bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increases in transforming growth factor‐β mRNA in hippocampus during response to entorhinal cortex lesions in intact and adrenalectomized rats
Authors: Nichols N. R. , Laping N. J. , Day J. R. , Finch C. E. 
Published: January 2005

AbstractTransforming growth factor‐β mRNA was detected with a rat TGF‐β1 coding sequence probe as a 2.5 kb band by RNA blot hybridization of total RNA from the adult male rat hippocampus. Following electrolytic lesions of the entorhinal cortex that cause hippocampal deaffer entation and synaptic remodeling, TGF‐β mRNA increases 5‐fold in ipsflateral hippocampus when compared with intact controls. This increase was independent of prior adrenalectomy or corticosterone‐replacement. These data demonstrate that TGF‐β gene expression increases in response to hippocampal deafferentation.
Complex expression pattern of tenascin during innervation of the posterior limb buds of the developing chicken
Authors: Martini R. , Schachner M. 
Published: January 2005

AbstractThe histological localization of the extracellular matrix glycoprotein tenasein was studied during the formation of peripheral nerves in the developing chick hindlimb (embryonic stages 21.5 to 30) by light and electron microscopic immunological methods to obtain insights into the molecule's functional role in the pathway formation by motor and sensory nerves. At stages 21.5 and 23, nerve roots and plexus were surrounded by high tenascin‐immunorenctivity, whereas the not yet innervated limb bud was not imiminoreactive. During inncrvation of the limb bud at stages 24.5 and 25, tenascin was detectable at the limb bud base and restricted in its expression to the proximal nerve regions. The nerve tips did not contact areas of elevated tenascin‐immunoreactivity. At stages 26 to 28 the dorsal and ventral trunks of the crural and sciatic nerves were surrounded by tenascin‐immunoreactivity, which was localized between Schwann and mesenchymal cells. The tips of the growing nerve had now reached the tenascin‐positive interface between bone and muscle anlagen. This interface was contacted tangentially rather than penetrated by the nerve tips. The medial and lateral femoral cutaneous nerves were surrounded by high and weak tenascin‐immunoreactivity, respectively. In both nerves, tenascin‐immunoreactivity was absent where the nerves branched extensively to innervate the skin. The cutaneous nerves diverging from the sciatic nerve were of very low tenascin‐immunoreactivity or tenascin‐negative at all developmental stages tested. At stages 29 and 30, muscle nerves, having just entered the ten‐ascin‐negative muscles, exhibited strong immunoreactivity, whereas the more proximally situated trunks of the sciatic nerve were weakly and discontinuously labeled, particularly at sites where smaller nerves were branching off. Since the cutaneous branches of the sciatic nerve were always of low tenascin‐immunoreactivity, the question was raised whether tenascin expression in the sciatic nerve depended on the presence of motor axons. Spinal cords of stage 19 or 20 embryos were therefore removed and tenascin expression was investigated at stages 26 and 27. Some of the residual nerves were weakly tenascin‐immunoreaetive, whereas others were tenascin‐negative. Our observations suggest that tenascin is not involved in the initial guidance of peripheral nerves to their targets. Rather, neuron‐induced tenascin appears to stabilize the proximal nerve trunks during a transient time period, possibly by preventing axons and Schwann cells from intermingling with the surrounding mesenchyme, thus, contributing to nerve fiber compaction. Conversely, nerve branching may be elicited by reduced levels of tenascin. Furthermore, tenascin may divert growth cones from the developing bone tissue and direct muscle afferents to their appropriate targets.
Stimulation of energy metabolism by α‐adrenergic agonists in primary cultures of astrocytes
Authors: Subbarao K. V. , Hertz L. 
Published: January 2005

AbstractNoradrenaline effects on glucose oxidation were studled in primary cultures of astrocytes. CO2 formation from labeled glucose was enhanced in the presence of; noradrenaline. The stimulatory effect by noradrenaline was exerted both on lactate formation (∼20%) I and on tricarboxylic acid activity (CO2 production from glutamate) (∼40%). The effect was, at least partly, exerted on the alpha‐ketoglutarate dehydrogenase step. The EC50 value for noradrenaline on lactate formation was significantly lower (60 nM) than that on oxidative metabolism (1,900 nM). Studies with specific adrenergic agonists and antagonists showed that various receptor subtypes are involved. Thus, the effect on lactate formation wasmediated exclusively by stimulation of an alpha1 receptor whereas oxidative metabolism was enhanced by both alpha1 and alpha2 receptor stimulation. No effects were exerted by beta receptor agonists or antagonists.
Morphology and antibody recognition of synthetic β‐amyloid peptides
Authors: Fraser P. E. , Duffy L. K. , O'Malley M. B. , Nguyen J. , Inouye H. , Kirschner D. A. 
Published: January 2005

