bluuebunny/crossref_metadata_2025_split huggingface dataset:
Damage to bulbospinal serotonin‐, tyrosine hydroxylase‐, and TRH‐containing axons occurs early in the development of experimental allergic encephalomyelitis in rats
Authors: White S. R. , Samathanam G. K. , Bowker R. M. , Wessendorf M. W. 
Published: January 2005

AbstractSpinal cord monoaminergic and peptidergic axonal damage occurring during the development of experimental allergic encephalomyelitis (EAE) was assessed using immunohistochemistry. Spinal cord axons immunoreactive for serotonin, catecholamines, or a thyrotropin‐releasing hormone marker peptide were found to be markedly swollen and distorted by the earliest stage of detectable paralysis during EAE development (the flaccid tail stage). As clinical signs progressed to complete hindlimb paralysis, axonal damage became increasingly extensive. Axonal damage was equally pronounced whether EAE was induced by inoculation with purified myelin basic protein or with whole spinal cord homogenate, suggesting that the damage did not result from an immune attack directed against specific monoaminergic and/or peptidergic antigens present in the inoculant. However, two observations suggested that mechanical or chemical factors associated with the inflammatory foci contribute to the axonal damage: first, distorted axons were nearly always located adjacent to blood vessels or the pial surface, sites at which inflammation occurs during EAE. Second, the severity of axonal damage correlated with the severity of the inflammation. The early onset of axonal damage during development of EAE and the close correlation that was found between the severity of axonal damage and the severity of clinical signs suggested that the axonal damage may contribute to the clinical signs of the disease.
Changes in PC12 cell morphology induced by transfection with 42C cDNA, coding for a member of the S‐100 protein family
Authors: Masiakowski P. , Shooter E. M. 
Published: January 2005

AbstractThe cloned DNA coding for 42C protein (light chain of calpactin I), whose mRNA is induced in PC12 cells by treatment with nerve growth factor (NGF), was reintroduced into these cells. A cell line was obtained in which the outgrowth of processes in the absence of added NGF, similar to that induced in the parental PC12 cells by the factor, was accompanied by high levels of 42C RNA. The apparent reason for this constitutive overexpression of 42C is the stable integration of multiple copies of the 42C DNA into the cell genome. These results further support the notion that S‐100 protein family, of which 42C is a member, may play an important role in development.
Immunohistochemical studies on cross‐transplantations between jimpy, shiverer, and normal newborn mice
Authors: Lachapelle F. , Lapie P. , Nussbaum J. L. , Gumpel M. 
Published: January 2005

AbstractCross‐transplantations of neural tissue have been performed between jimpy (jp), shiverer (shi), and normal mice. Taking advantage of the absence of immunodetectable myelin basic protein (MBP) in the shi brain, jp myelin has been identified in the shi recipient by using an anti‐MBP antiserum. By contrast, shi as well as normal myelin have been identified in the jp brain by using an anti‐C‐terminal hexapeptide of the proteolipid protein (PLP) (this PLP hexapeptide being absent in the jp PLP). When transplanted under homochronic conditions (newborn into newborn), jp oligodendrocytes (ODC) express their usual phenotype in a normal or a shi environment, suggesting that at birth the jp ODCs phenotype is strictly established and cannot be modified by environmental conditions. The reverse transplantations (newborn shi or normal into newborn jp brain) demonstrate that the jp environment does not modify the phenotype of normal or shi ODCs. Finally, these experiments demonstrated a normal timing of differentiation of jp axons and of jp ODCs.
Nicotinic acetylcholine receptor subtypes in human frontal cortex: Changes in Alzheimer's disease
Authors: Sugaya K. , Giacobini E. , Chiappinelli V. A. 
Published: January 2005

AbstractMolecular genetic and pharmacological studies have suggested that several subtypes of nicotinic acetylcholine receptors exist in the mammalian and avian brain. Combining 3H‐(−)‐nicotine, 125 I‐α‐bungarotoxin, and 125I‐κ‐bungarotoxin as ligands, we report here the first evidence for the existence in human frontal cortex of at least three different subtypes of nicotinic receptors. Autoradiographic analysis shows that specific 125I‐κ‐bungarotoxin binding sites are concentrated mainly in several cortical layers. We also show that κ‐bungarotoxin, but not κ‐bungarotoxin decreases the evoked release of 3H‐acetylcholine in rat cortical slices, indicating a likely presynaptic localization for some of the α‐bungarotoxin‐insensitive κ‐bungarotoxin sites in mammalian brain. The brains of patients with Alzheimer's disease show marked decreases in Bmax values for low‐affinity 125I‐κ‐bungarotoxin sites and both high‐ and low‐affinity 3H‐nicotine sites, whereas 125I‐κ‐bungarotoxin sites are not significantly different in number from age‐matched control brains. We conclude that Alzheimer's disease does not affect all subtypes of nicotinic receptors in the frontal cortex to the same extent.
Characterization of functional nerve growth factor‐receptors in a CNS glial cell line: Monoclonal antibody 217c recognizes the nerve growth factor‐receptor on C6 glioma cells
Authors: Kumar S. , Huber J. , Peña L. A. , Perez‐Polo J. R. , Werrbach‐Perez K. , de Vellis Jean 
Published: January 2005

