bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characteristics of the K‐252a‐induced increase in calcium uptake in PC12 cells
Authors: Nikodijevic B. , Aschkenasy M. , Dickens G. , Lachance C. , Guroff Gordon 
Published: January 2005

AbstractK‐252a treatment produced a 30–50% increase in the uptake of radioactive calcium by PC12 cells within 3–4 minutes. The increase in uptake was partially blocked by inhibitors of voltage‐operated calcium channels, such as nifedipine, but not by inhibitors of receptor‐operated calcium channels, such as nickel or suramin. Introduction of phosphatase 2A into the cells completely blocked the effect of K‐252a. Longterm treatment of the cells with either K‐252a or with nerve growth factor blocked the subsequent actions of either K‐252a or nerve growth factor on calcium uptake, but neither altered the subsequent action of the L‐channel agonist Bay K 8644 on calcium uptake. Calcium uptake was not stimulated by K‐252a in PC12nnr, cells that have little or no high‐affinity nerve growth factor receptors; cells expressing increased levels of high‐affinity nerve growth factor receptors showed a response to K‐252a comparable to that seen in parent PC12. The data suggest that the increased uptake of radioactive calcium produced by K‐252a is mediated by a mechanism very similar to that serving the increased calcium uptake produced by nerve growth factor. © 1995 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America
Colocalization of NGF and TSH‐like immunoreactivity in cultures of adult rat anterior pituitary cells
Authors: Burnham P. , Conner J. M. , Varon S. 
Published: January 2005

AbstractNerve growth factor (NGF) has been well‐characterized with respect to its role as a trophic agent for various peripheral nervous system (PNS) and central nervous system (CNS) neuronal populations. Recent evidence indicates that NGF may also play a functional role in endocrine systems, although investigations in this field are only beginning to define sites of action and molecular mechanisms involved in NGF endocrine interactions. A potential site for such an interaction to occur is within the pituitary. Previous investigations have demonstrated the presence of NGF and NGF receptors in the pituitary and our group has recently reported the presence of NGF‐like immunoreactivity exclusively within the thyrotrophic cells of the anterior pituitary of the adult rat. Since many questions regarding how NGF interacts in the anterior pituitary will be more efficiently addressed using an in vitro system, it was necessary to first determine if cultured adult anterior pituitary cells retain the NGF‐like staining and unique association of NGF with thyroid‐stimulating hormone‐producing cells seen in vivo. Results of the present investigation confirm that cultured anterior pituitary cells retain the characteristics previously observed in vivo and further demonstrate the stability of these cells and their specific NGF and pituitary hormone contents in culture for as long as 6 days. © 1995 Wiley‐iss, Inc.
Innervation of cutaneous structures in the mouse hind paw: A confocal microscopy immunohistochemical study
Authors: Navarro X. , Verdú E. , Wendelschafer‐Crabb G. , Kennedy W. R. 
Published: January 2005

AbstractThe normal innervation of structures in mouse foot pads was investigated with immunohistochemistry and confocal microscopy. Nerves were visualized by incubating Zamboni fixed, thick, frozen sections with antibodies to protein gene product 9.5 (PGP 9.5), vasoactive intestinal peptide, substance P, calcitonin gene‐related peptide, and protein zero. The antibodies were localized using cyanine 3.18 labeled anti‐rabbit gamma globulin. PGP 9.5 immunolocalization showed dense nerve bundles at the base of the foot pad with branches to larger blood vessels, sweat glands and epidermis. Sweat gland tubules were surrounded by numerous sudomotor axons; single fibers accompanied the sweat duct toward the skin's surface. Nerve bundles containing myelinated and unmyelinated axons ran through and around the centrally located sweat gland cluster to end in free nerve endings and Meissner's‐like corpuscles at the apex of the foot pad. Other bundles running parallel to the epidermis gave arcuate branches that supplied epidermis on the sides of the pads with a rich nerve network, principally with free nerve endings that often reached the most superficial cell layers of epidermis. Calcitonin gene‐related peptide‐immunoreactive (‐ir) nerves were distributed to dermis and epidermis in lower density than PGP 9.5‐ir fibers. Substance P‐ir fibers were less numerous; most terminated as free endings in deeper layers of epidermis. Vasoactive intestinal peptide‐ir nerves almost exclusively innervated sweat glands, ducts and blood vessels, but not epidermis. The mouse hind paw has potential to serve as a model system for investigations of functional and morphological changes that affect peripheral and au tonomic nerves under diverse experimental conditions. © 1995 Wiley‐Liss, Inc.
Intracellular routing of human amyloid protein precursor: Axonal delivery followed by transport to the dendrites
Authors: Simons M. , Ikonen E. , Tienari P. J. , Cid‐Arregui A. , Mönning U. , Beyreuther K. , Dotti C. G. 
Published: January 2005