AbstractTo elucidate the relationship between amyloid fibril formation in Alzheimer disease (AD) and the primary structure of the β‐amyloid protein (β‐AP), we investigated the ability of peptides sharing sequences with β‐AP to form fibrils in vitro and to recognize anti‐β‐amyloid antisera. The peptides, which were synthesized using a FMOC solid phase procedure and purified by HPLC, consisted of residues 6–25 from the putativeaqueous domain, residues 22–35, which overlaps the putative aqueous and transmembrane domains, and residues 1–38 and 1–40 representing nearly the full length of β‐AP. Electron microscopy of negative‐stained or thin‐sectioned preparations revealed that the peptides assembled into fibrils having different morphologies, some of which resembled in situ AD amyloid. Peptide 6–25 fibrils had diameters of 50–80 å and occasionally showed a central groove suggestive of constituent filaments. Cross sections of the fibril showed a penta‐ or hexameric arrangement ofglobular subunits with diameters of 25–30 å. Peptide 22–35 fibrils were helical, with a pitch of 1,100 å and a width of 120 A at its greatest and 50–60 å at its narrowest. The fibrils formed by peptides 1–38 and 1–40 were 70–90 å in diameter. When the peptide assemblies were singly oriented by sedimentation or doubly oriented in a magnetic field, their X‐ray diffraction patterns all showed reflections typical of a cross‐β pleated sheet conformation. The patterns differed mainly in their small‐angle equatorial intensity, which arises from the packing of fibrils having different widths. Antiserum raised to either native amyloid or to synthetic peptide β‐(l–28) was highly reactive in an inhibition‐ELISA assay to β‐(6–25) and β‐(1–38), but not to β‐(22–35), and immunostained β‐(1–40) on Western blots. These studies show that the β‐(6–25), β‐(l–38) and β‐(1–40) peptides can assemble into cross‐β fibrils that retain epitopes characteristic of AD amyloid.
Fetal rat septal cells adhere to and extend processes on basement membrane, laminin, and a synthetic peptide from the laminin A chain sequence
Authors: Jucker M. , Kleinman H. K. , Ingram D. K. 
Published: January 2005

AbstractResponses of rat embryonic septal cells to reconstituted basement membrane, laminin, and laminin A chain‐derived synthetic peptides were studied in culture. Dissociated fetal E16/17 septal cells were grown for three days on differently coated plastic substrata. Reconstituted basement membrane (Ma‐trigel), laminin, and a 19‐amino acid synthetic peptide CSRARKQAASIKVAVSADR‐NH2 (PA22‐2) from the laminin A chain sequence mediated cell‐substratum adhesion and promoted neurite outgrowth. In contrast, cells did not attach to or form processes on uncoated plastic or on plastic substrata coated with synthetic, laminin‐derived control peptides. Polyethylenimine (PEI) supported the adhesion and survival of fetal septal cells; however, when lami‐nin was added to the medium during cell plating or 18 hr afterward, a dose‐dependent increase was observed in neurite outgrowth of cells attached to this substratum. Cells grown for 6 days on PEI in the presence of laminin showed a determined increase in the number of cholinergic neurons as marked by acetylcholinesterase staining. These data suggest that the subpopulation of cholinergic septal neurons present in the septal cells studied here were also responding to laminin. The results of this in vitro study suggest potential uses for basement membrane, laminin, or synthetic peptides, sucha as PA22‐2, in fetal septal grafts to enhance regeneration in the damaged septo‐hippocampal system.
Myelin/oligodendrocyte‐specific protein: A novel surface membrane protein that associates with microtubules
Authors: Dyer C. A. , Hickey W. F. , Geisert E. E. 
Published: January 2005

