bluuebunny/crossref_metadata_2025_split huggingface dataset:
Microtubule‐associated protein tau is required for axonal neurite elaboration by neuroblastoma cells
Authors: Shea T. B. , Beermann M. L. , Nixon R. A. , Fischer I. 
Published: January 2005

AbstractNB2a/d1 neuroblastoma cells constitutively express multiple isoforms of the microtubule‐associated protein tau and incorporate this protein into the axonal neurites elaborated during serum deprivation. To examine whether or not tau played an essential role in axonal outgrowth, cells cultured in serum‐free medium were treated at 24 h intervals with antisense‐ and sense‐oriented cDNA oligonucleotides (25 or 36 mers that span or are upstream of tau initiation codon) and were simultaneously serum deprived. Oligonucleotide uptake was confirmed by determination of intracellular levels of radiolabeled oligonucleotides. Treatment for 48 h with tau antisense oligonucleotides reversibly inhibited the expression of tau and the number of neurite‐bearing cells compared with treatment with sense oligonucleotides. By contrast, tubulin expression was not affected. When cells were treated with antisense oligonucleotide simultaneously with serum deprivation, the initial outgrowth of neurites was unaffected, but continued neurite elongation was prevented. By contrast, neurite outgrowth at 4 h was inhibited when cells were pretreated with tau antisense 24 h before serum deprivation. Furthermore, intracellular delivery of antitau antiserum prevented neurite outgrowth and, in cells that had previously been deprived of serum for 24 h, induced retraction of existing neurites. These findings indicate that both the initiation and the continued outgrowth of neurites are dependent on tau and that pre‐existing cytoplasmic pools of tau can mediate initial neuritogenesis. © 1992 Wiley‐Liss, Inc.
The morphological localization and biochemical characterization of a synapsin I‐like antigen in the nervous system of Aplysia californica
Authors: Bongiovi M. E. , Ambron R. T. , Silverman A.‐J. 
Published: January 2005

AbstractSynapsins are a well‐characterized class of phosphoproteins found at synapses in the mammalian nervous system. One member of this family, synapsin I, has been extensively studied and shown to associate in a phosphorylation‐dependent manner with both small synaptic vesicles and cytoskeletal elements. Though the characteristics of synapsin I suggest an important function in synaptic transmission, its definitive role is still in question. In an effort to find a model system in which to test directly the function of synapsin I, we have looked in the nervous system of the marine mollusc Aplysia californica for synapsin I‐like antigens (SILA).Light microscope immunocytochemical studies using polyclonal and monoclonal antibodies to bovine brain synapsin I demonstrate Aplysia SILA in neuronal somata, in the neuropil, and at some identified synapses. Though SILA were exclusively associated with neuronal structures in Aplysia, the pattern of staining suggested that they are not present at all synaptic terminals. This interpretation was corroborated by ultrastructural studies in which SILA were present at some synaptic terminals but absent, or in low abundance, in adjacent terminals. In axons, SILA were associated with vesicles of 120–150 nm diameter, as well as with filamentous structures. Biochemical studies identified small amounts of SILA of 40 and 50 kD molecular weight that are recognized by several antibodies to mammalian synapsin I, and are acid extractable, collagenase‐sensitive phosphoproteins; these are criteria used to define synapsin I homologues in other species. Our studies indicate that SILA are present in neurons in Aplysia californica but suggested that they represent only a small percentage of the total protein within the nervous system. © 1992 Wiley‐Liss, Inc.
Nerve growth factor receptor gene expression in human peripheral blood lymphocytes in aging
Authors: Kittur Smita D. , Song L. , Endo H. , Adler W. H. 
Published: January 2005

AbstractNerve growth factor (NGF) has a modulating effect on immune function, which may occur as a consequence of binding to the NGF receptor (NGF‐R). To determine if mRNA for the gene coding for p75NGFR (low affinity NGF‐R) is present in lymphocytes, Northern blot analysis of mRNA from human peripheral blood lymphocytes (PBL) and purified T lymphocytes was initiated using cDNA probe for human p75NGFR. p75NGFR mRNA was present in PBL and T lymphocytes, and the mRNA in response to phytohemagglutinin stimulation showed maximum levels at 14 hr of stimulation. p75NGFR mRNA content when analyzed in PBL and T cells from volunteers of various ages showed that p75NGFR mRNA expression does not change with the age of the cell donor. © 1992 Wiley‐Liss, Inc.
Differential expression of the presynaptic protein SNAP‐25 in mammalian retina
Authors: Catsicas S. , Catsicas M. , Keyser K. T. , Karten H. J. , Wilson M. C. , Milner R. J. 
Published: January 2005

