bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential laminar expression of AMPA receptor genes in the developing rat visual cortex using in situ hybridization histochemistry. Effect of visual deprivation
Authors: Roβner Steffen , Kumar Ashok , Kues Wilfried , Witzemann Veit , Schliebs Reinhard 
Published: April 2003

AbstractThe postnatal development of laminar pattern of AMPA receptor mRNA subtypes GluR‐A through to GluR‐D (flip variants) in the visual cortex of both normally raised and monocularly deprived rats (one eyelid sutured at the age of 11 days) was studied using in situ hybridization histochemistry and computer‐assisted image analysis. The AMPA receptors GluR‐A through to GluR‐D transcripts exhibit a differential laminar expression pattern in the developing rat visual cortex. At birth the levels of GluR‐A transcripts are lower by about 50% in each visual cortical layer as compared to the adult values. In contrast, GluR‐B to GluR‐D mRNAs are expressed in all cases at higher levels at birth than in the adult brain.Unilateral eyelid closure at postnatal day 11 for several periods of time resulted in both transient and permanent changes in the laminar development of GluR‐A through to GluR‐C transcripts but hardly affected the GluR‐D mRNA subtype. The distinct laminar developmental pattern of AMPA receptor mRNAs in rat visual cortex as well as the differential effects of visual deprivation suggest specific roles of AMPA receptor subtypes during the early postnatal maturation of visual function.
Differential development of the stress response in congenital learned helplessness
Authors: King J.A. , Campbell D. , Edwards E. 
Published: April 2003

AbstractEarly in the development of the hypothalamic‐pituitary‐adrenal (HPA) axis, the rat undergoes a stress hyporesponsive period of blunted responses to several Stressors including cold exposure (CE) and maternal deprivation (MD). We examined the development of the axis by monitoring adrenocorticotropin hormone (ACTH) plasma levels in an animal model of depression and/or anxiety characterized by learned helpless (LH) behavior and a dysfunctional HPA axis in adult life. On postnatal day 7 there was no significant difference in basal plasma ACTH levels between congenital (cLH) and controls, but cLH animals showed a blunted response to CE (P<0.001). By postnatal day 14 there was a dramatic increase in ACTH response to CE (P<0.005). On postnatal day 21 baseline ACTH and response to CE were again significantly suppressed in cLH rats. Stress responsiveness to MD was present in all groups and was insignificantly different for all ages of development between groups. These findings suggest that rats with congenital learned helplessness undergo a differential response in the development of the HPA axis in that the axis was hypersensitive at postnatal day 14 and became hyporesponsive beyond day 14 and this may, in part, account for the dysfunctional stress response observed during adulthood.
Neuraminic acid specific lectins as markers of early cortical plate neurons
Authors: Adam E. , Dziegielewska K.M. , Saunders N.R. , Schumacher U. 
Published: April 2003

AbstractEarly cortical plate and subplate cells in the developing neocortex of many animal species and humans contain one specific plasma protein, fetuin. Fetuin is heavily glycosylated and it is possible that due to the large amount of sugars, this molecule may play a part in cellular recognition during brain development.Cellular and extracellular carbohydrates in the developing brain of the sheep were studied histochemically using a battery of fluorescein‐labelled lectins. Two neuraminic acid specific lectins, Sambucus nigra and Maackia amurensis, labelled consistently the fetuin‐positive cells as demonstrated by double labelling with lectins and antifetuin antibodies. Brain sections from other species, known to contain fetuin‐positive cells (fetal cow, postnatal tammar wallaby) showed a similar lectin staining pattern to that of the sheep fetus. Additionally, sections from species thought to contain fetuin in their developing brains that failed to cross‐react with available antifetuin antibodies (postnatal Monodelphis, fetal cat) also demonstrated lectin‐positive staining in the same neuronal cell population.Thus, neuraminic acid is a common and well conserved terminal carbohydrate in cortical plate and subplate neurons of the developing brain. Neuraminic‐specific lectins are useful markers for these neurons in addition to the more traditional use of immunocytochemical methods in studies of formation of the neocortex.
Acute effects of perinatal hypoxic insult on concentrations of dopamine, serotonin, and metabolites in fetal monkey brain
Authors: Binienda Zbigniew , Fogle C. Matthew , Slikker William , Ali Syed F. 
Published: April 2003

