bluuebunny/crossref_metadata_2025_split huggingface dataset:
NADPH‐Diaphorase histochemistry in the postnatal mouse cerebellum suggests specific developmental functions for nitric oxide
Authors: Brüning G. 
Published: January 2005

AbstractNADPH‐diaphorase histochemistry has been applied for the localization of nitric oxide synthase during the postnatal development of the mouse cerebellum. Staining for NADPH‐diaphorase during the first week after birth was confined to some but not all laminae of the immature cerebellum: NADPH‐diaphorase activity was located in the molecular/Purkinje cell layer and in inner parts of the internal granular layer. The external granular layer and the developing white matter were essentially unstained. Expression was earliest and very strong in parallel fibers and in the internal granule layer of the ventral part of the pyramis and the dorsal part of the uvula. Staining in the Purkinje cell layer was observed throughout the cerebellum. The presence of formazan deposits within Purkinje cells was verified by colocalization with calbindin D‐28k immunoreactivity. The distribution of NADPH‐diaphorase activity changed into the adult pattern between 8 and 12 days of age: Within the molecular layer, basket cells and their processes became strongly stained. Reaction product within Purkinje cells gradually disappeared. Likewise, strongly stained parallel fibers were no longer detectable. These results suggest that nitric oxide is involved in different processes in cerebellar development. © 1993 Wiley‐Liss, Inc.
Characterization of a Schwann cell neurite‐promoting activity that directs motoneuron axon outgrowth
Authors: Bolin L. M. , Shooter E. M. 
Published: January 2005

AbstractSchwann cells support and facilitate axonal growth during development and successful regeneration in the peripheral nerve. In the regenerating rat sciaticnerve, Schwann cells provide a trophic milieu for primary sensory, sympathetic, and motoneurons. We have characterized a neurotrophic activity produced by adult rat sciatic nerve Schwann cells and a spontaneously immortal Schwann cell clone (iSC). This activity elicits neurite outgrowth from chick embryo explants of both CNS and PNS. The iSC activity has been concentrated by cation‐exchange chromatography and compared to known neurotrophins in bioassay. Pooled bound fractions elicit neurite outgrowth from sympathetic, ciliary and motoneurons. In collagen matrix cocultures of iSC and E4 ventral horn(before motor axon extension to muscle targets), the iSC activity can direct the initial axonal extension from motoneurons. The data presented suggest that Schwann cell‐produced activity may mediate motoneuron axonal extension before contact with their peripheral source of neurotrophin. © 1994 Wiley‐Liss, Inc.
Guanosine‐5′‐(3‐O‐thio)triphosphate‐mediated stimulation of phosphoinositidase C in solubilized rat peripheral nerve myelin and its alteration in streptozotocin induced diabetes
Authors: Mathew J. , Eichberg J. 
Published: January 2005

AbstractThe regulation of phosphoinositidase C (PIC) activity by guanosine‐5′‐(3‐O‐thio)triphosphate (GTPγgMS) was characterized in a cholate‐solubilized peripheral myelin‐enriched fraction from rat sciatic nerve. The GTP analog maximally enhanced PIC‐catalyzed hydrolysis of exogenous phosphatidylinositol‐4,‐5‐bisphosphate (PIP2) in a dose‐dependent manner only within a narrow range of cholate concentrations. Maximal stimulation was attained at 0.6 μM GTPγS and could be completely prevented by 1 μM guanosine‐5′‐(2‐O‐thio)diphosphate. Neither adenylyl‐imidodiphosphate nor adenosine triphosphate (ATP) enhanced PIC activity. Carbamoylcholine (1 mM)added together with GTPγS increased the extent of PIP2 hydrolysis over that elicited by GTPγ increased the extent of PIP2 hydrolysis over that elicited by GTPγS alone and this stimulation was blocked by the muscarinic receptor antagonist, atropine (50 μM). In detergent solubilized myelin preparations from streptozotocin induced diabetic rats, a higher concentration of the guanine nucleotide analogn was required to achieve stimulation comparable to that obtained with corresponding preparations from normal animals. These results suggest that sciatic nerve myelin possesses muscarinic receptors coupled via a GTP‐binding protein to PIC and that this system can be reconstituted in detergent‐solubilized extracts. It is possible that the function of G Proteins in cell signaling is impaired in experimental diabetic neuropathy. © 1994 Wiley‐Liss, Inc.
Platelet‐derived growth factor receptor is expressed by cells in the early oligodendrocyte lineage
Authors: Ellison J. A. , de Vellis J. 
Published: January 2005

