bluuebunny/crossref_metadata_2025_split huggingface dataset:
Corticorubral connections: Ultrastructural evidence for homotypical synaptic reinnervation after developmental deafferentation
Authors: Fisher R. S. , Sutton R. L. , Hovda D. A. , Villablanca J. R. 
Published: January 2005

AbstractCorticorubral (CR) connections are reorganized after the red nucleus is deafferented by neonatal hemispherectomy. Our objective was to determine if the new decussating CR axons establish synaptic junctions with their target neurons. The ultrastructure of CR axonal terminal arbors was identified by the anterograde transport and histochemical labeling of wheat germ agglutinin lectin‐bound horseradish peroxidase injected unilaterally into the pericruciate neocortex of adult cats that received unilateral neonatal hemispherectomy (HEMI cases) and normal adult cats (control cases). The regional organization of undecussated and decussated CR arbors was nearly equivalent in the HEMI cases. The fine structure of both connections was uniform. Asymmetrical synaptic junctions were observed in frequent axodendritic and infrequent axosomatic boutons en passage and boutons terminaux. The undecussated arbors formed the principal connection in the control cases. However, the fine structures of the decussated and undecussated arbors were comparable and matched the arrangements in the HEMI cases. We conclude that developmental deafferentation redirects CR axons to provide stable synaptic afferents to new targets. The reinnervation is homotypical in terms of regional and fine structure organization. It is likely to be an important factor in chemically mediated neurotransmission that contributes to the sparing/recovery of function after brain damage.
Role of neuron‐target interactions in the development of a subpopulation of avian sensory neurons
Authors: Marusich M. F. , Weston J. A. 
Published: January 2005

AbstractSubpopulations of sensory neurons appear in embryonic dorsal root ganglia during development. In this paper, we examine what role neuron‐target interactions play in this process. Previous work has shown that alterations in the environment of developing sensory neurons regulate the proportion of neurons that express a cell surface antigen identified by the monoclonal antibody SN1 (Marusich et al.: Dev. Biol. 118: 505–510, 1986). We now report that neuron‐target interactions may also act to stabilize the phenotype of sensory neurons. Thus, older SN1− neurons, which would normally remain SN1− if left undisturbed in vivo, can express SN1 immunoreactivity in vitro when they are deprived of contact with their normal peripheral targets. We also demonstrate that naive sensory neurons, i.e., those that have never made contact with peripheral targets, can be identified and maintained in culture. At least some of these naive neurons (all of which are initially SN1−) can express SN1 immunoreactivity in vitro, in the absence of contact with normal peripheral targets. We conclude that subpopulations of sensory neurons may arise from naive neurons in the absence of neuron‐target interactions but that subsequent neuron‐target interactions may act to stabilize or modulate subpopulation‐specific phenotypes.
Identification and cDNA cloning of a new member of the L2/HNK‐1 family of neural surface glycoproteins
Authors: Gennarini G. , Rougon G. , Vitiello F. , Corsi P. , Di Benedetta C. , Goridis C. 
Published: January 2005

AbstractRabbit antibodies raised against a 135‐ to 140‐kD glycoprotein isolated from the culture medium of mouse forebrain explants were used for the identification and cloning of a complex of mouse neural cell surface glycoproteins. The antibodies recognized a 135‐kD surface protein which shared the L2/HNK‐1 epitope with several neural cell adhesion molecules. Three homologous complementary deoxyribonucleic acid (cDNA) clones were isolated from a mouse brain cDNA library prepared in the expression vector lambda gt11, one of which was sequenced and found to lack sequence homologies with known proteins. In Northern blots, this clone hybridized with a single 6.3 kb messenger ribonucleic acid (mRNA). In immunoblots of mouse brain extracts, antibodies raised in rabbits against the fusion protein encoded by it stained two glycoproteins of 135 and 90 kD, which we designated F3.135 and F3.90. In the developing mouse cerebellum, F3 antigenic sites were found predominantly on parallel fibers and on postmitotic neurons. In fetal brain cell cultures, F3 antigen was detected at the surface of cells with neuronal morphology, but the antibodies also stained some non‐neuronal cells in a pattern characteristic of matrix components. Because all proteins carrying the L2/HNK‐1 epitope identified so far have a role in cell adhesion, it can be anticipated that the F3 surface proteins also are involved in cellinteraction phenomena.
A Soluble brain molecule related to epidermal growth factor receptor is a mitogen inhibitor for astrocytes
Authors: Nieto‐Sampedro M. , Broderick J. T. 
Published: January 2005

