bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cells of the Arcuate Nucleus and Ventromedial Nucleus of the Ovariectomized Ewe that Respond to Oestrogen: A Study Using Fos Immunohistochemistry
Authors: Clarke I. J. , Pompolo S. , Scott C. J. , Rawson J. A. , Caddy D. , Jakubowska A. E. , Pereira A. M. 
Published: March 2003

AbstractOestrogen produces a positive feedback effect on the secretion of gonadotropin releasing hormone (GnRH) and luteinizing hormone (LH) when implanted into the ventromedial/arcuate nucleus of the ovariectomized (OVX) ewe. This has led to the belief that it is in this area of the hypothalamus that oestrogen causes the preovulatory surge in GnRH/LH. To date, however, the cell types that are integral to this response have not been identified. The present study aimed to examine cellular responsiveness to oestrogen in this region of the brain using Fos immunohistochemistry and further aimed to determine the cell type that shows an acute response to oestrogen. OVX ewes (n = 4–6 per group) were given i.m. injections of oestradiol benzoate or oil (vehicle) and were killed 1–6 h later. Brains were perfused for immunohistochemistry. The number of cells in the arcuate nucleus which were immunopositive for Fos was greater (two‐ to fourfold) in the oestradiol benzoate‐treated OVX ewes (n = 5) 1 h after injection. The number of Fos‐positive cells in the ventromedial hypothalamic nucleus was 10‐fold greater in the oestradiol benzoate‐treated ewes 1 h after injection. Because there were high levels of Fos‐immunoreactive cells in oil‐treated ewes, we repeated the experiment with i.v. injection of 50 µg oestrogen or vehicle (n = 5). With this latter procedure, we found that oestrogen injection caused a significant increase in the number of Fos immunoreactive cells in the arcuate nucleus within 1 h, but there was no response in the ventromedial hypothalamus. To further characterize the types of cells that might respond to oestrogen, we double‐labelled cells for Fos and either adrenocorticotropin hormone, neuropeptide Y or tyrosine hydroxylase (a marker for dopaminergic cells). These cell types could account for less than 30% of the total number of cells that were Fos‐positive and oestrogen treatment did not cause an increase in the Fos labelling of any of these types of cell. These data show that oestrogen activates cells of the arcuate/ventromedial hypothalamus within 1 h of injection and that this response could relate to the feedback effects of this gonadal hormone. The majority of cells that produce Fos following oestrogen injection are of unknown phenotype. The data further suggest that induction of cells of the ventromedial hypothalamic nucleus require more prolonged oestrogen stimulus than cells of the arcuate nucelus.
Chronic Antidepressant Treatments Decrease Pro‐Opiomelanocortin mRNA Expression in the Pituitary Gland: Effects of Acute Stress and 5‐HT1A Receptor Activation
Authors: Jensen J. B. , Mørk A. , Mikkelsen J. D. 
Published: March 2003

AbstractConsistent findings in depressed patients are hyperactivity in the hypothalamic‐pituitary‐adrenal (HPA) axis with high plasma concentrations of adrenocorticotropic hormone and cortisol. Long‐term antidepressant treatments seem to normalize this hyperactivity, suggesting a link between the HPA axis and the action of antidepressant treatments. The present study was carried out to study the effects of antidepressant treatments on pro‐opiomelanocortin (POMC) mRNA expression, with a focus on interaction with acute stress and 5‐HT1A receptor activation. Male rats were treated for 21 days with saline, citalopram, fluoxetine, moclobemide or desipramine, and the expression of POMC mRNA in the anterior pituitary was analysed by semi‐quantitative in situ hybridization. All antidepressants, but not saline, cocaine and haloperidol, reduced POMC mRNA expression. The decrease in POMC mRNA was not observed until 9 days of citalopram treatment. Decreased POMC mRNA levels were also observed after 14 days of repeated electroconvulsive stimulation. The decreased POMC mRNA levels did not affect the stress‐induced POMC mRNA increase, measured following swim stress and restraint stress. Finally, using Fos as a marker for neural activity, we showed attenuation of 8‐OH‐DPAT‐stimulated activity in the paraventricular nucleus following 21 days of citalopram treatment. In conclusion, antidepressant treatments decrease basal POMC mRNA expression without affecting the acute stress response, and the reduced POMC mRNA may be related to reduced 5‐HT1A‐stimulated hypothalamic output.
Paradoxical Effects of Chronic Morphine Treatment on the Temperature and Pituitary‐Adrenal Responses to Acute Restraint Stress: A Chronic Stress Paradigm
Authors: Houshyar H. , Cooper Z. D. , Woods J. H. 
Published: March 2003