AbstractOnly a few proteins are known to be exclusively expressed in central nervous system (CNS) myelin. A novel surface membrane protein expressed only in CNS myelin and oligodendrocytes of higher vertebrates has been identified by a monoclonal antibody. This CNS myelin/oligodendrocyte‐specific protein, IMOSP, has a molecular weight of 48 kDa and a pI of : Approximately 6.7. In the presence of the monoclonal antibody, MOSP remains on the surface of cultured oligodendrocytes but becomes associated with cytoplasmic microtubules. Our results suggest that MOSP plays an important role in membrane/cytoskeleton interactions during the formation and maintenance of CNS myelin. MOSP also may play a critical role in the pathogenesis of diseases of CNS myelin.
Characterization of ramified microglia in tissue culture: Pinocytosis and motility
Authors: Ward S. A. , Ransom P. A. , Booth P. L. , Thomas W. Eric 
Published: January 2005

AbstractFunctional properties of ramified microglia were investigated in primary cultures of rat cerebral cortical celts. These microglia could be readily identified in both fixed and living cultures through previously established features. Based on their destruction by 5 mM L‐leucine methyl ester, a high level of intrinsic endocytotic activity was established. When cultures were incubated with fluorescent latex beads to assess phagocytosis, little or no such activity was exhibited by ramified cells. However, when cultures were incubated with dyes or other soluble tracer compounds, these cells always exhibited labeling. This labeling was selective for ramified microglia in the cultures and was demonstrated using a variety of compounds, including trypan blue, lucifer yellow, horseradish peroxidase (HRP), and India ink. Intracellular label could be observed in vesicular structures; this localization corresponded to an active cellular process. Also, cellular labeling was inhibited by the presence of colchicine. These features supported the inference that the labeling was attributable to pinocytosis, and this process appeared to account for the vast majority of endocytotic activity in the ramified microglia. Possible physiological significance of this pinocytotic activity was indicated by the accumulation of various neurotransmitters/modulators: γ‐aminobutyric acid and vasoactive intestinal polypeptide (VIP). Ramified cells in these cultures have been previously noted to exhibit a constant and rapid pattern of motility, which was consistently observed here through time‐lapse video recording; pinocytosis and rapid motility were shown to concur in individual cells. Based on their high intrinsic pinocytotic activity and pattern of cellular motility, the ramified microglia specifically are suggested to serve a constitutive function of fluid cleansing within the interstitial spaces of brain tissue.
The neurotrophic factor, n‐hexacosanol, reduces the neuronal damage induced by the neurotoxin, kainic acid
Authors: Borg Jacques 
Published: January 2005

AbstractThe long‐chain fatty alcohol, n‐hexacosanol, has been shown to possess neurotrophic properties in vitro on rat CNS cultures (Borg et al., 1987) and to promote the survival of septal cholinergic neurons after experimental axotomy (Borg et al., 1990). Long‐chain alcohols have also been shown to be synthesized and metabolised by rat brain during development (Bishop and Hayra, 1981; Natarajan et al., 1984). The present study was undertaken in order to find out if a nonproteic neurotrophic factor like n‐hexacosanol may be able to reduce the neuronal damages induced by the excitatory amino acid, kainic acid. When administered chronically by intraperitoneal injection, hexacosanol (1 mg/kg) protected the pyramidal neurons of the hippocampus from the neurotoxic degeneration induced by an intracerebroventricular infusion of kainic acid in rats; the extent of the damage was limited to a small part of the CA3 region. Mor‐phometric analysis showed that 72% of the neurons that would have died following kainic acid injection were spared by hexacosanol. Moreover the increased locomotor activity induced by the neurotoxin was also inhibited by hexacosanol and the behavioral effect was statistically correlated to the extent of neuronal loss. The present study suggests a possible role for nonproteic neurotrophic compounds against neurotoxic damages on central neurons. Moreover the peripheral administration of hexacosanol may lead to a significant breakthrough in the treatment of excito‐toxin‐related human diseases.
Non‐competitive antagonists of N‐methyl‐D‐aspartate prevent spontaneous neuronal death in primary cultures of embryonic rat cortex
Authors: Drian M.‐J. , Kamenka J.‐M. , Pirat J.‐L. , Privat A. 
Published: January 2005