AbstractWe have studied the expression of the nerve terminal protein synaptosomal associated protein 25 (SNAP‐25) in the retina of adult rat, mouse, and monkey, as well as in the developing mouse retina. To evaluate SNAP‐25 expression, its distribution was compared to those of the synaptic vesicle‐associated proteins synapsin I and synaptophysin. In situ hybridization in adult rat retinas suggested that SNAP‐25 mRNA is mainly expressed by ganglion, amacrine, and horizontal cells, but not by photoreceptors and bipolar cells. In all species, the SNAP‐25 polypeptide was most abundant in the inner part of the inner and outer plexiform layers and was also found in the ganglion cell axons. In adult retina, synapsin I and synaptophysin were also mainly localized in synaptic fields and processes but all three proteins showed a distinct pattern of distribution. Finally, in mouse retina, the three proteins were first detectable at embryonic day 16 and subsequently showed developmentally regulated changes in their cellular localization. These results suggest that SNAP‐25 is predominantly expressed in specific subtypes of conventional synapses, but not ribbon synapses, and that it may also be involved in the physiology of nonvesicular terminals of horizontal cells. Our study also suggests that combinatorial expression of different components of the presynaptic specialization may contribute to synaptic functional diversity. © 1992 Wiley‐Liss, Inc.
Cold‐induced alterations in the binding of adrenomedullary nuclear proteins to the promoter region of the tyrosine hydroxylase gene
Authors: Miner L. L. , Pandalai S. P. , Weisberg E. P. , Sell S. L. , Kovacs D. M. , Kaplan B. B. 
Published: January 2005

AbstractIt is well documented that cold stress induces a rapid trans‐synaptically mediated increase in the relative abundance of rat adrenomedullary tyrosine hydroxylase (TH) mRNA. To investigate the transcriptional mechanisms regulating the cold stress response, we have employed a gel mobility shift assay, using DNA fragments prepared from the proximal 5′ flanking region of the bovine TH gene as a heterologous molecular probe. In pilot studies, this region of the bovine TH promoter (nucleotides −246 to +21) was fused to the bacterial reporter gene, chloramphenicol acetyltransferase, and the chimeric construct transfected into human neuroblastoma SK‐N‐BE(2)‐C, hepatoma HepG2, and rat pheochromocytoma PC‐12 cells. Results of this analysis indicate that the proximal 5′ flanking region of the bovine TH gene contains sufficient information to drive transient reporter gene expression in both human and rat catecholaminergic clonal cell lines. The findings derived from the gel mobility shift studies demonstrate that cold exposure causes rapid and selective alterations in the binding of adrenomedullary nuclear proteins to the proximal 5′ flanking region of the TH gene. The most striking cold stress‐induced alteration in DNA/nucleoprotein binding occurs in a region of the TH promoter (nucleotides −246 to −189) which contains an element bearing marked sequence similarity to an AP1 binding site and is highly conserved among animal species. This alteration occurs within 1 hr of cold exposure and persists for up to 48 hr after the onset of stress. The results of adrenal denervation experiments indicate that the cold‐induced change in DNA/nucleoprotein binding is neurally mediated, requiring intact sympathetic innervation of the gland. Formation of the cold‐induced DNA/nucleoprotein complex was inhibited by competition with a synthetic oligodeoxyribonucleotide containing a consensus sequence for the AP1 binding site. Pretreatment of adrenomedullary nuclear extracts with antibodies to either c‐Fos or c‐Jun also inhibited the cold‐induced alteration in DNA/nucleoprotein binding. Heat denaturation of the anti‐Fos or anti‐Jun antibodies, or preadsorption of the antibodies with their cognate antigenic peptides eliminated the inhibitory effect. Taken together, these findings suggest that the cold‐induced increases in adrenomedullary TH gene expression are mediated, at least in part, through the interaction of a phorbol ester‐responsive element and proto‐oncogene transcription factors. © 1992 Wiley‐Liss, Inc.
Nitric oxide synthase is critical in mediating basal forebrain regulation of cortical cerebral circulation
Authors: Raszkiewicz J. L. , Linville D. G. , Kerwin J. F. , Wagenaar F. , Arneric S. P. 
Published: January 2005

