bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neuritogenic effect of estradiol on rat ventromedial hypothalamic neurons co‐cultured with homotopic or heterotopic glia
Authors: Cambiasso M. J. , Díaz H. , Cáceres A. , Carrer H. F. 
Published: January 2005

AbstractIn sexually segregated cultures of dissociated neurons taken from ventromedial hypothalamus of rat fetuses at embryonic day 16 (E16), it is demonstrated that only neurons from males respond with increased axonal growth to the addition of 17‐β‐estradiol 100 nM (E2) to the culture medium. Moreover, this response is contingent upon co‐culture with heterotopic glia from a target region (amygdala), whereas in the presence of homotopic glia or in cultures without glia, E2 has no effect. It is concluded that before neurons are exposed to gonadal steroids in utero there is a sexual difference in the response to E2, probably explained by earlier maturation of neurons from males as compared to females. The possibility that the observed axogenic effect may be the consequence of an interaction among E2, cells equipped with specific receptors, and glia‐producing trophic factors is discussed. © 1995 Wiley‐Liss, Inc.
Widespread expression of the peripheral myelin protein‐22 gene (pmp22) in neural and non‐neural tissues during murine development
Authors: Baechner D. , Liehr T. , Hameister H. , Altenberger H. , Grehl H. , Suter U. , Rautenstrauss B. 
Published: January 2005

AbstractThe gene encoding the peripheral myelin protein PMP22 is affected by various mutations in the hereditary peripheral neuropathies Charcot‐Marie‐Tooth disease type 1A (CMT1A), Déjérine‐Sottas syndrome (DSS) and hereditary neuropathy with liability to pressure palsies (HNPP). In contrast to the recent remarkable progress in the genetics of the PMP22 gene, the biological function of PMP22 remains largely unknown. In this report, we have confirmed by using in situ hybridization techniques that high levels of PMP22 niRNA are present in maturing peripheral nerves of the 2‐week‐old mouse, a finding consistent with the PNS‐specific defect observed in hereditary peripheral neuropathies. However, high levels of PMP22 transcripts were also found in the villi of the adult gut, and PMP22 expression was detected in various non‐neural tissues during embryonic mouse development. In early embryogenesis (9.5 days postconception, dpc), PMP22 RNA expression appears restricted to the epithelial ectodermal layer. During early organogenesis (11.5 dpc), particularly high levels of expression are present in the capsule surrounding the liver and in the forming gut, while low levels of PMP22 mRNA can be fund in precartilagous condensations forming the vertebrae and the ventricular layer of the myelencephalon. During midgestation development (14.5 dpc to 16.5 dpc), the number of PMP22‐positive tissues increases, and high expression is detected in several mesoderm‐derived tissues, in particular connective tissues of the face region, bones including the vertebrae, the lung mesenchym, and in muscles. In addition, high expression is also found in ectoderm‐derived tissues, especially the epithelia of the lens and the skin. These findings strongly suggest that PMP22 serves not only a PNSspecific function but is also of broader biological significance in cell proliferation and/or differentiation. ©1995 Wiley‐Liss, Inc.
Comparative distribution of GAD65 and GAD67 mRNAs and proteins in the rat spinal cord supports a differential regulation of these two glutamate decarboxylases in vivo
Authors: Feldblum S. , Dumoulin A. , Anoal M. , Sandillon F. , Privat A. 
Published: January 2005