AbstractBody temperature and pituitary‐adrenal responses to restraint (15 min or 4 h) stress were evaluated in nondependent and morphine‐dependent rats. Male Sprague‐Dawley rats were treated twice daily with increasing doses of morphine (10–100 mg/kg, s.c.) for 16 days. Transmitters were implanted in the peritoneal cavity to monitor body temperature and blood was collected for hormone assays. Acute withdrawal from chronic morphine treatment was associated with reduced body weight, increased adrenal weight and decreased thymus weight. Sixteen days after termination of chronic morphine treatment, rats had recovered normal adrenal size, but still displayed marked thymus involution and reduced body weight. Restraint‐induced hyperthermia was attenuated in morphine‐dependent rats that had undergone 12‐h withdrawal. Sixteen days after withdrawal, rats still had not fully recovered the hyperthermic response to restraint. Chronic morphine treatment resulted in a marked elevation of basal corticosterone concentrations. Despite the negative‐feedback effects of elevated basal corticosterone concentrations, morphine‐dependent rats that had undergone 12‐h withdrawal displayed a potentiated and prolonged corticosterone response to restraint stress. In contrast, rats that had undergone 8‐day and 16‐day morphine withdrawal had recovered normal basal pituitary‐adrenal activity, but displayed significantly reduced and shorter adrenocorticotropic hormone and corticosterone responses to restraint. These results suggest that chronic morphine dependence is a chronic stressor, resulting in profound and long‐lasting changes in the temperature and pituitary‐adrenal responses to acute restraint stress in a time‐dependent manner. This morphine‐dependence model may be useful in understanding the role that hormonal stress responses play in the maintenance and relapse to opioid use in humans.
Differential Responsivity of the Hypothalamic‐Pituitary‐Adrenal Axis to Glucocorticoid Negative‐Feedback and Corticotropin Releasing Hormone in Rats Undergoing Morphine Withdrawal: Possible Mechanisms Involved in Facilitated and Attenuated Stress Responses
Authors: Houshyar H. , Galigniana M. D. , Pratt W. B. , Woods J. H. 
Published: March 2003

AbstractChronic morphine treatment produces profound and long‐lasting changes in the pituitary‐adrenal responses to stressful stimuli. The purpose of the present study was to explore the mechanisms involved in these altered stress responses. Chronic morphine administration increased basal plasma concentrations of corticosterone and adrenocorticotropic hormone (ACTH), which peaked at 36 h after the final morphine injection and returned to normal levels within 84‐h. Whole brain glucocorticoid receptor protein expression was reduced (approximately 70%) in morphine‐treated rats 4‐h after the final morphine injection and these levels recovered within 16‐h. Twelve hours following morphine withdrawal, rats displayed normal ACTH, but potentiated and prolonged corticosterone responses to restraint stress. Both the ACTH and corticosterone responses to restraint in acutely withdrawn rats were insensitive to dexamethasone. Furthermore, acutely withdrawn rats displayed reduced ACTH but prolonged corticosterone responses to peripheral corticotropin releasing hormone (CRH) administration. These findings suggest that the normal ACTH and enhanced corticosterone responses to stress in acutely withdrawn rats involved decreased sensitivity of negative‐feedback systems to glucocorticoids, reduced pituitary responsivity to CRH, and enhanced sensitivity of the adrenals to ACTH. Eight days following morphine withdrawal, rats displayed dramatically reduced ACTH, but normal corticosterone responses to restraint stress. These rats displayed enhanced sensitivity to dexamethasone and normal pituitary‐adrenal responses to CRH. These data suggest that the reduced ACTH responses to stress in 8‐day withdrawal rats involved increased sensitivity of negative‐feedback systems to glucocorticoids as well as reduced CRH and/or AVP function in response to stress. Taken together, the results of this study illustrate some of the mechanisms mediating altered stress responsivity in rats that have received chronic morphine treatment.
Sucrose Intake and Corticosterone Interact with Cold to Modulate Ingestive Behaviour, Energy Balance, Autonomic Outflow and Neuroendocrine Responses During Chronic Stress
Authors: Bell M. E. , Bhargava A. , Soriano L. , Laugero K. , Akana S. F. , Dallman M. F. 
Published: March 2003