AbstractA characteristic neuropathological feature of Alzheimer's disease is the cerebral deposition of amyloid plaques. These deposits contain b̃A4 amyloid peptide, a cleavage product of the transmembrane protein amyloid protein precursor (APP). Despite numerous studies on the processing of the different APP isoforms in non‐neuronal cells, little is known about its sorting and transport in neurons cf the central nervous system (CNS). To analyze this question we expressed in cultured rat hippocampal neurons the human APP 695, tagged at its N‐terminus with the myc epitope, using the Semliki forest virus (SFV) expression system. APP was first delivered from the cell body to the axon and later appeared also in the dendrites. Inhibition of protein synthesis at the time of axonal expression did not block the late appearance of the protein in the dendrites. An antibody directed against the myc tag, bound to the cell surface at 4°C at the time of axonal APP expression, could be chased to the dendritic domain after subsequent incubation at 37°C. These results suggest that the newly synthesized APP, after initial axonal delivery, may be transported to the dendrites by a transcytotic mechanism. The routing of APP in polarized neurons is different from that of polarized epithelial cells, in which the protein is delivered basolaterally, arguing for neuronal specific sorting and processing mechanisms. © 1995 Wiley‐Liss, Inc.
Demonstration of interleukin‐3 receptor‐associated antigen in the central nervous system
Authors: Konishi Y. , Chui D.‐H. , Kunishita T. , Yamamura T. , Higashi Y. , Tabira T. 
Published: January 2005

AbstractWe previously reported that interleukin‐3 (IL‐3) acts as a neurotrophic factor for cholinergic neurons. However, it has not yet been determined whether the action is derived from the interaction of IL‐3 with IL‐3 receptors. As the first step to study IL‐3 receptors in the central nervous system, we examined the presence and localization of IL‐3 receptor‐associated antigen (IL‐3RAA) in mouse and rat brain. Immunohistochemically, IL‐3RAA, which is closely involved both in the IL‐3 binding to IL‐3 receptors and the tyrosine phosphorylation in the signal transduction for IL‐3 in hematopoietic cells, was demonstrated in neurons throughout the brain. This was confirmed in primary cultured neurons and neuronal cell lines by immunocytochemistry and flow cytometry. The staining intensity varied among regions and the most intense immunoreactivity for IL‐3RAA was found in large neurons in the magnocellular basal nuclei, pyramidal cells in the cerebral cortex, and neuronal cells in some nuclei of the brainstem. Not only cholinergic cell lines derived from the septal region but also other neuronal cell lines exhibited IL‐3RAA immunoreactivity by flow cytometry. Therefore, we conclude that IL‐3RAA is present in a wide variety of neurons in the brain including cholinergic neurons of the basal forebrain. Western blot analysis revealed that the candidates for IL‐3RAA are 145, 100, and 50 kDa proteins both in neuronal and IL‐3‐dependent cell lines. © 1995 Wiley‐Liss, Inc.
Second generation cholinesterase inhibitors: Effect of (L)‐huperzine‐A on cortical biogenic amines
Authors: Zhu X.‐D. , Giacobini E. 
Published: January 2005

