‐expressing neurons made up a relatively large proportion of the MPOA and VBST projection to the periaqueductal gray. This study suggests that MPOA and VBST efferents project to a variety of regions to promote full maternal responsiveness.
Tập 9 Số 5 - Trang 369-384 - 1997
Chronic Administration of Leptin into the Lateral Ventricle Induces Sexual Maturation in Severely Food‐restricted Female Rats In many species, delayed sexual maturation occurs when metabolic conditions are not satisfactory. Recently, leptin was shown to be involved in the regulation of food intake and body mass. Furthermore, leptin administration was shown to advance sexual maturation in mice and to rescue sexual function in adverse metabolic conditions. We examined plasma leptin levels in female rats during development and evaluated the role of leptin on sexual maturation in rats subjected to food restriction. In normal rats, plasma leptin levels were low at day 24 of life, then steadily increased during the juvenile period, reaching 740 ±56 pg/ml at 40 days at time of vaginal opening (VO) and further increasing by day 60 (957±73 pg/ml). Food restriction initiated at day 25 strongly impaired this increase, in proportion to the severity of the restriction. With a daily food intake reduced to 7–8 g/day, that permanently prevented VO, plasma leptin levels were very low at day 53 (169 ±67 pg/ml). Following switch to ad libitum feeding, plasma leptin reached high levels within 2 days (1577±123 pg/ml), and VO occurred 4 days later. If the severe food restriction was maintained and a central infusion of leptin (10 μg/day) was initiated, a significant decrease in body weight compared with vehicle‐infused controls was observed. In these conditions, VO occurred in eight out of the nine leptin‐treated rats, representing induction of the process of sexual maturation confirmed by increases in ovarian and uterine weights. This induction of sexual maturation exclusively results from a central effect of leptin because no leak of the icv administered leptin to the general circulation was observed. These data suggest that the rising plasma levels of leptin in the prepubertal period represent a signal to the brain indicating that the young animal is metabolically ready to go through the process of sexual maturation.
Tập 10 Số 8 - Trang 627-633 - 1998