AbstractSeven monkeys (Macaca mulatta) were laparotomized under general anesthesia (halothane, nitrous oxide, oxygen). Fetal hypoxia was induced in four monkeys by occlusion of the umbilical cord with a hydraulic occluder for 5–6 min. Three sham‐operated fetuses served as controls. After unclamping, the fetuses were allowed to reperfuse for 20–30 min. To monitor hypoxia, the fetal electrocardiogram was recorded continuously. Hypoxic insult was associated with a decrease in fetal heart rate during the occlusion. After reperfusion, fetuses were immediately sacrificed and neocortex regions dissected on ice, frozen on dry ice and stored at −70°C. Dopamine, 3,4‐dihydroxyphenylacetic acid, homovanillic acid, serotonin, and 5‐hydroxyindoleacetic acid were assayed by high performance liquid chromatography with electrochemical detection (HPLC/EC) in hippocampus, caudate nucleus and cortical regions. In the hippocampus, there was a significant increase in 5‐hydroxyindoleacetic acid concentration. In prefrontal cortex, there was a trend toward an increase in serotonin but no effects on dopamine and homovanillic acid concentrations. Dopamine, serotonin and metabolites were not altered in the caudate nucleus. These data demonstrate that fetal hypoxia followed by reperfusion produced an increase in serotonin concentration measured within the hippocampus and selected cortical areas known to be targets of hypoxic injury.
Nicotine effects on the regulation of amyloid precursor protein splicing, neurotrophin and glucose transporter RNA levels in aged rats
Authors: Monteggia L.M. , Arneric S.P. , Giordano T. 
Published: April 2003

AbstractIt has been reported that an inverse relationship exists between nicotine intake and the incidence of Alzheimer's Disease (AD). Although nicotine has been reported to induce c‐fos, in the present study it was shown that this induction does not alter the accumulation of a number of transcripts associated with AD. Altered splicing patterns of Amyloid Precursor Protein (APP) and changes in neurotrophin and glucose transporter expression have been implicated in AD and behavioral deficits in rats. The effects of subacute administration of nicotine (12 mg/ml at 2.3 μl/hr for 14 days) on the abundance levels of APP, glucose transporter(GLUT) and neurotrophin transcripts were determined by rtPCR in the hippocampus, cortex, and striatum of aged (22–24 months) male Wistar rats. No significant differences between saline and nicotine infused rats were detected for APP abundance levels or ratio of the various isoforms. However, both groups had a higher level of APP transcripts containing the Kunitz Protease Inhibitor (KPI) domain in the hippocampus than in either the cortex or striatum. The mean percentages of APP 695 for the two groups were 75% in the hippocampus and 82 and 81% in the cortex and striatum, respectively (P<0.01). No changes in the abundance of GLUT1, GLUT3, nerve growth factor (NGF) or brain derived neurotrophic factor (BDNF) transcripts were detected. However, since both APP and GLUT1 are thought to be regulated post‐transcriptionally, the present results do not rule out a change at the protein level. Further work will be required to determine whether nicotine can influence the expression of these proteins which affect neuronal function.
Migration behavior of granule cells on laminin in cerebellar microexplant cultures from early postnatal reeler mutant mice
Authors: Nagata Isao , Terashima Toshio 
Published: April 2003