AbstractIn adrenalectomized (ADX) rats, either corticosterone replacement or increased sucrose intake will restore body weight gain, uncoupling protein‐1, fat depot mass, food intake and corticotropin‐releasing factor mRNA expression to normal. Here, we tested the potential interactions between sucrose intake and circulating corticosterone on behavioural, metabolic, autonomic and neuroendocrine responses to the stress of cold. Rats were left intact, sham‐ADX, or ADX and replaced with pellets that provided normal, basal (30%B) or high stress (100%B) constant circulating concentrations of corticosterone ± sucrose. More calories were consumed in cold than at room temperature (RT), provided that corticosterone concentrations were elevated above mean daily basal values in cold. Neither increased sucrose nor increased chow ingestion occurred in cold if the rats were ADX and replaced with 30%B. However, sucrose drinking in this group markedly ameliorated other responses to cold. By contrast, ADX30%B rats not drinking sucrose fared poorly, and none of the metabolic or endocrine variables were similar to those in sham‐ADX controls. ADX100%B group in cold, resembled intact rats without sucrose; however, this group was metabolically abnormal at RT. We conclude that drinking sucrose lowers stress‐induced corticosterone secretion while reducing many responses to cold; elevated corticosterone concentrations in the stress‐response range are essential for the normal integrated cold‐induced responses to occur.
Hormonal and Behavioural Responses of Paradoxical Sleep‐Deprived Rats to the Elevated Plus Maze
Authors: Suchecki D. , Tiba P. A. , Tufik S. 
Published: March 2003

AbstractActivation of the hypothalamic‐pituitary‐adrenal (HPA) axis is observed immediately after 96 h of paradoxical sleep (PS) deprivation. However, when individually or group PS‐deprived rats are challenged with a mild stressor, they exhibit a facilitation of the corticosterone response, and a faster return to basal levels than control rats. Because the housing condition influences coping behaviour, we tested whether the type of PS deprivation (individually or in group) influenced anxiety‐like behaviour in the elevated plus‐maze and the accompanying adrenocorticotropin (ACTH) and corticosterone responses. Individually (I‐DEP) or group deprived (G‐DEP) rats and their appropriate control groups were either killed immediately after 96 h of sleep deprivation (time‐point 0 or ‘basal’) or exposed to a 5‐min test on the elevated plus maze and sampled 5, 20 or 60 min after test onset. Control of I‐DEP rats showed reduced locomotor activity and augmented anxiety‐like behaviour, replicating the effects of social isolation. Although I‐DEP rats exhibited higher motor activity than cage control rats, these groups did not differ in regard to the percentage of entry and time spent in the open arms. G‐DEP rats, in turn, ambulated more, entered and remained longer in the open arms, exhibiting less anxiety‐like behaviour. PS‐deprived rats exhibited higher ACTH and corticosterone ‘basal’ secretion than control rats. For all groups, peak ACTH secretion was reached at the 5‐min time‐point, returning to unstressed basal levels 60 min after the test, except for G‐DEP rats, which showed a return at 20 min. Peak levels of corticosterone occurred at 5 min for PS‐deprived groups and at 20 min for control groups. G‐DEP rats showed a return to ‘basal’ unstressed levels at 20 min, whereas the I‐DEP and control groups did so at 60 min. A negative correlation between exploration in the open arms and hormone concentrations was observed. These data indicate that housing condition influences the subsequent behaviour of PS‐deprived rats in the EPM which, in turn, seems to determine the secretion profile of ACTH and corticosterone in response to the test.
Corticotropin‐Releasing Factor Neurones of the Central Nucleus of the Amygdala Mediate Locus Coeruleus Activation by Cardiovascular Stress
Authors: Curtis A. L. , Bello N. T. , Connolly K. R. , Valentino R. J. 
Published: March 2003