AbstractPrimary cultures of embryonic rat cerebral cortex were treated after 17 days in vitro for 10 min with a single dose of the non‐competitive antagonists of N‐methyl‐D‐aspartate (NMDA) receptor MK 801, TCP, and GK 11. They were then maintained in vitro for 31, 59, or 73 days, and then processed for the immu‐nocytochemical detection of neuron‐specific enolase (NSE). Immunoreactive cells were counted in treated and control cultures, and it was found that, except at 31 days, treated cultures contained far more NSE immunoreactive cells than controls. Moreover, this effect was dose‐dependent, since with both TCP and GK 11 neuron survival was significantly higher with, respectively, 20 μM and 5 μM than with the lowest concentration of 2.5 μM. We tentatively conclude that spontaneous neuron death occurring in primary cultures in vitro is at least partly related to the NMDA‐associated Ca++ property of the molecules we used is to block this channel. The relevance of this mechanism of cell death in vitro to neuronal death in vivo is discussed.
Migration patterns of donor astrocytes after reciprocal striatum–cerebellum transplantation into newborn hosts
Authors: Jacque C. , Suard I. , Collins P. , Baumann N. 
Published: January 2005

AbstractFragments of striatum or cerebellum from E 25 rabbit embryo were implanted into either the striatum or the mesencephalon of newborn mice. Implanted rabbit astrocytes were selectively identified by mono‐donal antibodies to the GFAP which are unable to combine with mouse GFAP. Previous investigations had shown that xenogenic astrocytes have the capacto migrate in host CNS. The purpose of this study was to compare the patterns of migration of transplant‐derived astroglial cells according to the topographic origin of the transplant and location of the grafting site. We found that the migration pattern of the grafted cells from any of both selected sites of implantation was independent from the topographic origin of the transplant. The routes as well as the distances of migration were similar after homo‐ or heterotopic transplantation. We conclude that astroglial cells or their precursors do not express information which would direct them to move specifically toward a defined region in the host brain according to the region of origin in the donor.
Monoclonal antibodies to the heavy neurofilament subunit (NF‐H) of torpedo cholinergic neurons
Authors: Faigon M. , Hadas E. , Alroy G. , Chapman J. , Auerbach J. M. , Michaelson D. M. 
Published: January 2005

AbstractPrevious studies from our laboratory suggest that Alzheimer'disease sera contain a repertoire of antibodies to the heavy neurofilament subunit (NF‐H) and that a subpopulation of these antibodies bind specifically to epitopes highly enriched in NF‐H isolated from the purely cholinergic electromotor neurons of Torpedo. In the present study, we prepared and characterized monoclonal antibodies (MAbs) that bind to epitopes specifically enriched in Torpedo cholinergic neurons. This was performed by a differential enzyme‐linked immunosorbent assay (ELISA) in which MAbs were selected that bind to epitopes much more abundant in the NF‐H protein of Torpedo cholinergic neurons than in NF‐H from the chemically heterogeneous Torpedo spinal cord. This yielded four MAbs, three of which (TC4, TC8, and TC21) were found to be specific to NF‐H and one (TC15) that reacts with both NF‐H and the medium‐size neurofilament sub‐unit NF‐M. Dephosphorylation abolishes the binding of MAbs TC4 and TC15 to Torpedo cholinergic NF‐H, partially reduces that of MAb TC21 and has no effect on the binding of MAb TC8. This suggests that the antigenic sites specific to Torpedo cholinergic NF‐H contain phosphoryiated as well as non phosphory‐lated epitopes. All the MAbs cross‐react with rat brain NF‐H.
Kinetics of dopamine and noradrenaline transport in synaptosomes from cerebellum, striatum and frontal cortex of normal and reeler mice
Authors: Efthimiopoulos S. , Giompres P. , Valcana T. 
Published: January 2005