AbstractL‐Huperzine‐A (Hup‐A), a natural cholinesterase inhibitor (ChEI) derived from the Chinese herb Huperzia serrata, was administered systemically (i.p.) or locally through the microdialysis probe into the rat cortex. Systemic Hup‐A significantly increased acetylcholine (ACh) levels above baseline at doses of 0.1, 0.3, and 0.5 mg/kg; the increases were 54%, 129%, and 220%, respectively. Norepinephrine (NE) and dopamine (DA) levels were also increased 121% and 129% above baseline at 0.3 mg/kg, and 143% and 153% at 0.5 mg/kg. Peak cholinesterase (ChE) inhibition was 23% at 60 min with the 0.3 mg/kg dose. Huperzine‐A, perfused through the microdialysis probe, produced a maximal increase of ACh levels of 3090% and 7790% at concentrations of 5 and 50 μM. The ACh increase seen at both concentrations lasted at least 6 hr. At the 5‐μM dose, NE and DA were increased by 214% and 386%; at the 50‐μM dose, NE and DA were increased by 216% and 1141%. There were no changes of 5‐HT levels. With local administration (via the probe), both doses produced facialforelimb seizures that lasted throughout the perfusion. Our results show that Hup‐A is a potent inhibitor of ChE which penetrates into the brain and produces a dose‐dependent increase of ACh, NE, and DA in rat cortex. This effect is seen with both systemic and local intracerebral administration, suggesting cortical as well as subcortical effects of the drug. © 1995 Wiley‐Liss, Inc.
GABA‐induced motility of spinal neuroblasts develops along a ventrodorsal gradient and can be mimicked by agonists of GABAA and GABAB receptors
Authors: Behar T. N. , Schaffner A. E. , Tran H. T. , Barker J. L. 
Published: January 2005

AbstractDuring embryogenesis, neuroblasts proliferate within germinal zones, then migrate to their final positions. Although many neurons migrate along radial glial fibers, evidence suggests that environmental factors, as yet unidentified, also influence neuroblast movement. In vivo, nerve growth factor (NGF) and ‐α‐aminobutyric acid (GABA) colocalize near target destinations of migratory neuroblasts. In vitro, embryonic spinal neurons migrate towards NGF and GABA (Behar et al.: J Neurosci 14:29‐38, 1994), implying that the molecules may act as chemoattractants in vivo. Here, we have used an in vitro assay of migration to show that migratory responses to these attractants develop along a ventrodorsal gradient that parallels terminal mitosis during cord development, and that GABA stimulates chemokinesis (motility without a gradient) via heterogeneous receptors involving separate signalling pathways. Both GABAA (muscimol) and GABAB (baclofen) agonists mimicked the effects of GABA in stimulating chemokinesis. Muscimol‐induced motility was only blocked by GABAA antagonists (bicuculline or picrotoxin), whereas migration to baclofen was blocked by antagonists of both GABAA and GABAB (2‐hydroxysaclofen) receptors. Migration to baclofen, but not muscimol, was abolished in the presence of 8‐bromo cAMP or pertussis toxin, indicating that the former, but not the latter, attractant may stimulate motility via Gi/Go GTP binding proteins, and that PKA may modulate migratory responses to baclofen. Migration to GABA was partially attenuated by each of the GABA receptor antagonists. These results lead us to conclude that the natural ligand stimulates neuroblast motility via heterogeneous receptors coupled to different signalling mechanisms. © 1995 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
AMPA receptors shape Ca2+ responses in cortical oligodendrocyte progenitors and CG‐4 cells
Authors: Holtzclaw L. A. , Gallo V. , Russell J. T. 
Published: January 2005

AbstractIntracellular calcium signals triggered by glutamate receptor activation were studied in primary cortical oligodendrocyte lineage cells and in the oligodendrocyte cell line CG‐4. Glutamate, kainate, and AMPA (30‐300 μM) increased [Ca 2+]i in both types of cells at the stage of oligodendrocyte progenitors (O‐2A; GD3+) or pro‐oligodendroblasts (04+). The peak amplitude of Ca2+ responses to glutamate receptor agonists was significantly larger in cortical cells. In CG‐4 and in cortical cells, the majority (more than 90%) of bipolar GD3+ or multipolar 04+ cells responded to kamate. In all the cells analyzed, kainate was more efficacious than AMPA and glutamate. The percentage of bipolar or multipolar cells responding to glutamate was significantly lower in the CG‐4 cell line than in primary cultures. Cellular responses typical of metabotropic glutamate receptor activation were observed in 20% of the cortical O‐2A progenitors, but in none of the CG‐4 cells. The AMPA‐selective antagonist GYKI 52466 blocked kainate‐induced Ca2+ responses in cortical O‐2A cells. The selective AMPA receptor modulator cyclothiazide (30 μM) greatly potentiated the effects of AMPA (30‐100 μM) on [Ca 2+]i in cortical and CG‐4 cells. Our findings indicate that Ca2+ responses in cells of the oligodendrocyte lineage are primarily shaped by functional AMPA receptors. © 1995 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Epidermal growth factor (EGF), transforming growth factor‐α (TGF‐α), and basic fibroblast growth factor (bFGF) differentially influence neural precursor cells of mouse embryonic mesencephalon
Authors: Santa‐Olalla J. , Covarrubias L. 
Published: January 2005

