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O F Almeida

Publications and source records attributed to O F Almeida.

At least 37 records · Page 2Linked to original sources
PubMed1996

Exacerbation of apoptosis in the dentate gyrus of the aged rat by dexamethasone and the protective role of corticosterone.

Glucocorticoid-induced cell loss in the dentate gyrus of rats of various ages was studied using the TUNEL procedure to detect apoptotic cells. A highly significant increase in the incidence of apoptosis was observed within the dentate hilus and granule cell layer within 24 h of a single injection of dexamethasone (DEX) in rats aged between 1 and 36 months; DEX-induced apoptosis was more pronounced with increasing age. Corticosterone (CORT) did not cause an increase in the rate of apoptosis above that found in age-matched controls. However, CORT pretreatment (3 h) resulted in a significantly attenuated DEX-induced apoptosis in both areas of the dentate gyrus. Serum CORT levels in saline-treated rats peaked at 6 months of age and reached a nadir at 36 months of age. The results indicate that (i) aged subjects are more susceptible to DEX in terms of dentate gyrus cell loss by apoptosis, (ii) CORT, which binds to Type I corticosteroid receptors with a high affinity, might serve to protect against the damaging effects of DEX which is a ligand of the Type II glucocorticoid receptor, and (iii) declining endogenous levels of CORT may increase the vulnerability of the dentate gyrus of aged rats to insult by DEX.

Aging↗
PubMed1996

The neurosteroid tetrahydroprogesterone attenuates the endocrine response to stress and exerts glucocorticoid-like effects on vasopressin gene transcription in the rat hypothalamus.

The neurosteroid tetrahydroprogesterone (5 alpha-pregnan-3 alpha-ol-20-one, allopregnanolone, THP), has been previously shown to counteract the anxiogenic effects of corticotropin-releasing hormone (CRH) and to interfere with noradrenergic and corticosteroid-mediated regulation of CRH release and gene transcription. Those observations indicated that, besides its sedative and analgesic activity, THP may also affect the neuroendocrine response to stress in a mode resembling that of corticosteroids. To examine this possibility, we compared the ability of THP, its precursor progesterone (P4), and the glucocorticoids dexamethasone (DEX) and corticosterone (CORT) to influence the pituitary-adrenal response to acute emotional stress and the adrenalectomy-induced increase in the gene transcription of the stress-related peptide arginine vasopressin (AVP) and of corticosteroid receptors (MR and GR) in the brain. Pretreatment of rats with a single dose of THP or P4 (50 micrograms/kg) significantly attenuated the elevation of plasma adrenocorticotropin (ACTH) and serum corticosterone after emotional stress; both steroids were, however, less potent than a similar dose of DEX. Administration of 1 mg of THP, CORT, or P4 to adrenalectomized (ADX) rats attenuated the increase in AVP mRNA levels in the ventromedial subdivision of the hypothalamic paraventricular nucleus (PVN), as compared with vehicle-treated ADX rats. However, whereas CORT and P4 influenced the ADX-induced increase in the transcription of both types of corticosteroid receptors in the hippocampus, these were unaffected by THP. In contrast to the glucocorticoids, THP and P4 failed to decrease plasma ACTH levels in rats deprived of endogenous steroids. These results demonstrate that the neurosteroid THP and its precursor P4 resemble glucocorticoids in their suppression of the pituitary-adrenal response to emotional stress; however, THP influences the transcription of glucocorticoid-responsive genes in brain structures involved in the regulation of the hypothalamo-pituitary-adrenal system in a fashion that is quite distinct from that obtained with glucocorticoids.

Adrenocorticotropic Hormone↗
PubMed1995

Corticosteroid regulation of gene expression and binding characteristics of vasopressin receptors in the rat brain.