AbstractRecent evidence indicates that the cerebellum has a dopaminergic system. In order to elucidate further the dopaminergic system in the cerebellum, we investigated the transport of dopamine (DA) in synaptosomal preparations of normal and reeler mice. For comparative purposes we also studied DA transport in synaptosomal preparations from striatum and frontal cortex and compared DA transport to nor‐adrenaline (NA) transport.[3H]‐DA transport into cerebellar synaptosomes was found to be a Na+‐dependent, two component system–a high affinity, low capacity and a low affinity, high capacity. In striatum [33H]‐DA is transported by a similar high but different low affinity component. Maximal velocities of both transport components in the striatum were higher than the corresponding ones in the cerebellum. In the frontal cortex we also observed two [3H]‐DA transport components with affinities significantly lower than those in cerebellum and striatum.[3H]‐NA transport into synaptosomes, prepared from the three brain regions studied, showed two transport components with similar Kt and Vmax values, except for the high affinity component in striatum whose affinity is lower.In reeler mice [3H]‐DA transport was different from normal only in the cerebellum where the maximal velocity for both transport components was significantly higher (2 x). In contrast, no significant difference was observed in the transport of [3H]‐NA.The accumulated [3H]‐DA from cerebellar slices was found to be releasable by K+ stimulation, in a Ca++‐dependent manner, and most of the released radioactivity was in the form of [3H]‐DA.These results indicate that in the cerebellum there is a low‐density dopaminergic system which is distinct from the corresponding noradrenergic system.
Epidermal growth factor and transforming growth factor α induce c‐fos gene expression in retinal muller cells in vivo
Authors: Sagar S. M. , Edwards R. H. , Sharp F. R. 
Published: January 2005

AbstractEpidermal growth factor (EGF) and transforming growth factor a (TGFα) are peptides that act at a common receptor and are mitogenic for immature astrocytes and trophic for developing brain neurons in vitro. However, a role for these growth factors in the mature nervous system has not been established. To investigate the actions of EGF and TGFα in the adult central nervous system (CNS) in vivo, the growth factors were injected into the vitreous cavity of adult male rabbits. After varying intervals, the retinas were examined for c‐fos mRNA by Northern blot hybridization or Fos (and Fos‐related antigen) protein by immunocytochemistry. EGF induction of c‐fos mRNA occurs within 30 min and persists more than 4 hr. Fos nuclear immunostaining is induced selectively in nuclei of Muller cells by both EGF and TGFα. Fos‐like immunoreactivity appears within 1 hr and persists more than 9 hr after EGF injection. These observations demonstrate that mature retinal Muller cells respond to exogenously applied EGF and TGFα in vivo, although the effect of the growth factors is not necessarily direct. The expression of c‐fos and other immediate early genes provides a short‐ term marker that can be used to investigate the role of growth factors in normal retinal physiology and responses to injury.
Hypothyroidism selectively reduces the rate and amount of transport for specific SCb proteins in the hyt/hyt mouse optic nerve
Authors: Stein S. A. , McIntire D. D. , Kirkpatrick L. L. , Adams P. M. , Brady S. T. 
Published: January 2005

AbstractThyroid hormone significantly affects molecular and neuroanatomical properties of the developing nervous system. Altered connectivity in hypothyroidism may reflect reductions in process growth, alterations in process maintenance, or changes in synaptogenesis or synaptic maintenance. These events are dependent on microtubules, neurofilaments, microfilaments, and associated molecular components. Reductions in delivery of microtubules and neurofilaments to the distal axon by slow component a (SCa) of axonal transport may contribute to the neuroanatomical abnormalities of hypothyroidism (Stein et al., J Neurosci Res 28:121–133, 1991). However, hypothyroidism might also affect the axon and synaptic connections by altering slow component b (SCb), which includes actin microfilaments and proteins that contribute to synaptic function, i.e., clathrin, HSC70 (clathrin uncoating ATPase), spectrin, and calmodulin. To determine the effect of hypothyroidism on SCb proteins, slow axonal transport was analyzed in optic nerves of hyt/hyt hypothyroid mice, which have severe primary hypothyroidism, and euthyroid control mice. Clathrin, spectrin, HSC70, and actin showed significant reductions in transport velocity in hyt/hyt optic nerves relative to euthyroid nerves, but the transport rate for calmodulin was less affected. However, the amount of calmodulin was significantly elevated in hyt/hyt nerve over euthyroid nerves. Hypothyroidism selectively reduces transport of SCb proteins, which are thought to play significant roles in synaptic function and in the growth cone. The effects of hypothyroidism on microtubules and neurofilaments combined with actions on SCb suggest that changes in neuronal function associated with reduced thyroid hormone during development and maturity (i.e., alterations in neuronal connectivity, nerve conduction, and synaptic function) may be mediated in part by effects on slow axonal transport.