AbstractGamma‐aminobutyric acid (GABA) synthesis can result from the action of at least two glutamic acid decarboxylase (GAD) isoforms, GAD65 and GAD67, possibly involved in distinct mechanisms. We have made the hypothesis that GAD65 may respond to short‐term changes and is present in neurons with a phasic activity, while GAD67 may rather provide GABA for the metabolic pool and for supporting tonic levels of synaptic transmission (Erlander et al.: Neuron 7:91–100, 1991; Feldblum et al.: J Neurosci Res 34:689–706, 1993). In the present work we have tested this hypothesis in the rat spinal cord where both types of activities have been identified. The correlation of GABA immunodetection with the distribution of GAD65 and GAD67 mRNAs and proteins has evinced in the dorsal horn a differential regulation of the two isoforms. In situ hybridization has revealed, in the dorsal horn, relatively higher levels of GAD67 mRNA than of GAD65, while immunodetection of the proteins demonstrated numerous punctate profiles with both GAD antisera. Reverse transcription‐polymerase chain reaction (RT‐PCR) data confirmed the abundance of the GAD67 transcripts compared to GAD65 in the rat spinal cord. In contrast, within the ventral horn, there was a greater number of GAD67‐immunoreactive (IR) profiles mostly located around motoneurons. The paucity of GAD65 immunoreactivity in the ventral horn cannot be related to a different accessibility of the antigens to the epitopes since on the same section a dense GAD65 staining was detected in the dorsal horn. Hence, a number of biochemical and electrophysiological data support the concept of the involvement of glycine as the major inhibitory system within the ventral horn which may explain the low levels of GAD transcription in this region. The paucity of GAD65 in the ventral horn may also reflect a functional difference, suggesting a predominance of GAD67 in neurons under tonic activity. In the dorsal horn, where neurons with phasic and tonic firing patterns have been disclosed, GAD65 may, in addition, provide GABA for responses to short‐term changes. ©1995 Wiley‐Liss, Inc.
Exogenous myelin basic protein promotes oligodendrocyte death via increased calcium influx
Authors: Tzeng S.‐F. , Deibler G. E. , DeVries G. H. 
Published: January 2005

AbstractTreatment of cultured oligodendrocytes (OLGs) with micromolar quantities of myelin basic protein (MBP) caused a rapid, MBP‐dose dependent cell death. In contrast, a 72‐hr incubation of OLGs with MBP peptides (1–44, 47–87, 88–151, or 152–167) at comparable concentrations had no effect on cell viability. MBP and MBP peptides (1–44 and 88–151) have been shown to interact with ganglioside GM1 (Tzeng et al.: J Neurochem Res: 42:758–767, 1995). This interaction has been reported to increase calcium influx. Therefore, using the fluorescent dye Indo‐1 and an ACAS laser cytometer, we examined the level of intracellular calcium in OLGs after MBP treatment. MBP was shown to provoke a rapid, dramatic, and sustained rise of intracellular calcium in most OLGs. The levels of elevated intracellular calcium were sustained and did not return to baseline even after 10 min. This increase of intracellular calcium was suppressed in the presence of EGTA, indicating that the [Ca2+]i rise was due to the entry of extracellular calcium. Incubation of cultured OLGs with MBP peptides (1–44 or 88–151) caused a modest and transitory elevation of intracellular calcium ions in a lower percentage of OLGs. The potent OLG cytotoxicity of intact MBP and the loss of potency after proteolysis raise the possibility that MBP proteolysis during demyelination protects OLGs from death. ©1995 Wiley‐Liss, Inc.
Neurotransmitter synthesis by SN6 cell lines, a family of hybrid cell lines of embryonic septal origin
Authors: Gallyas F. , Satoh J. , Endoh M. , Kunishita T. , Tabira T. 
Published: January 2005