Arginine-vasopressin (AVP) plays significant roles in neuroendocrine and autonomic regulation, and in processing of cognitive information. Its synthesis and secretion are subject to control by circulating glucocorticoids. The lateral septum and subdivisions of the hippocampus are innervated by AVP-ergic fibres and, together with AVP-producing neurons in the hypothalamic paraventricular nucleus, are major neural targets of glucocorticoid negative feedback. In this study, we investigated the effects of chronic adrenalectomy (ADX) and subsequent treatment with supraphysiological doses of corticosterone (B) on the gene expression of AVP receptors of the V1a subtype in the septum, hippocampus and hypothalamic arcuate (ARC) nucleus using semiquantitative in situ hybridization histochemistry. Adrenalectomy did not alter AVP receptor expression in any of the structures studied. Supplementation with B significantly decreased AVP receptor expression in the lateral septum and hippocampus, whereas receptor mRNA levels in the ARC were indistinguishable from those measured in controls. In a complementary study, we investigated the binding characteristics of V1 AVP receptors in membrane preparations from the hippocampus. Adrenalectomy significantly decreased the number of AVP binding sites, and chronic corticosteroid treatment was associated with a further suppression of AVP receptor concentrations in this structure. These results indicate that the gene transcription of V1a AVP receptors in the brain is regulated by circulating glucocorticoids in a site-specific fashion that largely reflects the corticosteroid sensitivity of the corresponding structure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1995

Implications of estrogen-dependent brain organization for gender differences in hypothalamo-pituitary-adrenal regulation.

Estrogens, derived from the aromatization of testosterone in the brain, account for sex-specific organization of neural circuits controlling gonadotropin release and sexual behavior. This study examines the possible organizing role of perinatal gonadal steroids in the manifestation of known, albeit unexplained, male-female differences in basal and stress-related adrenocortical secretion. We document here the existence of gender-specific differences in the gene expression of hypothalamic corticotropin-releasing hormone (CRH), and hippocampal and hypothalamic glucocorticoid receptors (GR), diurnal corticosterone secretion, as well as in the responsiveness of CRH and GR mRNA levels to exogenous estradiol. In addition, we report that neonatal estrogenization of female rats profoundly affects several regulatory substrates of the hypothalamo-pituitary-adrenal (HPA) axis, namely, the gene expression of CRH, arginine-vasopressin (AVP) and GR in the brain, and the responsiveness of these parameters to estrogen. The neonatal treatment appeared to "defeminize" a number of neuroendocrine mechanisms related to HPA function; these changes were reminiscent of those observed in earlier studies on sexual differentiation of reproductive behavior and hormonal secretion. The results indicate a pivotal role for estrogens during early development for the determination of gender-specific differences in HPA function in the mature animal and demonstrate for the first time that the brain-organizing actions of gonadal steroids may extend to nonreproductive neuroendocrine axes.

Adrenal Glands↗
PubMed1995

Lactation as a model for naturally reversible hypercorticalism plasticity in the mechanisms governing hypothalamo-pituitary- adrenocortical activity in rats.

Steady state levels of hypothalamic expression of the genes encoding corticotropin-releasing hormone (CRH), proopiomelanocortin (POMC), arginine vasopressin (AVP), and oxytocin (OT) were studied in rats to investigate the mechanisms underlying the transitions between hypercorticalism during lactation and normocorticalism upon weaning. During lactation, CRH mRNA levels and blood titers of adrenocorticotropin (ACTH) were found to be significantly reduced, although POMC mRNA levels in the anterior pituitary were not significantly different from those found in cycling virgin (control) rats; during all phases of lactation, an inverse relationship was observed between the blood levels of ACTH and corticosterone (CORT). Plasma prolactin (PRL) concentrations were elevated approximately 30-fold during lactation. Whereas steady state levels of OT mRNA were markedly increased throughout lactation, those of AVP mRNA were only transiently (initially) elevated, and the blood levels of these hormones were not significantly altered in lactating as compared with cycling virgin and postlactating rats. CRH and POMC gene expression and blood levels of ACTH, CORT, and PRL were normalized within 1-3 d of removal of suckling pups. The temporal relationships between the biosynthetic profiles of the various peptide hormones and the patterns of ACTH and CORT secretion during the two physiological states suggest that lactation-associated hypercorticalism does not merely result from increased ACTH secretion; although still not well substantiated at this time, the evidence points to contributory roles of PRL, OT, and AVP in the hypercorticalismic state found during lactation.