AbstractHypotensive stress engages corticotropin‐releasing factor (CRF) release within the rat locus coeruleus (LC), which activates LC neurones, initiating norepinephrine release in forebrain and activation of forebrain electroencephalographic activity. This study identified CRF afferents to the LC that are engaged during hypotensive stress. One of two potential CRF afferents, the central nucleus of the amygdala (CNA) or bed nucleus of the stria terminalis (BNST), was electrolytically lesioned and LC activation during hypotensive stress was quantified. Neither lesion altered LC spontaneous discharge rate or activation by intra‐LC administered CRF. By contrast, LC activation by hypotensive stress was greatly attenuated in CNA‐lesioned, but not BNST‐lesioned, rats. Hypotensive stress‐induced changes in transcriptional activation were immunohistochemically identified in CRF neurones that were retrogradely labelled from the LC region. c‐fos immunoreactivity was prevalent in the paraventricular nucleus of the hypothalamus (PVN), CNA and BNST. However, only the PVN contained a substantial number of neurones that were doubly immunolabelled for CRF and c‐fos, and few of these were retrogradely labelled from the LC. By contrast, immunoreactivity for the phosporylated form of cyclic AMP response‐element binding protein (PCREB) was prevalent in CRF neurones in the CNA and BNST. Moreover, approximately one‐third of the PCREB‐expressing CRF neurones in the CNA were retrogradely labelled from the LC. These electrophysiological and anatomical findings implicate the CNA as a primary source of CRF that activates the LC during hypotensive stress. Additionally, CREB phosphorylation, rather than c‐fos induction, is associated with hypotensive activation of CRF‐CNA neurones that project to the LC.
Effects of Leptin on Arcuate Pro‐Opiomelanocortin and Cocaine‐Amphetamine‐Regulated Transcript Expression Are Independent of Circulating Levels of Corticosterone
Authors: Vrang N. , Kristensen P. , Tang‐Christensen M. , Larsen P. J. 
Published: March 2003

AbstractIn the hypothalamic arcuate nucleus, neurones that coexpress cocaine‐amphetamine‐regulated transcript (CART) and α‐melanocyte‐stimulating hormone [α‐MSH; pro‐opiomelanocortin (POMC) derived] peptides exert catabolic actions and are stimulated by leptin. However, leptin treatment also affects other circulating factors that influence hypothalamic gene expression. Notably, the hypercorticosteronaemia of ob/ob mice is lowered by leptin treatment. To examine the interaction between glucocorticoids and leptin on POMC/CART mRNA expression, an experiment combining leptin and adrenalectomy (ADX) in leptin deficient ob/ob mice was carried out. Obese ob/ob and lean littermate Ob/? mice were ADX or sham‐operated. ADX mice received a pellet containing 25% corticosterone subcutaneously. Seven days postoperatively, mice were injected intraperitoneally for 5 days with either recombinant human leptin or vehicle. On the sixth day, the mice were decapitated and the brains removed and trunk blood was collected for corticosterone analysis. Plasma concentrations of corticosterone were elevated in all ob/ob groups compared to Ob/?. For both ob/ob and Ob/? groups, corticosterone concentrations exhibited a decline across groups: vehicle‐sham>leptin‐sham>ADX‐vehicle>ADX‐leptin. Leptin inhibited food intake and bodyweight in ob/ob‐sham and ob/ob‐ADX to a similar extent, whereas no effect of leptin was observed in Ob/? mice. Similarly, leptin caused an identical increase in arcuate POMC and CART mRNA expression in ob/ob‐sham and ob/ob‐ADX compared to vehicle. The present data support the view that leptin influences arcuate POMC and CART mRNA expression directly, and that the effect is not modulated by corticosterone across a wide range of circulating corticosterone concentrations.
Thyroid Hormone Regulation of N‐Methyl‐d‐Aspartic Acid Receptor Subunit mRNA Expression in Adult Brain
Authors: Lee P. R. , Brady D. , Koenig J. I. 
Published: March 2003

AbstractThyroid hormone is an essential modulator of brain development, but little is known about its actions in the adult brain. Hypothyroidism is associated with gene expression changes in both central and peripheral nervous tissue. Functional consequences of adult‐onset hypothyroidism include an inability to produce long‐term potentiation in rat hippocampus and impaired learning and memory in both rats and man. Long‐term potentiation is a form of learning that is dependent on functional N‐methyl‐d‐aspartic acid (NMDA)‐preferring ionotropic glutamate receptors. This work examines the expression of ionotropic glutamate receptor subunit mRNA following surgical thyroidectomy with or without thyroid hormone replacement. In situ hybridization histochemistry was used to determine the mRNA levels of the NMDA receptor subunits NR1, NR2A, NR2B, the AMPA receptor subunit GluR1, and the kainate receptor subunit KA2. Reducing circulating concentrations of thyroid hormone by surgical removal of the thyroid gland 2 weeks before sacrifice decreased the expression of NR1 mRNA exclusively in the hippocampus. Conversely, hyperthyroidism selectively reduced NR2B mRNA expression in the dorsal hippocampus. Altering thyroid hormone status had no effect on the expression of KA2 or GluR1 subunit mRNA. The regulation of expression of NR1 and NR2B mRNA by thyroid hormone is a novel mechanism for explaining the relationship between thyroid hormone and cognitive function.
Photoperiodic and Temporal Influences on Chemosensory Induction of Brain Fos Expression in Female Prairie Voles
Authors: Hairston J. E. , Ball G. F. , Nelson R. J. 
Published: March 2003