AbstractPreviously, we reported the presence of multiple neurotransmitters in subclones of SN6, a septal cholinergic hybrid cell line. To obtain information concerning the functionality of these transmitters, we measured transmitter contents, activities of transmitter‐producing enzymes, and the effect of serum‐free culture medium in two different batches (SN6.1.6 and SN6.10.2.2) and two subclones of the SN6 cell line (SN6.2a and SN6.1b). Except for SN6.1b, SN6 cell lines and subclones had basically the same neurotransmitter characteristics. Among the transmitters, only acetylcholine seemed to be functional. Monoamine oxidase was missing and activity of aromatic amino acid decarboxylase was diminished in SN6 cell lines. Even in serum‐containing medium, SN6.1b had a more mature morphology than the other cell lines, and it contained choline acetyltransferase and acetylcholine but not tyrosine hydroxylase or catecholamines. Similar characteristics were acquired by the mother cell line in response to serum‐free conditions. Thus, SN6.1b is the most mature of these central cholinergic neuronal cell lines, at least with regard to neurotransmitter profiles. ©1995 Wiley‐Liss, Inc.
Perinatal morphine II: Changes in cortical plasticity
Authors: Germani E. , Lesma E. , De Biasi S. , Di Giulio A. M. , Bertelli A. , Gorio A. 
Published: January 2005

AbstractWe have previously shown that perinatal exposure to morphine impairs reactive plasticity of serotonin (5‐HT) neurons following selective neonatal lesion (Gorio et al., J Neurosci Res 34:462–471, 1993). This study shows that morphine inhibits also that the compensatory sprouting of intact axons after partial denervation. Neonatal 6‐OHDA injection causes norepinephrine (NE) depletion in the frontal cortex, which triggers a compensatory increase of dopamine, serotonin (5‐HT), and met‐enkephalin content correlated by the increased density of tyrosine hydroxylase– and 5‐HT–positive axons. In perinatal morphine‐treated rats, no compensatory changes are observed after neonatal 6‐OHDA depletion of NE in the frontal cortex. ©1995 Wiley‐Liss, Inc.
Attenuation and recovery of nerve growth factor receptor mRNA in dorsal root ganglion neurons following axotomy
Authors: Krekoski C. A. , Parhad I. M. , Clark A. W. 
Published: January 2005

AbstractThe actions of nerve growth factor (NGF) are mediated by two receptor proteins, trk and p75. Recent evidence indicates that NGF upregulates the expression of both trk and p75 in responsive neurons including rat dorsal root ganglion (DRG) neurons. Axotomy by disconnecting the neuron from its source of target‐derived NGF is predicted to lead to the downregulation of trk and p75 expression. However, previous studies of the effects of axotomy on trk and p75 mRNA expression in rat DRG have yielded discrepant results. We report that following sciatic nerve crush, trk and p75 mRNA levels in L4‐L6 DRG decrease to ∼50% of control levels at 4–14 days, return to control levels by 30 days, and are increased by ∼30% at 60 days. Similar changes are observed following nerve transection although mRNA levels are slower in returning to normal and do not exceed control levels at later timepoints. Thus, trk and p75 expression decline early following target disconnection and later recover irrespective of target reinnervation. These observations indicate that target derived NGF is required for the maintenance of NGF receptor expression in adult rat DRG neurons and that non‐target derived factors can appropriate this function following peripheral nerve injury. © 1996 Wiley‐Liss, Inc.
OX‐40 antibody enhances for autoantigen specific Vβ8.2+ T cells within the spinal cord of lewis rats with autoimmune encephalomyelitis
Authors: Weinberg A. D. , Lemon M. , Jones A. J. , Vainiene M. , Celnik B. , Buenafe A. C. , Culbertson N. , Bakke A. , Vandenbark A. A. , Offner H. 
Published: January 2005