Adrenal Cortex↗
PubMed1995

Regulation of rat mineralocorticoid receptor expression in neurons by progesterone.

We have studied the effects of progesterone on the transcription of the mineralocorticoid receptor (MR) gene in neurons in vitro and in vivo. Progesterone treatment caused a 2.5-fold increase in activity of the MR promoter in transiently transfected N2A neuroblastoma cells. Similarly, MR promoter activity in GH3 pituitary cells was increased 2-fold after treatment with the specific progesterone receptor agonist R5020, with an even greater induction after priming with 17 beta-estradiol. Progesterone treatment also produced a dose-dependent increase in MR messenger RNA (mRNA) levels in primary hippocampal neuron cultures. In vivo, chronic administration of progesterone to estrogen-primed adrenalectomized/ovariectomized rats significantly increased MR mRNA levels in all hippocampal subfields, as determined by semiquantitative in situ hybridization histochemistry. Whereas chronic estradiol treatment decreased MR mRNA levels in the hippocampus, progesterone administration in the absence of estradiol priming was without any effect. These results indicate that 1) progesterone increases MR mRNA levels in vitro and in vivo; 2) the stimulatory effects of progesterone are at least partially mediated by induction of MR promoter activity; and 3) estrogen priming is essential for the effect of progesterone upon MR mRNA in vivo. Further, they suggest the possibility of heterologous regulation of corticosteroid receptors in the brain, whereby the responsiveness of the limbic-hypothalamo-pituitary-adrenal system to corticosteroids may be modulated.

Adrenal Glands↗
PubMed1994

Evidence that nor-binaltorphimine can function as an antagonist at multiple opioid receptor subtypes.

This study examined the influence of acute and repeated administration of the kappa-opioid receptor antagonist, nor-binaltorphimine, upon opioid-induced antinociception as measured by the tail-pressure test. A single intracerebroventricular (i.c.v.) injection of nor-binaltorphimine (30 micrograms) administered 1, 10 or 30 days prior to algesiometric testing prevented the analgesic effect of the kappa-opioid receptor agonist, (5 alpha, 7 alpha, 8 beta)-(-)-N- methyl-N-(7-(1-pyrrolidinyl)-1-oxaspiro(4,5)dec-8-yl)benzenacet amide (U69593). The analgesic effect of the mu-opioid receptor agonist, [D-Ala2,N-methyl-Phe4,Gly5-ol]enkephalin (DAMGO), and the delta-opioid receptor agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE), was not modified. In contrast, when nor-binaltorphimine was administered repeatedly (twice daily i.c.v. administration of 30 micrograms nor-binaltorphimine for 10 days), the analgesic effect of DAMGO, DPDPE as well as U69593 was abolished. In the case of mu- and delta-opioid receptor agonists, this abolition was apparent when testing occurred 1 or 2, but not 5 days after termination of nor-binaltorphimine treatment. This treatment regimen also resulted in a long-lasting antagonism (e.g. 20 days) of U69593-induced analgesia. These data show that, depending on the treatment regimen employed, nor-binaltorphimine can function as a selective kappa-opioid receptor antagonist, or as an antagonist at multiple opioid receptor subtypes. Further, they demonstrate that nor-binaltorphimine functions as a long-lasting kappa-opioid receptor antagonist in vivo.

Amino Acid Sequence↗
PubMed1994

Endogenous kappa-opioid systems in opiate withdrawal: role in aversion and accompanying changes in mesolimbic dopamine release.

The kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI) was recently shown to potentiate certain overt withdrawal signs in morphine-dependent rats. The present study sought to further assess this phenomenon by examining the influence of nor-BNI treatment upon the conditioned place aversion associated with the naloxone-precipitated withdrawal syndrome. In addition, in vivo microdialysis studies were conducted in morphine-dependent rats to determine whether nor-BNI treatment can modify withdrawal-induced changes in basal dopamine (DA) release within the mesolimbic system. Rats were pretreated with either saline or a single dose of nor-BNI and then received ascending doses of morphine for 10 days. A withdrawal syndrome was then precipitated by the administration of naloxone (1 mg/kg SC). In rats which received chronic morphine injections, administration of naloxone produced a characteristic withdrawal syndrome and a marked aversion for an environment previously associated with naloxone-precipitated withdrawal. Nor-BNI treatment potentiated most overt signs of physical dependence. This treatment also resulted in a greater withdrawal-induced place aversion. Morphine-dependent rats exhibited a marked reduction in basal mesolimbic DA release. An even greater decrease in basal DA release was observed in nor-BNI treated rats. These results suggest that endogenous kappa-systems are important in the modulation of mesolimbic DA release and the accompanying place aversion which occurs during opiate withdrawal.

Animals↗
PubMed1994

The neurosteroid tetrahydroprogesterone counteracts corticotropin-releasing hormone-induced anxiety and alters the release and gene expression of corticotropin-releasing hormone in the rat hypothalamus.

The ring-A-reduced progesterone derivative 5 alpha-pregnan-3 alpha-ol-20-one (tetrahydroprogesterone) is synthesized under normal physiological conditions in the brain and is a potent modulator of the GABA receptor. This neurosteroid has significant sedative and anxiolytic properties. Corticotropin-releasing hormone plays a major role in stress-induced activation of the hypothalamo-pituitary-adrenal axis, and sustained hyperactivity of hypothalamic corticotropin-releasing hormone-producing neurons may be causally related to both, increased pituitary-adrenal secretion and behavioural symptoms observed in anxiety and affective disorders. We investigated the effect of tetrahydroprogesterone on corticotropin-releasing hormone-induced anxiety, the basal and methoxamine-stimulated release of corticotropin-releasing hormone from hypothalamic organ explants in vitro, and adrenalectomy-induced up-regulation of the gene expression of corticotropin-releasing hormone in the hypothalamic paraventricular nucleus in rats. At doses of 5 and 10 micrograms i.c.v., tetrahydroprogesterone counteracted the anxiogenic action of 0.5 microgram of corticotropin-releasing hormone. Tetrahydroprogesterone did not alter the basal release of corticotropin-releasing hormone in vitro, but suppressed the stimulatory effect of the alpha 1-adrenergic agonist methoxamine on this parameter. Measurements of the steady-state levels of mRNA coding for corticotropin-releasing hormone by quantitative in situ-hybridization histochemistry revealed that tetrahydroprogesterone was equipotent with corticosterone in preventing adrenalectomy-induced up-regulation of peptide gene expression. Systemic administration of tetrahydroprogesterone also restrained adrenalectomy-induced thymus enlargement. These results demonstrate that tetrahydroprogesterone has anxiolytic effects that are mediated through interactions with hypothalamic corticotropin-releasing hormone in both, genomic and non-genomic fashions.

Animals↗
PubMed1994

Reduced availability of milk after central injections of corticotropin-releasing hormone in lactating rats.