AbstractThe astrocyte mitogenic activity of normal and injured rat brain extracts was greatly enhanced by antibodies to epidermal growth factor receptor (EGFR). The antibodies appear to act by removing from the extracts inhibitory molecules immunologically related to EGFR. Three molecular species recognized by anti‐EGFR antibody in brain extracts (molecular weights 41, 52, and 69 kilodaltons) did not seem to originate from EGFR proteolysis. The increase in astrocyte mitogenic activity in brain tissue following injury correlated with a reduction in the levels of soluble EFGR‐cross‐reacting material and a decrease in mitogen inhibitory activity. The decrease in EGFR‐related mitogen inhibitor also correlated with a large increase in astrocyte membrane EGFR immunoreactivity, and intracerebral injection of antibodies to EGFR caused the appearance at the injection site of numerous EGFR‐positive reactive astrocytes. Invasion of brain tissue by EGF/EGFR‐related blood components may be the signal that initiates astrocyte activation. EGFR‐related immunoreactive molecules are also present in extracts of other tissues and may have a general role in the control of cell division.
Enzyme translocation in the course of regeneration of central primary afferent terminals in the substantia gelatinosa of the adult rodent spinal cord
Authors: Knyihár‐Csillik E. , Kreutzberg G. W. , Csillik B. 
Published: January 2005

AbstractSynaptic circuitry in the upper dorsal horn, disorganized due to transganglionic degenerative atrophy (evoked by blockade of retrograde axoplasmic transport in the related peripheral nerve), begins to be reestablished by a process of regenerative synaptoneogenesis as soon as retrograde transport is resumed. Central axons of type C primary sensory neurons, terminating in substantia gelatinosa Rolandi, as well as their cells of origin in dorsal root ganglia are specifically and selectively labeled by the enzyme thiamine monophosphatase (TMPase). Under normal conditions, TMPase is localized in axolemmal membranes at the electron histochemical level. In axonal growth cones of regenerating central terminals, only negligible TMPase reaction was found. In axonal filopodia and young nerve sprouts, there appears an increasing number of intraaxonal grains of the reaction product. Vanicous swellings (beads) of regenerating axonal sprouts are transformed into scalloped (sinusoid) en passant terminals. TMPase reaction end product, present initially in the axoplasm of beads and scalloped terminals, is successively translocated to the axolemmal membrane in the course of cytochemical maturation. Structural regeneration and cytochemical maturation of central terminals of primary sensory neurons are completed 60 days after crush injury to the related peripheral axons, i.e., about 7 weeks after the peripheral nerve has regenerated.
Reversibility and prevention of intraspinal peptidergic loss caused by sciatic nerve lesions
Authors: Di Giulio A. M. , Tenconi B. , Mantegazza P. , Gorio A. 
Published: January 2005

AbstractWe have investigated the reversibility and prevention of peptidergic losses in the lumbar spinal cord caused by permanent resection of sciatic nerve. The lesion triggers a series of degenerative events involving the substance P sensory imput as well as met‐enkephalin interneurons of the substantia gelatinosa. The degenerative processes are evident 10 days after sciatic nerve lesion and are gradually reversible as shown by radioimmunoassay and quantitative immunocytochemistry. Recovery begins 30 days postlesioning and full restoration is observed at 90 days. Serotonin (5‐HT) turnover is markedly affected by sciatic nerve lesion as soon as 24 hr postlesioning, when 5‐HT metabolism is enhanced, returning to control levels just preceding the peptide alterations; 5‐HT metabolism then undergoes a transient period of hypoactivity which correlates with the beginning of the peptidergic restorative processes. Altogether these results, with previous observations showing that 5‐HT depletion prevents metenkephalin interneurons degeneration triggered by the lesion (Di Giulio et al.: J Neurosci Res 18:443–448, 1987), suggest a role for 5‐HT in the synaptic plasticity of the substantia gelatinosa of the spinal cord. The administration of gangliosides (10 or 50 mg/kg) to sciatic‐nerve‐lesioned animals fully prevented the metenkephalinergic degeneration without affecting the degenerative atrophy of the lesioned substance P sensory imput.
Interleukin‐1 Interaction with neuroregulatory systems: Selective enhancement by recombinant human and mouse interleukin‐1 of in vitro opioid peptide receptor binding in rat brain
Authors: Wiedermann C. J. 
Published: January 2005