AbstractThis study sought to determine whether the activity of nitric oxide synthase (NOS) is an important physiological link required to mediate increases in cortical cerebral blood flow (CBF) elicited by electrical microstimulation of the basal forebrain (BF). Changes in cortical CBF were assessed in urethane anesthetized rats using laser‐Doppler flowmetry. Microstimulation of the BF elicited stimulus‐locked increases in CBF that were dependent on frequency and current intensity (up to 280% of control at 50 Hz). Infusion of the potent NOS inhibitor NG‐nitro‐L‐arginine (L‐NNA) resulted in significant dose‐related reductions in the BF‐elicited response at 50 Hz (3.75–60 mg/kg, i.v.), significant elevation in resting mean arterial pressure (MAP) from 106 to 160 mmHg, and modest 21% reductions in resting CBF. The stereoisomer NG‐nitro‐D‐arginine (D‐NNA) was without any effect on CBF, although at higher concentrations MAP was elevated to levels comparable to those obtained with L‐NNA. Infusion of arginase was also without effect on resting or BF‐elicited CBF responses. In contrast, L‐arginine (100–400 mg/kg, i.v.) significantly potentiated the BF‐elicited response up to an additional 38%, without affecting resting CBF or MAP. This study suggests that NO, or a related nitroso precursor formed by NOS, has a critical role in mediating regulation of cortical CBF by BF neurons. © 1992 Wiley‐Liss, Inc.
Neurofilament and tubulin mRNA expression in schwann cells
Authors: Roberson M. D. , Toews A. D. , Goodrum J. F. , Morell P. 
Published: January 2005

AbstractFeeding of elemental tellurium to weanling rats blocks synthesis of cholesterol (a major component of myelin), and causes demyelination of the sciatic nerve. Expression of mRNA for myelin‐specific genes in Schwann cells is downregulated. We now demonstrate specificity for Schwann cell injury in that expression of mRNAs for neurofilament subunits and for class II β‐tubulin (parameters sensitive to axonal injury) is unaltered in neurons of the dorsal root ganglia. An unexpected result was that in tellurium‐treated rats there was marked upregulation of expression of mRNAs coding for the light and medium neurofilament subunits (“neuron‐specific” proteins) as well as that for class II β‐tubulin (the major neuronal β‐tubulin isotype) in Schwann cells. Expression of these “neuronal” mRNA species was also detected in distal stumps of transected nerves at times when Schwann cells were undergoing dedifferentiation. © 1992 Wiley‐Liss, Inc.
S‐100β and insulin‐like growth factor‐II differentially regulate growth of developing serotonin and dopamine neurons in vitro
Authors: Liu J. P. , Lauder J. M. 
Published: January 2005

AbstractTo study the phenotypic specificity of S‐100β and insulin‐like growth factor II (IGF‐II) for developing monoamine neurons, serotonin (5‐HT) neurons from the embryonic day 14 (E14) rostral raphe or dopamine (TH) neurons from the substantia nigra/ventral tegmental area were cultured for 3 days in vitro (3 DIV) in the presence of these factors. Neuronotrophic effects were analyzed by computer‐assisted morphometry of 5‐HT and TH‐immunoreactive neurons. S‐100β significantly increased several parameters of neurite outgrowth by 5‐HT neurons but inhibited the spatial extent (field area) of TH neurites. IGF‐II promoted growth of cell bodies of both phenotypes, but only stimulated neurite outgrowth by TH neurons. S‐100β and IGF‐II differentially affected the number of GFAP immunoreactive cells from raphe and substantia nigra, but these effects did not correlate with the specificity of neuronotrophic effects. S‐100β and IGF‐II immunoreactivities were expressed in glial cultures derived from the same brain regions, raising the possibility that these factors have autocrine effects on glia as well as paracrine actions on neurons. The results of this study suggest that specificity of neuronotrophic factors for particular embryonic neurons may be correlated with their neurotransmitter phenotype. © Wiley‐Liss, Inc.
Developmental changes in nerve growth factor level in rat serum
Authors: Murase K. , Takeuchi R. , Iwata E. , Furukawa Y. , Furukawa S. , Hayashi K. 
Published: January 2005