AbstractThe behaviors of neuroblasts of granule cell neurons and their precursor cells on a poly‐l‐lysine/laminin substratum were examined in cerebellar microexplant cultures from early postnatal reeler mutant and normal mice. The total numbers of migrating neuroblasts and their precursor cells or blast cells derived from the mutant cerebellum were markedly reduced in comparison with their normal counterparts. However, no difference was shown between these two strains in either the numbers of blast cells or neuroblasts that migrated from single explants. In addition, all behaviors examined, such as migration of neuroblasts and the proliferation of blast cells in culture were identical between both genotypes. Thus, behaviors of both granule cells and their precursors in the cerebellar cortex of reeler mutant mouse may be qualitatively identical to those of normal counterparts, but precursors of granule cells in the external germinal layer of the cerebellar cortex may be reduced in the reeler mouse.
The survival of cultured mouse cerebellar granule cells is not dependent on elevated potassium‐ion concentration
Authors: Mogensen Helle S. , Hack Nicola , Balázs Robert , Jørgensen Ole Steen 
Published: April 2003

AbstractThe effects of K+‐induced membrane depolarization were studied on the survival and biochemical parameters in mouse and rat cerebellar granule cells grown in micro‐well cultures. Cell numbers were determined by estimating DNA content using the Hoechst 33258 fluorochrome binding assay. DNA from degenerated cells was removed by prior DNAase treatment. These DNA estimates of cell numbers were comparable with values obtained by direct counting of fluorescein diacetate‐stained viable cells. In agreement with previous studies, the survival of rat granule cells was promoted by increasing the concentration of K+ in the medium from 5 to 25 mM throughout a 7‐day culture period. In contrast, mouse granule cells survived in culture containing ‘low’ K+ (5 or 10 mM), as well as in the presence of ‘high’ K+ (25 mM). On the other hand, several biochemical parameters in mouse granule cells were markedly increased by cultivation in ‘high’ as compared with ‘low’ K+‐containing media, demonstrated by increased fluorescein diacetate esterase activity, enhanced rate of NADPH‐dependent tetrazolium reduction, augmented 2‐deoxy‐d‐glucose accumulation and increased N‐methyl‐d‐aspartate‐evoked 45Ca2+ influx. It was concluded that although cultivation in ‘high’ K+ promotes biochemical differentiation in mouse cerebellar granule cells, these cells differ from their rat counterparts in that they do not develop a survival requirement for K+‐induced membrane depolarization.
Intracerebroventricular injection of streptozotocin induces discrete local changes in cerebral glucose utilization in rats
Authors: Duelli Roman , Schröck Helmut , Kuschinsky Wolfgang , Hoyer Siegfried 
Published: April 2003

AbstractThe purpose of the present study was to investigate whether or not cerebral glucose utilization is changed locally after damage of the neuronal insulin receptor by means of intracerebroventricular (icv) streptozotocin (STZ) administered in a subdiabetogenic dosage (1.5 mg/kg bw.). STZ was administered at the start of the study, and 2 and 21 days later bilaterally into the cerebral ventricles in rats of a mean age of 18 months. The local distribution of cerebral glucose utilization was analyzed in conscious rats on the 42nd day after the first STZ injection using the quantitative (14C)‐2‐deoxyglucose method. Of the 35 brain structures investigated from autoradiograms of brain sections, 17 showed a reduction in glucose utilization. Decreases in glucose utilization were observed in the frontal, parietal, sensory motor, auditory and entorhinal cortex and in all hippocampal subfields. In contrast, glucose utilization was increased in two white matter structures. The decrease in cerebral glucose utilization observed in cortical and hippocampal areas in the present study may correspond to changes in morphobiological parameters which have been found in patients with Alzheimer's disease. The present data are in accordance with the hypothesis that an impairment in the control of neuronal glucose metabolism at the insulin receptor site may exist in sporadic dementia of Alzheimer type (DAT), and can be studied by the icv STZ animal model.
Hyperglycemia delays rostral initiation sites during neural tube closure
Authors: Peng Ying , Finley Brent E. , Fechtel Kim 
Published: April 2003