AbstractInterleukin‐1 (IL‐1) exerts a wide variety of biological effects on various cell types and may be regarded as a pleiotropic peptide hormone. Biological evidence suggests that IL‐1 participates in the modulation of central nervous system physiology and behaviour in a fashion characteristic of neuroendocrine hormones. In this investigation, recombinant (r) human (h) IL‐1 and r mouse (m) IL‐1 were examined for their modulation of opioid peptide receptor binding in vitro. Experiments were performed on frozen sections of rat brain. Receptor binding of radiolabeled substance P and of radiolabeled neurotensin were not significantly affected by the presence of rIL‐1s. Recombinant IL‐1s, however, significantly enhanced specific binding of 125I‐beta‐endorphin (125I‐beta‐END) and of D‐ala2‐(tyrosyl‐3,5‐3H)enkephalin‐(5‐D‐leucine) (3H‐D‐ALA), equipotently and in a concentration‐dependent manner with maximal activity occurring at a concentration of 10 LAF units/ml. The increased binding of 125I‐β‐END and 3H‐D‐ALA was blocked steroselectively by (−)‐naloxone and by etorphine, suggesting detection of opiate receptors. In addition, brain distribution patterns of receptors labeled in the presence of rIL‐1s corresponded to patterns previously published for opiate receptors. Autoradiographic visualization of receptors revealed that rIL‐1s in the different areas of the brain exert their effect on opioid binding with comparable potencies. The data suggest that certain central nervous system effects of IL‐1s may be mediated by their selective interaction with opiatergic systems at the receptor level.
Potassium‐stimulated calcium uptake in astrocytes and its potent inhibition by nimodipine
Authors: Hertz L. , Bender A. S. , Woodbury D. M. , White H. S. 
Published: January 2005

AbstractElevation of the extracellular potassium concentration above its “resting” level of 5.4 mM stimulated uptake of 45Ca2+ in primary cultures of astrocytes. This effect was only observed when cells were exposed to excess potassium shortly after their exposure to 45Ca2+ and was potently inhibited (IC50 ⋍ 3 nM) by the calcium channel blocker nimodipine. In contrast, nimodipine exerted little effect on unstimulated basal uptake of 45Ca2+. These findings suggest that the therapeutic benefit of calcium channel blockers in epilepsy may result in part from the ability of these drugs to prevent calcium entry into astrocytes during seizures when the extracellular potassium is elevated four‐ to fivefold above normal.
Pharmacological characterization of the glutamate receptor in cultured astrocytes
Authors: Backus K. H. , Kettenmann H. , Schachner M. 
Published: January 2005

AbstractCultured astrocytes from neonatal rat cerebral hemispheres are depolarized by the excitatory neurotransmitter glutamate. In this study we have used selective agonists of different neuronal glutamate receptor subtypes, namely, the N‐methyl‐D‐aspartate (NMDA), kainate, and quisqualate type, to characterize pharmacologically the glutamate receptor in astrocytes. The agonists of the neuronal quisqualate receptor, α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole‐4‐propionic acid (AMPA) and quisqualate, depolarized the membrane. Kainate, an agonist of the neuronal kainate receptor, depolarized astrocytes more effectively than quisqualate. Combined application of kainate and quisqualate depolarized astrocytes to a level which was intermediate to that evoked by quisqualate and kainate individually. Agonists activating the neuronal NMDA receptor, namely NMDA and quinolinate, were ineffective. Application of NMDA did not alter the membrane potential even in combination with glycine or in Mg2+‐free solution, conditions under which neuronal NMDA receptor activation is facilitated. The nonselective agonists L‐cysteate, L‐homocysteate, and β‐N‐oxalylamino‐L‐alanine (BOAA) mimicked the effect of glutamate. Dihydrokainate, a blocker of glutamate uptake, did not, and several antagonists of neuronal glutamate receptors only slightly affect the glutamate response. These findings suggest that astrocytes express one type of glutamate receptor which is activated by both kainate and quisqualate, lending further support to the notion that cultured astrocytes express excitatory amino acid receptors which have some pharmacological similarities to their neuronal counterparts.
Superoxide dismutase and cytochrome oxidase activities in light and heavy synaptic mitochondria from rat cerebral cortex during aging
Authors: Vanella A. , Villa R. F. , Gorini A. , Campisi A. , Giuffrida‐Stella A. M. 
Published: January 2005