AbstractIn serum, nerve growth factor (NGF) forms a complex with α2‐macroglobulin (α2M), which formation inhibits the immunoreactivity between NGF and its antibodies. For measuring the serum level of NGF, it is thus necessary to liberate NGF from the NGF‐α2M complex and prevent reformation of such complex. The pretreatment of rat serum with 1 M guanidine hydrochloride for a few hours and operation of the enzyme immunoassay (EIA) in the presence of guanidine hydrochloride provided a reliable means for determination of the NGF level in serum. By this procedure we followed the serum NGF level in rats developmentally. It increased from prenatal day 2 to postnatal day 5 and decreased slightly at postnatal week 3, thereafter remaining constant throughout adulthood. In pregnant rats, the NGF level in serum increased threefold to fivefold before birth and then decreased rapidly. These data suggest that serum NGF level may reflect the demand for this molecule during establishment of the peripheral nervous system. © Wiley‐Liss, Inc.
Neuromuscular junctions contain NP185: The multifunctional protein is located at the presynaptic site
Authors: Perry D. G. , Li S. , Hanson V. , Puszkin S. 
Published: January 2005

AbstractThe NP185 polypeptide (AP3) is a multifunctional component isolated from brain endocytic vesicles, which binds to tubulin and clathrin light chains, decoated vesicles, synaptic vesicles, and the synaptosomal plasma membrane (Su et al., 1991). The NP185 molecules are expressed during avian cerebellar synaptogenesis and appear to function in CNS regions rich in synaptic terminals (Perry et al., 1991). In this report we describe double‐labelling experiments with avian embryonic striated muscle fibers demonstrating the exclusive presence of the brain‐specific protein at the neuromuscular junction. We used indirect rhodamine immunofluorescence labeling with a monoclonal antibody (mAb‐8G8) to mark the location of NP185 in muscle combined with fluorescein‐alpha‐bungarotoxin to mark the postsynaptic location of the acetylcholine receptors (AChRs). We show that the distribution of both NP185 and AChRs has an overall correlation, but the location of NP185 is circumscribed to presynaptic structures adjacent but not overlapping with postsynaptic structures displaying the AchRs. To confirm the identity of NP185, the molecule was extracted from both tissues, partially purified, immunoprecipitated, and identified in Western blots with the mAb 8G8. The mAb reacted with an identical 185 kD protein band purified from both tissues. Based on its properties and specific neuronal location, the NP185 molecule may function in motor nerve terminals by screening membrane proteins, identifying areas of the synaptic plasma membrane, and to anchor these elements with structural proteins for their recycling and transport within the neuronal cellular compartments. © 1992 Wiley‐Liss, Inc.
Interleukin‐2 inhibits the GABA‐induced Cl‐ current in identified Aplysia neurons
Authors: Sawada M. , Hara N. , Ichinose M. 
Published: January 2005

AbstractThe effects of extracellularly applied recombinant human interleukin‐2 (rhIL‐2) on the γ‐aminobutyric acid (GABA)‐induced Cl‐ current recorded from identified neurons (R9 and R12) of Aplysia kurodai were investigated with conventional voltage‐clamp and pressure ejection techniques. Bath‐applied rhIL‐2 (10–40 U/ml) reduced the GABA‐induced current in the neurons without affecting resting membrane conductance and the holding current. The suppressing effect of rhIL‐2 on the current was completely reversible. Heat‐inactivated rhIL‐2 was without effect. These results suggest that the immunomodulator IL‐2 can modulate the GABA‐induced response in the nervous system. © 1992 Wiley‐Liss, Inc.
Gene therapy of maliganant brain tumors: A rat glioma line bearing the herpes simplex virus type 1‐thymidine kinase gene and wild type retrovirus kills other tumor cells
Authors: Takamiya Y. , Short M. P. , Ezzeddine Z. D. , Moolten F. L. , Breakefield X. O. , Martuza R. L. 
Published: January 2005