AbstractNeural tube defects contribute greatly to perinatal loss, physical handicap, mental retardation and other developmental defects, yet the mechanisms through which they occur are poorly understood. One hindrance to the study of these defects at the cellular and molecular levels is the low frequency with which they arise in susceptible animals. The present study utilizes a culture system for the study of rodent exencephaly, an animal model of human anencephaly, in which a high frequency of affected animals are obtained by culture in hyperglycemic rat serum. Rat embryos were dissected at day 9.5 from timed‐pregnant Sprague‐Dawley dams and cultured under standard conditions developed by New [Biol. Rev. (1978) 53, 81–122]. Embryos cultured under elevated glucose conditions are able to close the caudal neural tube with the failure of neural tube closure limited to the rostral neuralepithelium. In this report we present the novel finding that, although at the end of culture frequently only the hindbrain region remains open, the normal sequence of events expected during rostral closure anterior to the hindbrain is markedly delayed. In embryos cultured in hyperglycemic serum, both rostral initiation sites II and III are significantly delayed. The degree of delay increases with increasing glucose concentration in the culture medium.These studies support the use of this defined in vitro model of anencephaly for studies of the molecular and cellular bases underlying the failure of hindbrain closure and demonstrate that sufficient numbers of affected animals can be produced to obtain significant results. The similarity of our findings with hyperglycemia‐induced exencephaly to studies in mouse strains that are genetically susceptible to anencephaly suggest that the mechanisms underlying these different routes to failure of neural tube closure share common precursor events.
Coincidental appearance of the α1 subunit of the gaba‐a receptor and the type ibenzodiazepine receptor near birth in macaque monkey visual cortex
Authors: Hendrickson Anita , March Derrick , Richards Grayson , Erickson Andra , Shaw Christopher 
Published: April 2003

AbstractThe expression of subtypes of the GABA‐A/benzodiazepine receptor complex has been studied during pre‐ and postnatal development of Macaca monkey visual cortex using complementary radioligand and immunocytochemical labeling. Type I benzodiazepine receptors were labeled directly by [3H]zolpidem. Type II receptors were determined by the amount of binding for [3H]flunitrazepam (FZ) persisting in the presence of the type I‐specific ligand CL218872. Monoclonal antibody bd24 was used to label α1 subunits and bd17 to label β2 and β3 subunits of the GABA‐A receptor. Radioligand binding data and bd17 immunoreactivity indicated that type II benzodiazepine receptors were present by fetal day (Fd) 74 (44% of gestation). Immunoreactivity for the β2/β3 subunits increased until 3–6 weeks after birth, and then declined somewhat into adulthood. Neither radioligand labeling for type I receptors nor immunocytochemical staining for the α1 subunit were apparent until mid‐gestation. Both markers appeared shortly before birth in layer 4C, and then in other cortical layers after birth. Immunoreactivity for the α1 subunit increased steadily after birth until it became more intense than that for β2/3 subunits in the adult. Quantitative densitometry of CL218872 competition for [3H]FZ binding showed that type I/II distribution was 22%/78% at Fd103; 42%/58% at Fd131; 67%/33% at 9 months; and 61%/39% in adult visual cortex.This “switch” between benzodiazepine receptor subtypes overlaps the postnatal critical period for geniculostriate development, suggesting that the change from type II to type I receptors and the appearance of α1 subunits may play a decisive role in the maturation of geniculocortical axon terminations and cortical response properties. It remains to be shown whether this ‘switch’ is dependent on functional visual input.
The manufacturing strategy formulation process: Linking multifunctional viewpoints
Authors: Menda Rafael , Dilts David 
Published: April 2003