Corticotropin-releasing hormone (CRH) plays a major role in activating the pituitary-adrenal axis in stress; its central application may therefore be expected to mimic stress. Since stress reportedly disrupts lactation, experiments were designed to study the effects of CRH administration upon the transfer of milk from rat mothers to their pups and to examine some of the possible underlying physiological mechanisms. CRH was administered intracerebroventricularly to primiparous rats on the 8th day of lactation immediately prior to being reunited with 8 of their overnight-separated pups. Changes in litter weights were measured for a period of up to 4 h as an index of milk procurement by the young (milk transfer); a qualitative assessment of maternal behaviour was also made. Treatment of dams with 0.1-1 nmol CRH resulted in a dose-dependent reduction in the amount of milk obtained by the pups. Conscious mothers treated with CRH initially showed intense behavioural activation; these events (mainly hyperlocomotion and grooming) in the mother resulted in reduced opportunities for nipple attachment by the pups and, thus, milk transfer. On the other hand, milk transfer was also significantly reduced in urethane-anaesthetized mothers treated with CRH, indicating that behavioural activation cannot have been the sole factor underlying the CRH-induced inhibition of milk transfer in awake dams. Although oxytocin (OT) release is stimulated by a variety of stressors, the possibility of an inhibitory effect of CRH upon OT secretion and/or disruption of the reflex arc serving milk ejection was considered. The peripheral administration of OT (100 mU/rat s.c.) did not, however, surmount the inhibitory actions of CRH upon milk transfer.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1994

Oxytocin-stimulated release of adrenocorticotropin from the rat pituitary is mediated by arginine vasopressin receptors of the V1b type.

Previous work showed the existence of receptors for arginine vasopressin (AVP) in the anterior pituitary; these receptors were classified as belonging to a distinct AVP receptor subtype, referred to as AVP-V1b receptors, and are thought to mediate the well documented ACTH-releasing activity of AVP. In the present work, high affinity receptors for another neurohypophyseal hormone, oxytocin (OT), were also shown to be present within the rat anterior pituitary; to this end, [125I]d(CH2)5[Tyr(Me)2Thr4Tyr-NH2(9)]OVT was used as a ligand in receptor binding studies. Experiments on dispersed rat anterior pituitary cells in a superfusion system confirmed earlier reports that OT acts as an additional secretagogue of ACTH, with significant effects first seen at concentrations as low as 1 nM. Further studies addressed the question of whether stimulation of ACTH release is mediated by OT receptors or whether receptors for AVP (V1b receptors) might serve this role. For this, highly selective agonist and antagonist ligands of the OT receptor and nonselective agonist and antagonist ligands of the V1b receptor were employed. Neither the OT receptor agonist Thr4Gly7OT nor the OT receptor antagonist des-Gly(NH2)9d(CH2)5-[Tyr(Me)2 Thr4]OVT displayed any influence on basal ACTH release, and des-Gly(NH2)9d(CH2)5-[Tyr(Me)2Thr4]OVT did not interfere with OT-induced ACTH release; these results indicated that OT promotes ACTH release through a receptor(s) other than the OT receptor itself. Evidence for the involvement of AVP V1b receptors was provided by the observation that the AVP receptor antagonist dP[Tyr(Me2)]AVP completely abolished OT-elicited increases in ACTH release. Thus, AVP V1b receptors mediate the actions of two structurally related peptides on ACTH secretion; the role of OT receptors in adenohypophyseal function remains to be determined.

Adrenocorticotropic Hormone↗
PubMed1993

Intrahypothalamic neuroendocrine actions of corticotropin-releasing factor.