AbstractWe report the loaclization of PDGFRα mRNA (PDGFRα) in phenotypically defined cells during the first postanatal week of rat forebrain development. Using a method of combined immunocytochemistry and in situ hybridization we have demonstrated the cellular colocalization of PDGFRα mRNA with GD3 ganglioside or 04 sulfatide, phenotypic markers of oligodendrocytes, in the gray and white matter of the dorsal cerebral cortex at all ages studies. Population analysis of the PDGFRα+/G3+ and PDGFRα+/analysis of the PDGFRα+/GD3+and PDGFRα+/04+ cells revealed that three populations express PDGFRα: GD3+, GD3+/04+, and 04+, corresponding to two lineage stages, progenitor and preoligodendrocyte, in oligodendrocyte development. Immature oligodendrocytes, identifice by galactocerebroside immunoreactivity, did not express detectable levels of PDGFR α mRNA. Post‐mitotic neurons, identifice by immunoperodxidase localization of the 68 kD neurofilament, and astrocytes identified by S‐100 or GFAP immunoreactivity were also negative for PDGFRα mRNA occured in oligodendrocyte cell populations which are post‐migratory and proliferative, but which do not express myelin proteins characteristic of post‐mitotic oligodendrocytes. © 1994 Wiley‐Liss, Inc.
Satellite cells in slow and fast rat muscles differ in respect to acetylcholinesterase regulation mechanisms they convey to their descendant myofibers during regeneration
Authors: Dolenc I. , Črne‐Finderle N. , Eržen I. , Sketelj J. 
Published: January 2005

AbstractThe hypothesis of satellite cell diversity in slow and fast mammalian muscles was tested by examining acetylcholinesterase (AChE) regulation in muscles regenerating (1) under conditions of muscle disuse (tenotomy, leg immobilization) in which the pattern of neural stimulation is changed, and (2) after cross‐transplantation when the regenerating muscle develops under a foreign neural stimulation pattern. Soleus (SOL) and extensor digitorum longus (EDL) muscles of the rat were allowed to regenerate after ischemic‐toxic injury either in their own sites or had been cross‐transplanted to the site of the other muscle. Molecular forms of AChE in regenerating muscles were analyzed by velocity sedimentation in linear sucrose gradients. Neither tenotomy nor limb immobilization significantly affected the characteristic pattern of AChE molecular forms in regenerating SOL muscles, suggesting that the neural stimulation pattern is probably not decisive for its induction. During an early phase of regeneration, the general pattern of AChE molecular forms in the cross‐transplanted regenerating muscle was predominantly determined by the type of its muscle of origin, and much less by the innervating nerve which exerted only a modest modifying effect. However, alkali‐resistant myofibrillar ATPase activity on which the separation of muscle fibers into type I and type II is based, was determined predominantly by the motor nerve innervating the regenerating muscle. Mature regenerated EDL muscles (13 weeks after injury) which had been innervated by the SOL nerve became virtually indistinguishable from the SOL muscles in regard to their pattern of AChE molecular forms. However, AChE patterns of mature regenerated SOL muscles that had been innervated by the EDL nerve still displayed some features of the SOL pattern. In regard to AChE regulation, muscle satellite cells from slow or fast rat muscles convey to their descendant myotubes the information shifting their initial development in the direction of either slow or fast muscle, respectively. The satellite cells in fast or slow muscles are, therefore, intrinsically different. Intrinsic information is expressed mostly during an early phase of regeneration whereas later on the regulatory influence of the motor nerve more or less predominates. © 1994 Wiley‐Liss, Inc.
Differential expression patterns of mRNAs for members of the fibroblast growth factor receptor family, FGFR‐1–FGFR‐4, in rat brain
Authors: Yazaki N. , Hosoi Y. , Kawabata K. , Miyake A. , Minami M. , Satoh M. , Ohta M. , Kawasaki T. , Itoh N. 
Published: January 2005