AbstractGrowth factors are key elements in the process of neural cell differentiation. We examined the effects of classical mitogens on neural precursor cells, by culturing mouse cells of the embryonic (13.5 days postcoitum) mesencephalon and treating them with epidermal growth factor (EGF), transforming growth factor‐β (TGF‐β), basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and transforming growth factor‐β (TGF‐ β). Our initial results show that EGF, TGF‐α or bFGF, but not NGF or TGF‐β, induced general proliferation of the cultured cells, followed by formation of colonies. Combinations of these three growth factors suggest that most cells with the capacity to form colonies responded to EGF, TGF‐α, or bFGF. The number of colonies increased significantly when EGF, but not TGF‐α, was used in combination with bFGF. Furthermore, a population responding only to EGF + bFGF was detected in the dorsal mesencephalon. The colony‐forming activity of bFGF was dependent on insulin, but bFGF and insulin cooperation was indirect since we could not observe colony formation in subcultures of cells derived from colonies, even in the presence of insulin. Cells obtained from our colonies displayed neuronal and glial morphology and expressed markers of both neurons and astrocytes; nestin, a marker of neural precursor cells was also expressed in the majority of colonies. Growth factors also influenced neuronal maturation; the best neurite outgrowth was obtained from cells derived from bFGF‐induced colonies cultured in the presence of EGF + bFGF. These data indicate the existence of neural precursor cells in the embryonic mesencephalon that respond differentially to growth factors. © 1995 Wiley‐Liss, Inc.
Ligands for EPH‐related tyrosine kinase receptors are developmentally regulated in the CNS
Authors: Carpenter M. K. , Shilling H. , Vandenbos T. , Beckmann M. P. , Cerretti D. P. , Kott J. N. , Westrum L. E. , Davison B. L. , Fletcher F. A. 
Published: January 2005

AbstractElk is a member of the eph family of receptor‐like tyrosine kinases. Although its function is unknown, elk is postulated to play a role in nervous system development. Using Northern analysis, we examined the developmental regulation of RNAs encoding elk, and several ligands for the eph family of RTKs, the LERKs. Expression of elk, LERK‐1, and LERK‐2 RNAs is high in all regions examined in the embryonic and postnatal rat brain and decreases to low levels with age. One exception is the adult olfactory bulb which continues to express a moderate level of LERK‐2. In contrast, moderate LERK‐4 expression was limited to the developing hippocampus and cerebral cortex. These data indicate that elk and some of the LERKs may play a role in nervous system development, maintenance, and/or regeneration. © 1995 Wiley‐Liss, Inc.
Long‐term hippocampal slices: A model system for investigating synaptic mechanisms and pathologic processes
Authors: Bahr B. A. 
Published: January 2005

AbstractOrganotypic cultures provide a unique strategy with which to examine many aspects of brain physiology and pathology. Long‐term slice cultures from the hippocampus, a region involved in memory encoding and one that exhibits early degeneration in Alzheimer's disease and ischemia, are particularly valuable in this regard due to their expression of synaptic plasticity mechanisms (e.g., long‐term potentiation) and responsiveness to pathological insults (e.g., excitotoxicity). Long‐term slices can be prepared from hippocampi at the second or third postnatal week of development and thus incorporate a number of relatively mature features; further signs of maturation and the preservation of adult‐like characteristics occur over succeeding weeks. The stability of the cultured slice renders it an appropriate model for studying (1) prolonged regulation/stabilization events linked to synaptogenesis and certain forms of plasticity, (2) temporal patterns of cellular atrophy associated with pathogenic conditions such as ischemia and epilepsia, and (3) slow processes associated with aging and agerelated pathologies. © 1995 Wiley‐Liss, Inc.
Immunolabeling of the Na+/C1− dependent “orphan” transporter Rxt1 in the rat central nervous system
Authors: Masson J. , Langlois X. , Lanfumey L. , Gérard C. , Aïdouni Z. , Giros B. , Hamon M. , El Mestikawy S. 
Published: January 2005