AbstractThe specific activities of superoxide dismutase (SOD) and cytochrome oxidase (COX) in light and heavy synaptic mitochondria from rat cerebral cortex at different ages (4, 8, 12, 16, 20, and 24 months) have been measured. The specific activity of COX was significantly higher in light synaptic mitochondria than in heavy ones at all ages examined. However, no significant difference during aging was shown. A marked decrease of SOD in light and heavy synaptic mitochondria during aging was observed.
Expression of nerve growth factor receptors by human peripheral blood mononuclear cells
Authors: Morgan B. , Thorpe L. W. , Marchetti D. , Perez‐Polo J. R. 
Published: January 2005

AbstractIn the rat, nerve growth factor (NGF) has been shown to affect immune reactivity by binding to cell surface receptors on a subpopulation of splenic mononuclear cells. This binding occurs in a specific and saturable fashion to what appear to be low‐affinity (type II) NGF receptors (NGFR). Immunofluorescence studies here showed that NGFR are also present on a proportion of human peripheral blood mononuclear cells (PBMC). Equilibrium binding studies demonstrated that the binding of NGF to its receptors on PBMC occurs with a single equilibrium binding constant (mean) of 2.11 × 10−9 M. The number of receptors per cell was determined to be approximately 6.94 × 103 receptors/cell. These results would suggest a role for NGF in the regulation of immune function in man, as well as in animals.
Isolation of a Thy‐1‐like glycoprotein from cat brain: Distribution in retina and brain defined by monoclonal antibodies
Authors: Saleh M. , Bartlett P. F. 
Published: January 2005

AbstractThy‐1 is a glycoprotein primarily expressed in the nervous system of a large number of vertebrate species. A concanavalin‐A binding glycoprotein with a molecular weight of 25, 000 daltons has been isolated from cat brain, which corresponds to the Thy‐1 molecule isolated in other species. Monoclonal antibodies were generated against this cat Thy‐1 molecule, and immunohistochemical staining on adult cat brain frozen sections demonstrated a localisation of the molecule to regions rich in synapses. In the cerebellum, the immunoperoxidase staining with the antibodies was intense in the molecular layer, the fibres of the granular layer, and the Purkinje cell bodies. This distribution of Thy‐1 is consistent with that seen with the rodent and chicken Thy‐1 molecule. In the retina, one antibody (WEHY‐MS‐1) detected the cat Thy‐1 molecule in the ganglion cell layer and on fibres of the inner plexiform and inner nuclear layers. Another antibody (WEHY‐MS‐2) produced a similar retinal staining pattern except that the ganglion cell layer was devoid of Thy‐1. Although the Thy‐1 molecule in the rodent and chicken retina have been reported in the ganglion cell and inner plexiform layers, there have been no consistent reports of Thy‐1 in the inner nuclear layer. This suggests that this putative cat Thy‐1 molecule may have a retinal distribution pattern different from that seen in other species.
Purification and culture of adult rat dorsal root ganglia neurons
Authors: Delree P. , Leprince P. , Schoenen J. , Moonen G. 
Published: January 2005

AbstractTo study the trophic requirements of adult rat dorsal root ganglia neurons (DRG) in vitro, we developed a purification procedure that yields highly enriched neuronal cultures. Forty to fifty ganglia are dissected from the spinal column of an adult rat. After enzymatic and mechanical dissociation of the ganglia, myelin debris are eliminated by centrifugation on a Percoll gradient. The resulting cell suspension is layered onto a nylon mesh with a pore size of 10 μm. Most of the neurons, the diameter of which ranged from 17 μm to > 100 μm, are retained on the upper surface of the sieve; most of the non‐neuronal cells with a caliber of < 10 μm after trypsinization go through it. Recovery of neurons is achieved by reversing the mesh onto a Petri dish containing culture medium. Neurons to non‐neurons ratio is 1 to 10 in the initial cell suspension and 1 to 1 after separation. When these purified neurons are seeded at a density of 3, 000 neurons/cm2 in 6 mm polyornithine–‐laminin (PORN‐LAM) coated wells, neuronal survival (assessed by the ability to extend neurites), measured after 48 hr of culture, is very low (from 0 to 16%). Addition of nerve growth factor (NGF) does not improve neuronal survival. However, when neurons are cultured in the presence of medium conditioned (CM) by astrocytes or Schwann cells, 60–80% of the seeded, dye‐excluding neurons survive. So, purified adult DRG neurons require for their short‐term survival and regeneration in culture, a trophic support that is present in conditioned medium from PNS or CNS glia. As NGF has no survival‐promoting effect on these purified adult neurons, the trophic effect of CMs is likely to be mediated by non‐NGF molecule(s).
TIS gene expression in cultured rat astrocytes: Induction by mitogens and stellation agents
Authors: Arenander A. T. , Lim R. W. , Varnum B. C. , Cole R. , de Vellis J. , Herschman H. R. 
Published: January 2005