AbstractWe have examined the region‐specific expression of mRNAs for four members of rat FGF receptor family, FGFR‐1, FGFR‐2, FGFR‐3, and FGFR‐4, in rat brain by in situ hybridization. The FGFR‐1, FGFR‐2, and FGFR‐3 mRNAs were expressed widely but differentially in the brain. However, the FGFR‐4 mRNA was not expressed in the brain. The FGFR‐1 mRNA was strongly expressed in several regions including the hippocampus, cerebellum, and pedunculoptine tegmental nucleus. The FGFR‐2 mRNA expression was high in the choroid plexus, and moderate in the fiber‐rich regions (the corpus callosum, external capsule, and internal capsule) and the olfactory bulb. The FGFR‐3 mRNA was expressed diffusely in the brain. We have also examined the cellular localization of these mRNAs in the brain. Although the FGFR‐1 mRNA was expressed preferentially in neurons, the FGFR‐2 and FGFR‐3 mRNAs were expressed preferentially in glial cells. The present findings that the FGFR‐1, FGFR‐2, and FGFR‐3 mRNAs were expressed widely but with region‐and cell‐specificity in the brain indicate that these receptors have different roles in the brain. © 1994 Wiley‐Liss, Inc.
Differential expression of two mRNA species indicates a dual function of peripheral myelin protein PMP22 in cell growth and myelination
Authors: Bosse F. , Zoidl G. , Wilms S. , Gillen C. P. , Kuhn H. G. , Müller H. W. 
Published: January 2005

AbstractTwo peripheral myelin protein PMP22 transcripts, CD25 and Sr13, have been identified by Northern blot and RNA‐polymerase chain reaction (PCR) methods in rat. The CD25 and SR13 mRNA species (each approximately 1.8 kb in size) differ significantly in their 5′‐untranslated region (5′‐UTR) sequences but encode the same protein. While CD25 mRNA is largely confined to the peripheral nervous system, the Sr13 transcript is more ubiquitously expressed in rat tissues. Both transcripts are differentially expressed during postnatal sciatic nerve development, while CD25 expression steadily increases from low levels in neonates up to a maximum at postnatal day 14, SR13 mRNA levels are elevated at birth but decrease throughout adulthood. CD25 and Sr13 transcripts are expressed at very low constant levels in developing and adult brain. In degenerating and regenerating segments of injured peripheral nerve changes in CD25 mRNA levels clarly resemble the expression pattern of other myelin genes, whereas expression of SR13 is inversely correlated with the time course of Schwann cell proliferation. In cultured rat meningeal fibroblast SR13 mRNA expression is strictly growth arrest‐specific and independent of forskolin. On the other hand, regulation of CD25 mRNA levels in these cells is more complex with respect to interfering effects of serum and forskolin. In cultured Schwann cells neither CD25 nor SR13 expression is growth arrest‐specific. However, both transcript levels are consistently enhanced by forskolin under all conditions of cell growth tested. Expression of CD25 (but not SR13) depends on high Schwann cell density. Our results substantiate the hypothesis that PMP22 serves two biological functions, one related to cell growth (SR13) and another to myelination (CD25). © 1994 Wiley‐Liss, Inc.
Changes of β‐amyloid precursor protein splice patterns in brain cell aggregate cultures
Authors: Gebicke‐Haerter P. J. , Appel K. , Honegger P. , Berger M. 
Published: January 2005

AbstractThe splice pattern of β‐amyloid precursor protein (β‐APP) has been studied in a variety of neuronal and glial cells and in brain cell aggregate cultures by the polymerase chain reaction (PCR). The brain‐typical pattern, in which β‐APP695 is the dominant form, has been found only in aggregate cultures but not in any of the other cell types including neuronal cell lines. Selective elimination of glial cells from aggregates resulted in increased quantities of β‐APP695, whereas removal of neurons led to a reduction of β‐APP695 and to an elevation of β‐APP751 and β‐APP770. This shift of splice pattern was not observed in cocultures of the neuronal cell line PC 12 with primary astrocytes combined in a variety of cellular ratios. Blood serum, which is an essential component of these cultures, tested on aggregates, did not reduce the amount of β‐APP695 or have any marked effects on splice patterns generally. From these results it is concluded that investigations on brain‐typical splicing of β‐APP require primary neurons. Neuronal cell lines may be no suitable model systems. Splicing events favoring production of β‐APP695 may mark an important, very early step of amyloid formation in the brain. © 1994 Wiley‐Liss, Inc.
Identification of Gal(β1–3)GalNAc bearing glycoproteins at the nodes of ranvier in peripheral nerve
Authors: Apostolski S. , Sadiq S. A. , Hays A. , Corbo M. , Suturkova‐Milosevic L. , Chaliff P. , Stefansson K. , Lebaron R. G. , Ruoslahti E. , Hays A. P. , Latov N. 
Published: January 2005