Most studies of the neuroendocrine effects of corticotropin-releasing factor (CRF) have focused on its role in the regulation of the pituitary-adrenal axis; activation of this axis follows release of the peptide from CRF-containing terminals in the median eminence. However, a sizeable proportion of CRF fibres terminate within the hypothalamus itself, where synaptic contacts with other hypothalamic neuropeptidergic neurons (e.g. gonadotropin-releasing hormone-containing and opioidergic neurons) have been identified. Here, we summarize physiological and pharmacological data which provide insights into the nature and significance of these intrahypothalamic connections. It is now clear that CRF is a potent secretagogue of the three major endogenous opioid peptides (beta-endorphin, Met-enkephalin and dynorphin) and that it stimulates opioidergic neurons tonically. In the case of beta-endorphin, another hypothalamic peptide, arginine vasopressin, appears to be an essential mediator of CRF's effect, suggesting the occurrence of CRF synapses on, or in the vicinity of, vasopressin neurons; morphological support for this assumption is still wanting. Evidence for direct and indirect inhibitory effects of CRF on sexual behaviour and secretion of reproductive hormones is also presented; the indirect pathways include opioidergic neurons. An important conclusion from all these studies is that, in addition to its better known functions in producing adaptive responses during stressful situations, CRF might also contribute to the coordinated functioning of various components of the neuroendocrine system under basal conditions. Although feedback regulation of hypothalamic neuronal activity by peripheral steroids is a well-established tenet of endocrinology, data on modulation of the intrahypothalamic actions of CRF by adrenal and sex steroids are just emerging. Some of these newer findings may be useful in framing questions related to the mechanisms underlying disease states (such as depressive illness) in which CRF has been strongly implicated.

Animals↗
PubMed1993

Oxytocin binding sites in rat limbic and hypothalamic structures: site-specific modulation by adrenal and gonadal steroids.

Basal density and estrogen induction of oxytocin binding sites in limbic and hypothalamic structures of the rat brain were investigated by semi-quantitative autoradiography following chronic administration of dexamethasone or progesterone. The selective oxytocin receptor antagonist d(CH2)5[Tyr(Me)2,Thr4,Tyr-NH2(9)] ornithine-vasotocin was used as a ligand for oxytocin binding sites. Estrogen administration increased ligand binding in all sites investigated. Dexamethasone treatment significantly increased ligand binding in the bed nucleus of the stria terminalis, lateral ventral septum and amygdala to an extent which was comparable to that of estradiol alone. In the hypothalamic ventromedial nucleus, dexamethasone significantly decreased basal levels of oxytocin binding. Estrogen administration subsequent to dexamethasone failed to cause a further increase in oxytocin binding in all structures investigated. Chronic progesterone treatment significantly increased basal oxytocin receptor density in the limbic structures, decreased it in the ventromedial nucleus, and prevented estrogen-induced increases in ligand binding in all areas studied with the exception of the medial preoptic area. These findings demonstrate that, in addition to gonadal steroids, glucocorticoids differentially and site-specifically modulate cerebral oxytocin binding sites. The evidence for glucocorticoid and gestagen influences on oxytocin receptors and their inducibility by estrogen may be relevant to the understanding of mechanisms leading to impairment of oxytocin-related behaviours.

Adrenal Cortex Hormones↗
PubMed1993

Pituitary-adrenal function and hypothalamic beta-endorphin release in vitro following food deprivation.

Basal and dexamethasone-suppressed adrenal glucocorticoid secretion and hypothalamic beta-endorphin (BE) release in vitro were investigated in rats deprived of food for 24, 48, 72, and 96 h. Fasting for up to 48 h neither caused significant changes in serum corticosterone levels nor in the suppressive effect of dexamethasone. Food deprivation for 72-96 h resulted in increased basal serum corticosterone, diminished suppression by dexamethasone, and a significant involution of the thymus. Basal in vitro BE release from hypothalamic explants was significantly increased after the first day of food deprivation, and in vitro perifusion with corticotropin-releasing hormone (CRH) failed to enhance BE release further. With continuing food deprivation, basal BE release remained significantly greater than that from hypothalami originating from normally fed control rats. The stimulatory effect of CRH on BE release was only partially restored after 2 days of fasting. The results suggest that food deprivation for more than 2 days increases basal glucocorticoid secretion, and signs of impairment in hypothalamic-pituitary-adrenal regulation become apparent. These findings might be implicated in the pathogenetic mechanisms of endocrine dysregulation in diseases related to caloric reduction.

Adrenal Glands↗
PubMed1992

Hypothalamic corticotropin-releasing hormone and opioid peptide neurons: functional changes after adrenalectomy and/or castration.