AbstractThe Vβ8.2 T cell receptor (TCR) component is the predominant Vβ gene product associated with antigen specific CD4+ T cell response to the major encephalitogenic epitope of myelin basic protein (MBP) in Lewis rats. Lewis rats were actively immunized with MBP in complete Freund's adjuvant and the Vβ8.2 positive and negative cells were analyzed for IFN‐γ mRNA production and OX‐40 cell surface expression during the onset of EAE. The Vβ8.2+ T cells isolated from the spinal cord produced the majority of mRNA for IFN‐γ and also showed a marked enhancement for OX‐40 expression compared to Vβ8.2+ T cells isolated from the lymph nodes. Only a fraction of IL‐2 receptor positive T cells examined ex vivo from the inflammatory compartments co‐expressed the OX‐40 antigen. These results suggested that OX‐40 cell surface expression could be used to identify and isolate the most recently activated T cells ex vivo. OX‐40+ T cells isolated from the spinal cord were highly enriched for the Vβ8.2 T cell receptor component compared to OX‐40− or unsorted spinal cord lymphocytes. OX‐40+ T cells isolated from the spinal cord had an enhanced response to MBP, whereas OX‐40+ cells isolated from the lymph nodes responded to both MBP and purified protein derivative. These data suggest that activated T cells can be isolated and characterized with the OX‐40 antibody which only respond to the antigens present at the local site. The data also imply that isolation of OX‐40+ T cells will be useful in identifying Vβ biases and autoantigen specific cells within inflamed tissues even when the antigen specificity is unknown. © 1996 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America
Methylphenylpyridium ion (MPP+) enhances glutamate‐induced cytotoxicity against dopaminergic neurons in cultured rat mesencephalon
Authors: Sawada H. , Shimohama S. , Tamura Y. , Kawamura T. , Akaike A. , Kimura J. 
Published: January 2005

AbstractParkinson's disease is characterized by chronic progression of dopaminergic neuronal death, the mechanism of which is still unknown. Although methyl‐4‐phenylpyridium ion (MPP+) or MPP+‐like substance, that can reduce mitochondrial complex I activity, is supposed to be a causative agent for Parkinson's disease, it is difficult to explain the chronic neuronal degeneration for years. It is important to identify other putative agents capable of causing chronic cell death besides MPP+. We hypothesized that treatment with small doses of MPP+, not causing severe damage to dopaminergic neurons but merely reducing the activity of mitochondrial complex I, can be a model of Parkinson's disease, and that glutamate can be a putative agent causing chronic neuronal degeneration. Using primary culture of the rat mesencephalon, we investigated glutamate‐induced cytotoxicity against dopaminergic and non‐dopaminergic neurons with or without the pretreatment with MPP+. Brief exposure to glutamate showed similar cytotoxicity against both dopaminergic and non‐dopaminergic neurons. An N‐methyl‐D‐aspartate receptor antagonist completely blocked the glutamate‐induced cytotoxicity against both dopaminergic and non‐dopaminergic neurons. In the dopaminergic neurons, MPP+ caused cytotoxicity that was not blocked by co‐administration of MK‐801. After pretreatment with small doses of MPP+, sub‐lethal doses of glutamate caused severe cell damage restricted to dopaminergic neurons, suggesting that MPP+ potentiates the glutamate‐induced cytotoxicity only against dopaminergic neurons. As glutamate is putatively capable of causing cytotoxicity against dopaminergic neurons, the present findings might be important in considering the pathogenesis of dopaminergic neuronal degeneration and a possible therapeutic application of glutamate receptor antagonists in Parkinson's disease. © 1996 Wiley‐Liss, Inc.
Alterations of dopamine release by rat caudate putamen tissues superfused with α2‐Macroglobulin
Authors: Hu Y.‐Q. , Liu B.‐J. , Dluzen D. E. , Koo P. H. 
Published: January 2005