AbstractA subset of human anti‐GM1 ganglioside antibodies cross‐reacts with Gal(β1–3)GalNAc bearing glycoproteins in peripheral nerve and spinal cord. The same oligosaccharide determinant is recognized by the lectin peanut agglutinin (PNA) which binds at the nodes of Ranvier in intact peripheral nerve. The Gal(β1–3)GalNAc bearing glycoproteins were isolated using PNA lectin affinity chromatography followed by separation on Western blot, and the proteins were subjected to partial amino acid sequence analysis. Two major PNA binding glycoproteins were identified in peripheral nerve and spinal cord; one had an approximate molecular weight of 120 kD and had sequence homology to the oligodendrocyte‐myelin glycoprotein (OMgp). The other migrated between 70 and 80 kD and had sequence homology to the hyaluronate binding domain of versican, which has been reported to share sequence homology with the 70 kD proteins hyaluronectin and the glial hyaluronic acid binding protein (GHAP). By immunocytochemistry, OMgp was localized to the paranodal region of myelin, and the protein homologous to the hyaluronate binding domain of versican was localized to the nodal gap in peripheral nerve. These PNA binding glycoproteins might be target antigens for autoantibodies in peripheral nerve. © 1994 Wiley‐Liss, Inc.
Type‐2 astrocytes have much greater susceptibility to heat stress than type‐1 astrocytes
Authors: Juurlink B. H. J. 
Published: January 2005

AbstractThe present investigations were undertaken to examine the susceptibility of type‐2 astrocytes to elevated temperature. Type‐2 astrocytes are much more easily injured by temperature elevation than type‐1 astrocytes. This may be related to cellular redox potential. Type‐1 astrocytes have a greater cytosolic NAD redox potential (i.e., higher NADH:NAD levels) than type‐2 astrocytes as evidenced by a 9‐fold higher ratio of lactate to pyruvate released into the medium by type‐1 astrocytes than type‐2 astrocytes. Heat stress causes the induction of hsp‐72 in both type‐2 and type‐1 astrocytes; however, hsp‐72 protein expression is retained for a longer period of time by the type‐2 astrocyte. A possible basis for the greater sensitivity of type‐2 astrocytes to stress may be a poorer ability to scavenge free radicals. This differential sensitivity of one neural cell type relative to another to elevated temperature may be of significance in understanding the effects of hyperthermia on the developing brain. © 1994 Wiley‐Liss, Inc.
Differential expression of immediate early genes in distinct layers of rat cerebral cortex after selective immunolesion of the forebrain cholinergic system
Authors: Roßner S. , Perez‐Polo J. R. , Wiley R. G. , Schliebs R. , Bigl V. 
Published: January 2005

AbstractThe aim of this study was to show whether reduction or loss of cortical cholinergic activity results in any particular change in the expression of the proto‐on‐cogenes c‐fos and/or c‐jun. To produce cortical cholinergic hypofunction, the monoclonal antibody, 1921gG, to the low‐affinity nerve growth factor receptor p75NGFR coupled to a cytotoxin, saporin, was used as an efficient and selective immunotoxin for cholinergic neurons in rat basal forebrain. Brain sections of adult rats that had received an intracerebro‐ventricular injection of 4 μg of the 1921gG‐saporin were subjected to in situ hybridization using oligonucleotides to detect c‐fos and c‐jun mRNA. Autoradiographs obtained were evaluated by quantitative image analysis. Seven days following injection of the immunotoxin there was a dramatic loss in acetylcholinesterase staining in frontal, parietal, piriform, temporal, and occipital cortices, hippocampus, and olfactory bulb, but not in the striatum and cerebellum. In situ hybridization revealed a considerable increase in the level of c‐fos mRNA in the lateral septum following the cholinergic lesion, whereas in the medial septum both c‐fos and c‐jun mRNA were elevated. Immunolesioning led to a distinct and specific increase in the level of c‐jun but not c‐fos mRNA in the parietal and occipital cortex that was restricted to cortical layer IV.These data suggest that reduced cortical cholinergic activity differentially regulates expression of c‐fos/c‐jun genes in distinct cortical regions of the rat brain. © 1994 Wiley‐Liss, Inc.
Gonadal steroid control of preprocholecystokinin mRNA expression in the limbic‐hypothalamic circuit: Comparison of adult with neonatal steroid treatments
Authors: Micevych P. E. , Abelson L. , Fok H. , Ulibarri C. , Priest C. A. 
Published: January 2005