AbstractPrairie voles (Microtus ochrogaster) typically stop breeding during winter. Male prairie voles respond to winter day lengths with gonadal regression, whereas female voles are relatively unresponsive to photoperiod. Unlike commonly studied laboratory rodents, female prairie voles do not exhibit spontaneous oestrous cycles. Instead, females are induced into oestrus by chemosensory cues from conspecific male urine. The present study investigated the interaction among day length, chemosensory cues and the initial brain responses during oestrus induction in female voles. A single drop of male conspecific urine, saline or skimmed milk was applied to the nares of female prairie voles housed for 9 weeks in either long (LD 16 : 8 h) or short (LD 8 : 16 h) days. Animals were killed 0.5, 1, 2 or 24 h after chemosensory treatment and their brains were processed for Fos immunocytochemistry. Body mass and ovarian fat pad mass were higher, but uterine and ovarian mass were lower, in short‐day compared to long‐day females. Regardless of photoperiod, Fos‐ immunoreactivity increased in the granule layer of the accessory olfactory bulb (AOB), the supraoptic nucleus and bed nucleus of the stria terminalis (BNST) (anterior medial) in females treated with male urine compared to the two control groups. Fos staining intensified in the AOB, medial and posterocortical medial amygdala and BNST (posterior ventral), 1 h and 2 h after urine treatment. In the medial preoptic area, anterior and lateral hypothalamus, and ventromedial nucleus of the hypothalamus, Fos‐immunoreactivity was elevated in females 2 h after receiving urine. Overall, long‐day females displayed higher Fos expression in response to urine than females maintained in short days. These results identify a putative neural circuitry of oestrus induction in this species, and provide an approximate time line of activation in the brain circuit responsible for oestrus induction in prairie voles.
Triumvirate nursing for personality disordered patients: crossing the boundaries safely
Authors: Melia  , Moran  , Mason  
Published: March 2003

As the issue of the treatment and effective management of personality disordered patients comes under close scrutiny in the wake of the Fallon Inquiry, we offer a brief overview of the nature of the challenges involved in nursing this difficult group of patients. Traditional methods of setting limits and defining boundaries are no longer convincing amidst the allegations of multidisciplinary staff being culpable, at one level or another, for their contribution in this tragic inquiry. In this paper we offer a strategic mechanism of constructing nursing care for this difficult group of patients and provide a framework for crossing boundaries safely through a multidisciplinary framework. We term this triumvirate nursing.Nursing management of those patients considered to have personality disorders is traditionally very difficult. This difficulty, in part, stems from the inability of nurses to strategically develop therapeutic relationships in a safe manner. Crossing boundaries is a necessary part of therapeutic exploration and relationship building; triumvirate nursing offers a safe mechanism for undertaking this. Creative thinking is a necessary part of the future development of the nursing management of these disorders.
Sleep‐disordered breathing in a predominantly African‐American pediatric population
Authors: STEPANSKI E. , ZAYYAD A. , NIGRO C. , LOPATA M. , BASNER R. 
Published: March 2003

SummaryThe goal of this study was to characterize sleep and respiratory parameters in children with sleep‐disordered breathing (SDB) as compared to children without SDB. Data are from 198 children and adolescents referred for sleep center evaluation, 128 of whom were diagnosed with SDB. In children with SDB, obesity (> 95% wgt for age) was more common than being severely underweight (< 5% wgt for age), but only the older children with SDB were heavier than age‐matched normal sleepers. Children with SDB had increased EEG arousals; sleep architecture was not otherwise significantly different from the non‐SDB group. African‐American children with SDB had significantly greater oxygen desaturation with obstructive events compared to Caucasian and Latino children. It appears that the role of obesity as a risk factor for obstructive sleep apnea (OSA) increases in children above the age of 8‐years. Additionally, African‐American children with SDB may be at increased risk for hypoxemia and cardiovascular consequences of SDB.