AbstractMonoamine‐activated alpha‐2‐macroglobulin (α2M) has been shown to decrease the dopamine concentrations in rat caudate putamen (CP) in vivo as well as inhibit choline acetyltransferase activities in the culture of basal forebrain neurons. In this study, we further investigated the effects of methylamine‐activated α2M (MA‐α2M) upon striatal rlopaminergic function by determining whether a direct infusion of this glycoprotein will alter dopamine (DA) release in vitro from superfused CP tissue fragments. In experiment 1, an infusion of 2.8 μM MA‐α2M produced a statistically significant increase in DA release compared with control superfusions. In experiment 2, varying doses (0, 0.7, 1.4, 2.8, 4.1 μM) of MA‐α2M were tested for their capacity to alter DA release. Only the 2.8 μM dose of MA‐α2M was effective in producing a significant increase of DA release. In experiment 3, the normal form of α2M (N‐α2M) at 2.8 μM was compared with the control superfusions. The infusion of N‐α2M produced an increase in DA release which was substantially lower than the DA increase induced by MA‐α2M, and not significantly different from that of the control superfusion. These results show that MA‐α2M, like some other neurotoxins, can markedly alter CP dapaminergic function as indicated by the acute increase in DA release following infusion of this glycoprotein, and these effects are exerted at a relatively narrow range of doses. Taken together, these data suggest that this glycoprotein, if allowed to accumulate in the central nervous system (CNS), may promote some neurodegenerative changes that can occur in disorders like Parkinson's disease. © 1996 Wiley‐Liss, Inc.
Disappearance of actin‐binding protein, drebrin, from hippocampal synapses in alzheimer's disease
Authors: Harigaya Y. , Shoji M. , Shirao T. , Hirai S. 
Published: January 2005

AbstractThe actin‐binding protein drebrin is localized in postsynaptic terminals in adult brain and is considered to be related to synaptic plasticity. Immunocytochemical study demonstrated that widespread drebrin immunoreactivity was observed in hippocampal formations of control human brains, while Alzheimer's disease (AD) brains showed remarkable reductions in this immunoreactivity. Western blot analysis demonstrated that drebrin E (116 kD) as well as drebrin A (125 kD) presented in adult human brains, and that these isoforms were decreased in parallel in AD brains. On the other hand, synaptic vesicle‐specific 38‐kD protein (SVP‐38), a presynaptic marker was not so changed in AD brains in comparison with control brains by both techniques. These findings suggest that drebrin E and A in the adult human brain may be co‐localized in postsynaptic terminals, and that drebrin may be more sensitive as a marker of synaptic damage than SVP‐38, and that the disappearance of drebrin may contribute to the pathogenesis of memory disturbance in AD. © 1996 Wiley‐Liss, Inc.
Identification and topography of neuronal cell populations expressing; TNFα and IL‐1α in response to hippocampal lesion
Authors: Tchélingérian J.‐L. , Le Saux F. , Jacque C. 
Published: January 2005

AbstractIn previous studies, we have shown that a traumatic lesion to the hippocampus of adult mice induces the transitory expression of TNFα and IL‐1α by neurons of different brain areas and also by glial cells at the site of injury. The aim of the present study was to establish whether the expression of TNFα and IL‐1α is restricted to defined subpopulations, or else is common to most of the central neuronal populations. Using polyclonal anti‐GAD 67, anti‐TH and monoclonal anti‐ChAT, and anti‐5‐HT antibodies in a double‐labeling immunohistochemical procedure in combination with murine anti‐TNFα and anti‐IL‐1α polyclonal antibodies, we show that most GABAergic, catecholaminergic, and serotoninergic neurons, and a subgroup of the cholinergic neurons, express these cytokines. Although not immunohistochemically characterized, neurons in some glutamatergic structures such as the hippocampus and the prefrontal cortex also express these cytokines. Thus, we conclude that the capacity of central neurons to express cytokines like TNFα and IL‐1α in reaction to a brain Injury is not restricted to peculiar neuronal subtypes, but could include most of the neuronal populations of the brain. © 1996 Wiley‐Liss, Inc.
Effects of MF‐268, a new cholinesterase inhibitor, on acetylcholine and biogenic amines in rat cortex
Authors: Zhu X.‐D. , Cuadra G. , Brufani M. , Maggi T. , Pagella P. G. , Williams E. , Giacobini E. 
Published: January 2005