AbstractThe neuropeptide cholecystokinin (CCK) is involved in the regulation of female, but not male, reproductive behavior. In both sexes, estrogen regulates the expression of CCK in adulthood within the bed nucleus of the stria terminalis and medial amygdaloid nucleus. These areas are parts of an interconnected limbic system‐hypothalamic circuit, the development of which is influenced by estrogen during the early postnatal period. This is the same period during which central nervous system (CNS) expression of CCK is dramatically increased, suggesting that the male and female patterns of CCK expression may be the result of early postnatal exposure to estrogen. In the present experiment, the expression of preprocholecystokinin (pCCK) mRNA was determined by in situ hybridization with an isotopically labeled pCCK complementary RNA and emulsion autoradiography in animals whose neonatal and adult gonadal steroid levels had been manipulated. The number of pCCK‐expressing cells in animals that were gonadectomized as adults was determined by neonatal estrogen, but stimulation with steroids in adulthood induced a similar number of pCCK‐expressing cells in both sexes in the medial amygdala and bed nucleus of the stria terminalis. Neonatal treatment of females with estrogen or testosterone, followed by ovariectomy in adulthood, eliminated the sex difference in pCCK mRNA expression. Males treated neonatally with the aromatase inhibitor androstenedione (to block metabolism of testosterone to estrogen) and orchidectomized in adulthood had a level of pCCK mRNA expression that was similar to that of ovariectomized females. These data suggest that, during neonatal development, estrogen determines the constitutive expression of pCCK mRNA in the medial amygdala and bed nucleus of the stria terminalis, resulting in higher levels of pCCK mRNA expression in males than in females. However, exogenous gonadal steroids induce the same levels of pCCK mRNA expression in adult females, indicating that the levels of gonadal steroids and the patterns of their secretion are the predominant influences on the sexually dimorphic adult levels of pCCK mRNA expression. © 1994 Wiley‐Liss, Inc.
Activation of adult human derived microglia by myelin phagocytosis in vitro
Authors: Williams K. , Ulvestad E. , Waage A. , Antel J. P. , McLaurin J. 
Published: January 2005

AbstractThe present study was designed to determine the extent to which cultured glial cells phagocytose normal central nervous system (CNS) myelin and CNS myelin opsonized with serum or purified antibody against myelin basic protein (MBP). Glial cells studied were mixed cultures (consisting of astrocytes, microglia, and oligodendrocytes) and enriched microglia established from adult human brain specimens and enriched astrocytes from fetal human brain. A human monocytic cell line, THP‐1, was included as a control. Uptake of 125I‐labelled myelin was followed over a 24 hr time period. An assay of oxidative burst (30 min) and cytokine bioassays measuring IL‐1, IL‐6, and tumor necrosis factor (TNF) production (6‐‐48 hr) were used to investigate short‐ and longterm activation of phagocytosing cells. Maximum myelin uptake by phagocytosing glial cells occurred within 12‐‐24 hr following myelin incubation. Opsonization of myelin prior to the phagocytosis assay resulted in greater myelin uptake by mixed glial cell cultures, microglia, and THP‐1 cells over that of nontreated myelin. The magnitude of myelin phagocytosis by astrocytes was considerably lower than microglia and THP‐, and was not affected by myelin opsonization. Within 30 min of myelin phagocytosis, microglia and THP‐1 cells underwent oxidative burst; opsonization of myelin by purified anti‐MBP IgG and heat‐inactivated serum enhanced the microglial oxidative burst activity. Production of IL‐1, TNF, and most markedly IL‐6 by microglia was increased following 12‐‐24 hr of myelin ingestion. Our data demonstrate that myelin phagocytosis by adult human‐derived microglia occurs in vitro, is augmented when myelin is opsonized, and results in the activation of microglia as assessed by oxidative burst and cytokine production. © 1994 Wiley‐Liss, Inc.