AbstractPrevious studies have shown that the mRNA encoding the Na+/Cr− dependent “orphan” transporter Rxt1 is expressed exclusively in the central nervous system (CNS). In the present study, specific antibodies were raised in rabbits for the detailed mapping of this transporter in the rat. The C‐terminal part of Rxtl was fused with glutathione‐S‐transferase (Rxtlct GST) and the resulting fusion protein was used as antigen. The specificity of the antiserum toward Rxtl was confirmed by immunofluorescent, Western blot, and immunoautoradiographic experiments. In cerebral cortex membranes, Rxtl‐like material recognized by the antiserum is a glycosylated protein of 97‐116 kDa. This protein was the most abundant in the caudate‐putamen, followed, in decreasing order, by the cerebral cortex ≈︁ hippocampus > cerebellum > brainstem > spinal cord. In contrast, no immunoreactive material could be detected in peripheral tissues (tongue, thymus, heart, lung, spleen, kidney, adrenals, liver, skeletal muscle, intestine, testis). Immunoautoradiographic labeling with affinity‐purified anti‐Rxtlet‐GST antibodies showed high levels of Rxtl‐like material in the olfactory bulb, cerebral cortex, striatal complex, hippocampal formation, superior layer of the anterior colliculus, cortex, and deep nuclei in the, cerebellum. The regional distribution of Rxtl‐like material generally matched that of GABAergic and glutamatergic projections in agreement with previous in situ hybridization data. © 1995 Wiley‐Liss, Inc.
Immunolocalization of GLUT1 and GLUT3 glucose transporters in primary cultured neurons and glia
Authors: Maher F. 
Published: January 2005

AbstractImmunofluorescence analysis was used to study the cellular localization of glucose transporters 1 and 3 (GLUT1 and GLUT3) in primary rat neuronal and glial cultures. In primary cultured cerebellar granule neurons and cortical neurons, GLUT3 was detected in a pattern consistent with a generalized cell surface distribution. GLUT3 distribution corresponded most closely with the neural cell adhesion molecule (NCAM), and showed overlapping but distinct distributions compared to synaptophysin, microtubule‐associated protein 2 (MAP2), neurofilament protein, and growth‐associated protein (GAP43). Culture of neurons in the presence of glia did not alter the cellular localization of GLUT3. GLUT1 was detectable in primary cerebellar granule neurons both at the cell surface and in the cytoplasm, and appeared decreased in neurons cocultured with glia. GLUT1, but not GLUT3, was detected in glial fibrillary acidic protein (GFAP)‐positive astrocytes present in mixed neuronal‐glial cultures derived from cerebellum and cerebral cortex, as well as in cortical astrocyte cultures. GLUT1, but not GLUT3, was also detected in microglia and oligodendrocytes present in these cultures. This study indicates a generalized cell surface expression of the glucose transporters expressed in neurons and glia, rather than selective targeting to different cellular domains or subcellular locations. © 1995 Wiley‐Liss, Inc.This article is a US Government work and, as such, is in the public domain in the United States of America.
Developing oligodendroglia express mRNA for insulin‐like growth factor‐I, a regulator of oligodendrocyte development
Authors: Shinar Y. , McMorris F. A. 
Published: January 2005

AbstractInsulin‐like growth factors IGF‐I and IGF‐II are potent inducers of oligodendrocyte development. Because IGF‐I is produced, in some cases, by the same cells that respond to it (autocrine/paracrine action), we examined the possibility that IGF‐I is expressed by developing oligodendroglial cells. We employed a sensitive method, reverse transcriptase‐polymerase chain reaction (RT‐PCR), to detect IGF‐I mRNA in purified populations of oligodendroglial cells isolated from rat brain during the period of oligodendrocyte development. Cells were purified by fluorescence activated cell sorting (FACS), using antibodies to the cell surface antigenic markers 04 and galactocerebroside (GC). RNA was isolated from the sorted cells, reverse‐transcribed, and PCR‐amplified, using a strategy that recognizes IGF‐I mRNA but not DNA. The amplified band was identified as IGF‐I by size, hybridization to an IGF‐I‐specific antisense probe, and restriction analysis. IGF‐I mRNA was detected in O4‐positive/ GC‐negative oligodendrocyte precursors and, more weakly, in GC‐positive oligodendrocytes. IGF‐I mRNA could be detected reproducibly in RNA extracted from 100‐cell samples of O4‐positive cells, making it unlikely that the mRNA was derived from contaminants in the FACS‐sorted cell populations. We conclude that IGF‐I is expressed by developing oligodendroglia. Autocrine expression of IGF‐I by developing oligodendroglial cells suggests that oligodendrocyte development is, in part, autoregulatory. © 1995 Wiley‐Liss, Inc.