AbstractWhile there has been considerable research on thecontentof manufacturing strategy, there is a paucity of literature concerning theprocessof manufacturing strategy formulation [Ward, P.T., Brickford, D.J., Leong, G.K., 1996. Configuration of manufacturing strategy, business strategy, environment, and structure, J. Manage., 22(4) 597–626; Leong, G.K., Snyder, D.L., Ward, P.T., 1990. Research in the process and content of manufacturing strategy, Omega, 18(2) 109–122]. Many researchers have highlighted the need to overcome this deficiency by studying the process of developing manufacturing strategy [Adam, E.E., Swamidass, P.M., 1989. Assessing operations management from a strategic perspective, J. Manage., 15(2) 181–203; Anderson et al., 1989; Leong, G.K., Snyder, D.L., Ward, P.T., 1990. Research in the process and content of manufacturing strategy, Omega, 18(2) 109–122]. To effectively link the manufacturing strategy of a firm to the needs of the marketplace, critical competitive factors or order‐winning criteria must be understood and agreed upon both by operations and marketing managers [Hill, T.J., 1983. Manufacturing's strategic role, J. Operational Res. Soc., 34(9) 853–860; Hill, T.J., 1994. Manufacturing Strategy—Text and Cases, 2nd edn., Irwin, Homewood, IL]. For this study, we created and examined a process of establishing a set of order‐winning criteria for a consumer pharmaceuticals firm which involved the participation of sixteen managers from seven functional areas over four months. The foundation of the process was developed by Hill [Hill, T.J., 1989. Manufacturing Strategy—Text and Cases. Irwin, Homewood, IL; Hill, T.J., 1994. Manufacturing Strategy—Text and Cases, 2nd edn., Irwin, Homewood, IL], however it was soon evident that additional steps were required. The expanded process we developed both exposed significantly differing views among the managers and raised several questions with important managerial and research implications.
Advanced manufacturing technology: Implementation policy and performance
Authors: Small Michael H. , Yasin Mahmoud M. 
Published: April 2003

AbstractThis article investigates the relationships between adoption of various advanced manufacturing technologies (AMT), the way that firms plan for and implement them, and their eventual performance. Data obtained from 125 manufacturing firms in the U.S. is used to test several hypotheses which were derived from an extensive review of the AMT implementation literature. The four research questions that drive this study are: (1) What types of planning and installation activities have firms utilized to support their AMT adoptions?, (2) do differences in the level of effort applied to these activities have any impact on the eventual performance of the systems?, (3) are firms that are using integrated technologies, such as FMC/FMS and CIM, applying higher levels of effort on these planning and installation activities than other firms?, and (4) Are these firms achieving higher levels of success than firms that are not using the integrated technologies. The results indicate that firms adopting integrated technologies had exerted significantly higher levels of effort on strategic planning and team‐based project management and had also achieved higher levels of performance across a wider range of performance factors than other firms. In addition, firms that had exerted higher levels of effort on developing human factors appeared to be achieving more of the benefits of AMT than their counterparts. The overall results and the research and practical implications of this study are discussed.
Postnatal phencyclidine‐induced deficit in adult water maze performance is associated with N‐methyl‐d‐aspartate receptor upregulation
Authors: Sircar Ratna 
Published: April 2003

AbstractThe N‐methyl‐d‐aspartate (NMDA) receptor plays an important role in developmental plasticity. Earlier, we have shown that blocking the NMDA receptor with the non‐competitive antagonist phencyclidine (PCP), during a brief postnatal period, disrupts the water maze performance in young juvenile rats (starting at 25 days of age). We now show the long‐term effects of postnatal phencyclidine exposure on spatial learning and memory. Male and female rats were exposed to PCP (1 and 5 mg/kg) or saline, from postnatal days 5–15, and their performance in the Morris water maze (MWM) was tested both as adolescents (starting on postnatal day (PD) 35) and as adults (starting on postnatal day 60). Separate groups of adult male and female postnatal PCP‐treated and saline‐treated rats were sacrificed and saturation [3H]MK‐801 binding experiments were carried out in their hippocampi and frontal cortices; hippocampus and frontal cortex have high densities of NMDA receptors and both regions are important in spatial learning and memory. Postnatal PCP administration disrupted the water maze performance both in adolescent and adult rats of both sexes. Adult male and female rats treated postnatally with PCP had increased maximal [3H]MK‐801 binding in the hippocampus and frontal cortex compared to same‐sex saline‐treated controls. Taken together, repeated postnatal PCP (RPP) administration impaired the acquisition of spatial learning in adolescent and adult male and female rats, and this cognitive deficit was associated with increased [3H]MK‐801 labeled NMDA receptor in the hippocampus and frontal cortex. These findings are consistent with the hypothesis that PCP treatment during the postnatal period produces deficits in the water maze performance by disrupting the developing glutamatergic system.