AbstractThe expression of a number of TIS genes (Lim et al.:Oncogene 1:263–270, 1987) was examined in secondary cultures of rat neocortical astrocytes treated with mitogens and stellation agents, to study the early nuclear events which accompany the induction of glial proliferation and/or differentiation. Tetradecanoyl phorbol acetate (TPA), epidermal growth factor, and firoblast growth factor, three mitogens for astrocytes, stimulated marked, rapid, and transient increases in TIS gene mRNAS. TIS10, which is not expressed in rat PC12 pheochromocytoma cells, could be induced by these mitogens in rat astrocytes. Dibutyryl cyclic adenosine monophosphate and forskolin, which induce rapid stellation in astrocytes, and ganglioside GM1, a potent mitogen as well as an antagonist of the induction and maintenance of stellation, all induced TIS gene expression. Thus, a broad range of agents which elicit both proliferative and differentiation responses in astrocytes are capable of inducing a family of genes that may play a role in the early events of signal transduction.
UDP galactose: Ceramide galactosyltransferase, CDP choline:1, 2‐diacyl‐sn‐glycerol phosphocholine transferase, and microsomal reductases in major regions of the developing rat brain in nutritional stress
Authors: Padmini S. , Rao P. Srinivasa 
Published: January 2005

AbstractThe influence of nutritional inadequacy during the active growth phase of the developing brain, coinciding with myelinogenesis, was examined in rat pups. Developmental profiles of enzyme activities involved in biosynthesis of myelin membrane lipids, and those of associated pathways which generate precursor compounds for such biosynthetic reactions, were followed as functions of age in major anatomical regions of the brain. It was observed that while galactosyltransferase and choline phosphotransferase activities were significantly diminished, the microsomal cytochrome reductases, which contribute to the process of fatty acid elongation and desaturation, were also lowered. An attempt at adaptative increase of enzyme activity, in response to the stress, was apparent in the case of glycerol‐3‐phosphate dehydrogenase, which could possibly explain, in part, the lower susceptibility of phospholipid biosynthesis to impairments induced by nutritional insufficiency.
Evidence from neuronal heterokaryons for a trans‐acting factor suppressing THY‐1 Expression during neuronal development
Authors: Saleh M. , Bartlett P. F. 
Published: January 2005

AbstractThe expression of Thy‐1 on developing sensory neurons cultured in vitro is strictly regulated and follows a temporal course identical to that observed in situ. We have investigated the role of trans‐acting factors in this innate regulation by constructing heterokaryons between mature Thy‐1.1+ expressing neurons and immature Thy‐1.2− neurons. It has been observed by immunofluorescence that within 16 hr of fusion, Thy‐1.1 expression is suppressed in such heterokaryons. However, this suppression is reversible, and after 3–4 days in vitro, at the time at which Thy‐1.2 is normally expressed, there is re‐expression of the Thy‐1.1 molecule producing Thy‐1.1+/Thy‐1.2+ co‐expressing heterokaryons. As nuclear fusion does not occur, it appears that a developmentally regulated diffusible suppressor molecule is responsible for these observations.
Patterns of proto‐oncogene expression in human glioma cell lines
Authors: LaRocca R. V. , Rosenblum M. , Westermark B. , Israel M. A. 
Published: January 2005

AbstractPreviously reported studies have suggested that variations in the pattern of proto‐oncogene expression within a specific tumor type may denote an underlying difference in the biology and clinical behavior of those tumors. To more sensitively characterize malignant tumors of the central nervous system, we have used Northern blot hybridization analysis to determine the patterns of expression of seven proto‐oncogenes in 20 cell lines established from biopsy specimens of patients with malignant glioma. The following proto‐oncogenes are expressed at detectable levels in 30 μg of total RNA from most glioma cell lines examined: c‐myc (20/20), c‐mil/raf‐1 (18/18), neu (19/20), c‐erbB (19/20), and c‐myb (17/20). In contrast, only half of the cell lines expressed detectable c‐sis (10/20). In none of the cell lines tested was N‐myc (0/20) mRNA detected. Morphologic analysis of these 20 cell lines revealed three different growth patterns: bipolar, epithelial, and pleomorphic‐glial. Detectable levels of c‐sis mRNA typically occurred with either an epithelial or pleomorphic‐glial morphology. The pleomorphic‐glial subgroup was also characterized by the expression of glial fibrillary acidic protein.