AbstractMF‐268 bitartrate [(3a S, 8a R)‐1,2,3,3a,8,8a‐hexahydro‐1,3a,8‐trimethylpyrrolo[2,3‐b]indol‐5‐ol[8‐(cis2, 6‐dimethyl‐morpholin‐4‐yl)octyl]‐carbamate L‐bitartrate hydrate; Mediolanum Farmaceutici, Milan, Italy] is a pseudo‐reversible carbamate‐type cholinesterase inhibitor (ChEI) which interacts with the catalytic and regulatory anionic site of the enzyme. Its effects on extracellular levels of acetylcholine (ACh), norepinephrine (NE), dopamine (DA), and serotonin (5‐HT, 5‐hydroxytryptamine) were studied in rat cortex by using a microdialysis technique coupled with high‐performance liquid chromatography‐electrochemical detection (HPLC‐ECD). Conscious, freely moving rats were systemically [per os (p.o.) and subcutaneously (s.c.)] administered MF‐268 with no ChEI in the probe. Cholinesterase inhibition in brain was assayed in parallel experiments.Oral administration of MF‐268 (0.5, 2.0, and 5.0 mg/kg) produced a significant increase of extracellular ACh in cortex; the maximal increase was 300% [not significant (n.s.)], 460% and 1,200%, respectively. Maximal cholinesterase (ChE) inhibition was 2.3% (n.s.) at 9 hr and 9.7% (P < .05) at 12 hr after the 2.0 and 5.0 mg/kg doses, respectively. Norepi nephrine and DA levels were increased 180% and 100% after the 5.0 mg/kg dose, respectively; 100%, and 60% after the 2.0 mg/kg dose, respectively; and 70% for both amines after the 0.5 mg/kg dose, respectively. The elevation lasted at least 5 hr with the 2.0 and 5.0 mg/kg doses. There were no major changes in 5‐HT levels at these three doses.Subcutaneous administration (0.5 and 2.0 mg/kg) produced a maximal 360% (5.5 hr) and 2,500% (5 hr) increase in extracellular ACh, respectively. Maximal ChE inhibition was 13% (0.5 mg/kg) and 41% (2.0 mg/kg). Neither 0.5 nor 2.0 mg/kg produced a consistent modification of NE. Only a transient increase in DA was seen with the 0.5 mg/kg dose. There were no changes in 5‐HT levels at these two doses. MF‐268‐treated animals showed slight cholinergic side effects (chewing, tremor) at both doses.MF‐268 administered intracortically through the microdialysis probe at a concentration of 50 p.M induced a 5,900% increase in ACh levels at 6 hr. This effect started 30 min after injection and continued throughout the period of administration. MF‐268 produced a significant decrease in NE levels (−44%) starting at 30 min, and a slight but significant increase in DA levels of 45% at 2.5 hr. A significant increase of 5‐HT (58%) was also observed starting at 4 hr. Slight symptoms of cholinergic toxicity were observed during intracortical administration. © 1996 Wiley‐Liss, Inc.
Optimisation of processing conditions for infrared drying of cashew kernels with testa
Authors: Hebbar Umesh H , Ramesh MN 
Published: January 2005

AbstractCashew kernels are thermally processed to facilitate the removal of their outer skin (testa). Infrared (IR) processing of cashew kernels for differential drying is a novel approach. Processed cashew kernels are valued for their colour, size and texture. The kinetics of colour change and the effect of thermal processing on compressive strength (indicator of brittleness) during IR drying of cashew kernels were investigated. Kernels with testa were dried for different durations (15–55 min) over a range of temperatures (55–95 °C). The change in colour was expressed as total colour difference and browning index. The colour values increased with increasing drying temperature and duration, indicating darkening of the kernel colour. Increase in drying duration reduced the compressive strength, imparting the desired brittleness to the kernel. Optimisation of the drying conditions by response surface methodology and the peelability factor indicated that the best results could be obtained when cashew kernels were dried at 55 °C for 55 min. Copyright © 2004 Society of Chemical Industry