AbstractTumor cells infected with a retrovirus vector (VIK) containing the herpes simplex virus thymidine kinase (HSV‐TK) gene can be selectively killed by treatment with nucleoside analogues, such as ganciclovir. To mediate delivery of the HSV‐TK gene to “recipient” tumor cells, “donor” C6 rat glioma cells infected with the VIK vector (C6VIK) were superinfected with wild type Moloney murine leukemia virus (WT Mo‐MLV). These modified donor cells (C6VIKWT) produced both wild type retrovirus and the VIK vector. In culture, C6VIKWT cells were 300‐fold more sensitive to the toxicity of ganciclovir than were C6VIK cells, suggesting that the presence of wild type retrovirus contributed to the toxicity. Co‐culture of C6VIKWT cells with the C6 subline, C6BAG, sensitized the latter to ganciclovir treatment. Nude mice inoculated subcutaneously with a mixture of C6VIKWT and C6BAG cells showed regression of subsequent tumors when treated with ganciclovir. The observations show that tumor cells modified in culture by infection with a retrovirus bearing the HSV‐TK gene and wild type retrovirus are not only sensitive to ganciclovir, but can transfer this sensitivity to neighboring “naive” tumor cells in culture and in vivo. © 1992 Wiley‐Liss, Inc.
Expression of the T‐lymphocyte activation gene, F5, by mature neurons
Authors: Arai M. , Prystowsky M. B. , Cohen J. A. 
Published: January 2005

AbstractF5 was first identified as an mRNA expressed by activated but not resting T‐lymphocytes. Subsequent studies suggested that it also is selectively expressed by mature neurons. Although the F5 protein coding sequence is highly conserved, the function of the F5‐encoded protein is unknown. The present studies were undertaken to define the anatomic distribution, cellular specificity, and developmental pattern of F5 mRNA expression in the mouse nervous system, addressing specifically the question of whether the expression pattern of F5 corresponds to that of known ligand‐receptor or signal‐transduction systems. The use of a nonradioactive in situ hybridization method and paraffin‐embedded sections provided excellent morphological preservation and a high degree of cellular resolution. F5 mRNA was detected in the central nervous system, peripheral nervous system, and retina in cells having the location and morphological features of neurons. Combined in situ hybridization histochemistry for F5 mRNA and immunofluorescence staining for cell‐specific markers confirmed that neurons expressed F5 mRNA but astrocytes did not. The neuronal expression of F5 mRNA had two interesting features. First, the level of expression appeared to correlate directly with the size of the neuronal perikarya, the length of the axonal projection, or the extent of dendritic arborization. Second, F5 mRNA appeared late in post‐natal development. These observations are of interest because of preliminary data suggesting that F5 may function as a substrate for protein kinase C, which demonstrates a similar expression pattern in the nervous system. © 1992 Wiley‐Liss, Inc.
MHC class II‐positive microglia in human brain: Association with alzheimer lesions
Authors: Perlmutter L. S. , Scott S. A. , Barrón E. , Chui H. C. 
Published: January 2005

AbstractCells of the mononuclear phagocytic system (MPS) present foreign antigen on their cell surfaces bound to major histocompatibility complex (MHC) class II molecules. Previous studies of normal human brain samples reported MHC class II expression primarily by perivascular MPS cells and white matter microglial cells. Marked increases in MHC class II‐expressing microglia have been shown in many neuropathologic disorders, including Alzheimer's disease (AD). A close morphologic association between these cells and Alzheimer senile plaque β‐amyloid has been demonstrated. The present study used a mixed aldehyde fixative to enhance the localization of MHC class II‐expressing MPS cells in non‐AD and AD brain. Two antibodies against MHC class II (HLA‐DR; LN3), as well as the lectin Ricinus communis agglutinin (which recognizes both ramified and activated microglia) were used for light and electron microscopic analyses. We now report that MHC class II‐expressing ramified microglia are distributed in a uniform reticular array throughout the grey, as well as the white matter in non‐AD cases. In AD cases, immunolabelled cells had the morphology of activated microglia, with darkly stained plump somata and short, thick processes. Microglia clustered around senile plaque amyloid and neurofibrillary tangles (NFT), rather than forming the uniform array characteristic of control tissue. Finally, we report that perivascular MPS cells are found in a morphologic relationship with vascular amyloid identical to that seen between microglial cells and senile plaque β‐amyloid. These data suggest that MHC class II‐expressing cells may be involved in the degradation of NFT‐laden neurons and the posttranslational modification of extracellular‐NFT epitopes. In addition, both parenchymal and perivascular MPS cells are ideally situated to uptake and process the β‐amyloid protein precursor and deposit β‐amyloid on senile plaques, NFT, and the cerebrovasculature. © 1992 Wiley‐Liss, Inc.