The influences of short- and long-term castration and adrenalectomy (or both) upon corticotropin-releasing hormone (CRH) mRNA levels, CRH peptide levels, and endogenous opioid peptide (EOP) content in the hypothalamus, and basal and CRH-stimulated EOP release in vitro, were examined. Gonadal and adrenal steroids regulated the function of these hypothalamic peptidergic systems in terms of peptide synthesis, storage pools, and secretion. The steroids were also found to alter the sensitivity of EOPergic neurons to CRH. In some cases, evidence was obtained for an interaction between gonadal and adrenal steroids in determining neuronal function (seen as additive or counteractive effects). A finding of major importance was that the response of these peptidergic systems was markedly influenced by the duration of steroid deprivation, the results of chronic treatment often being opposite to those of acute treatment. Lastly, inspection of the data on peptide synthesis, storage and release, revealed that there was no simple relationship between these three parameters even within a single type of peptidergic neuron.

Adrenalectomy↗
PubMed1992

Photoperiod-driven changes in reproductive function in male rhesus monkeys.

Environmental lighting, which regulates seasonal breeding in many animal species, has not been examined as a regulator of reproduction or puberty in man or nonhuman primates. In this study we examined the effects of controlled alternating long and short daily photoperiods, independent of other environmental variables, on testicular size and function in rhesus monkeys. Sixteen animals, some pubertal, others prepubertal, were individually caged indoors in light-controlled rooms. They were subjected to a 32-week "year" with alternating 16-week cycles of long (16 h of light and 8 h of darkness) or short (8 h of light and 16 h of darkness) days. Animals were examined every 2 weeks over four 32-week "years". Body weight, testicular diameter, and testicular volume were measured, and blood was collected for testosterone and PRL determinations. We found that although short days did not trigger testicular development in prepubertal animals, testicular growth was markedly enhanced by short days in postpubertal animals, accompanied by increased plasma testosterone levels and reduced PRL levels. In long days, testes regressed, testosterone levels fell, and PRL levels rose. The periodicity of testicular size, as determined by spectral analysis, showed a strong signal at a cycle length of 31 +/- 13 weeks, but no signal at intervals close to the natural 52-week year, indicating that the observed periodicity is induced by the changes in lighting, rather than by circannual changes in other variables. These studies establish that changes in photo-period alone can modulate reproductive function in a higher primate and suggest that the onset of puberty is not directly driven by seasonal fluctuations in day length.

Animals↗
PubMed1991

Adrenalectomy and experimental hypercorticalism modulate the basal, corticotropin-releasing-hormone- and arginine-vasopressin-stimulated release of hypothalamic beta-endorphin.

Recent in vitro studies have shown that the release of hypothalamic beta-endorphin (beta-END), like that of adenohypophysial origin, is enhanced by both corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). However, whereas AVP merely synergizes with CRH in the pituitary, it seems to be essential for the release of hypothalamic beta-END by CRH. The present paper reports on the effects of long-term adrenalectomy (ADX) and subsequent replacement with supraphysiological doses of corticosterone (compound B, CB) upon the in vitro basal and CRH- and AVP-stimulated release of beta-END from the rat hypothalamus. Basal release of beta-END was significantly elevated by ADX, and returned to control levels following CB overdosage. Both ADX and CB replacement significantly reduced the stimulatory effect of CRH (10(-8) M) upon beta-END release. ADX caused no significant change in the AVP (10(-6) M)-induced release of beta-END. However, the AVP-stimulated release of beta-END was completely abolished in ADX rats treated with a high dose of CB. The hypothalamic content of beta-END was also measured following ADX and subsequent CB treatment. Compared with control tissues, those from ADX animals had significantly greater contents of beta-END; the hypothalami from rats with experimentally induced hypercorticalism had markedly reduced concentrations of the opioid peptide. Measurements of basal release and content of AVP in the hypothalamus following long-term ADX and CB treatment revealed that AVP neuronal activity is also subject to manipulations of the glucocorticoid hormone environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