AbstractThe biological effects of nerve growth factor (NGF) have been shown to be mediated by the high‐affinity form of the nerve growth factor receptor (NGF‐R) in sympathetic and sensory neurons, and in PC12 cells. We report here that the central nervous system C6 rat glioma cell line likewise expresses functional high‐affinity NGF‐Rs. The expression of NGF‐R mRNA in C6 cells can be up‐regulated by cycloheximide and its own ligand, NGF; and it can be rapidly down‐regulated by epidermal growth factor (EGF). Furthermore, C6 cells display NGF responsiveness by expressing c‐fos mRNA within 30 minutes of treatment with NGF; and after 4—5 days of NGF exposure, C6 cells cease dividing as measured by [3H]‐thymidine uptake, change shape, and reveal neurite‐like ‐processes. Scatchard analysis of [125 I]‐labelled bound to solubilized C6 cells confirms the presence of both high‐ and low‐affinity receptor protein. Cross‐linking radiolabeled NGF to its receptor in the presence or absence of excess unlabeled NGF, followed by immunoprecipitation with monoclonal antibody (mAb) 192‐IgG (a known anti‐NGF‐R antibody) and SDS‐PAGE reveals a 100 kD band corresponding to the NGF/NGF‐R complex. An identical band is observed when the immunoprecipitation is carried out with mAb 217c, suggesting that the 217c epitope is related to NGF‐R. The 217c antibody was generated against C6 cells and shown to be a cell surface antibody (Peng et al., Science 215:1102–4, 1982); several investigators have used it subsequently as an immunocytochemical marker for Schwann cells. The significance of NGF‐Rs in a CNS glial cell line is unclear, but association of NGF with the control of proliferation and/or differentiation of primitive glial cells is suggested.
Effect of gender on glucose utilization rates in healthy humans: A positron emission tomography study
Authors: Miura S. A. , Schapiro M. B. , Grady C. L. , Kumar A. , Salerno J. A. , Kozachuk W. E. , Wagner E. , Rapoport S. I. , Horwitz B. 
Published: January 2005

AbstractPositron emission tomography (PET) was used with 18fluorodeoxyglucose to see if gender differences in resting cerebral glucose utilization could be detected. Thirty‐two healthy subjects (15 women and 17 men; age range: 21–38 yr) were examined using a high‐resolution PET scanner to determine the regional cerebral metabolic rate for glucose (CMRglc) in 65 gray matter regions of interest. Whole brain CMRglc did not differ significantly between the two genders, nor did any of the regional CMRglc values. Only 1 of 65 ratios of regional‐to‐whole brain CMRglc differed significantly between men and women, which is consistent with chance. These results indicate that there are no differences in resting regional cerebral glucose utilization between young men and women.
Effects of light/dark‐ and dark‐rearing on synaptic morphology in the superior colliculus and visual cortex of the postnatal and adult rat
Authors: Bakkum B. W. , Benevento L. A. , Cohen R. S. 
Published: January 2005

AbstractServeral synaptic parameters, previously shown to undergo alterations with changes in the internal and external environment, were examined in the visual system of light/dark‐ and dark‐reared postnatal and adult rats. Animals were raised in either 14hr light/10 hr dark (Lt/Dk) or in total darkness (Dk). The specific synaptic parameters in the superficial layers of the superior colliculus (SC), visual cortex (laminae II/III and IV) (VC), and, as contro, the auditory cortex (laminae II/III and IV) (AC), examined during the postnatal period (i.e., postnatal days 7,14,21, and 28) and in the adult (i.e., day 56) included:(1) mean number of synapses, (2) mean synaptic length, (3) percentages of perforated postsynaptic densities, (4) percentages of asymmetric and symmetric synapses, (5) percentages of dendritic, spinous, anmd somatic synapses, and (6) percentages of synapses with positive, negative, or no curvature. Developmental patterns in rats rearded in normal lighting conditions were noted. Specifically, in the SC and VC of Lt/Dk animals, the number of synapses increased up to postnatal day in the mean number of synapses increased; no significant changes in the mean number of synapses between PND =28 and 56 were detected in any of the areas examined. Changes in synaptic length in the SC and VC were not observed during postnatal development or in the adult in any of the aforementioned brain areas. Low percentages of postsynaptic densities (PSDs) were found at all time points and in all brain areas during the postnatal period. Increases in perforated PSDs were seen at PND = 56 compared to PND = 28 in the VC. In the VC and AC, there was decrease in symmetric synapses with age. Asymmetric synapses were prevalent in all brain areas at PND = 28 AND 56. dendritic synapses predominated in the SC, while spinous synapses were the preponderant type in the VC and AC during postnatal development and in the adult, A decrease in the percentage of spinous synapses in the SC was observed at PND = 56 vs. PND = 28. A decrease in the percentage of negatively curved synapses with age and a trend toward a concomitant increase in the percentage of positively curved synapses were seen in all brain areas during development and in the adult. Quantitative analyses of the SC and VC tissues examined from all postnatal animals demonstrated no significant differences between Lt/Dk and Dk animals in all the synaptic parameters measured. On the other hand, similar analyses of adult synapses in the SC and VC showed a significantly smaller mean number of synapses in rats dark‐reared to adulthood as compared to those raised in normal lighting conditions. Dark‐rearing had no effect on synaptic number at any time point in the auditory cortex, indicating that this is a specific light effect. Therefore, the effects of visual deprivation on synaptic numbers occur during early adulthood and not during postnatal development.
Changes in glial fibrillary acidic protein mRNA expression after corticospinal axotomy in the adult hamster
Authors: Kost‐Mikucki S. A. , Oblinger M. M. 
Published: January 2005

AbstractWe examined changes in the expression of glial fibrillary acidic protein (GFAP) mRNA during Wallerian degeneration in the corticospinal system of the adult Golden hamster following axotomy. GFAP is the product of a type III intermediate filament (IF) gene that is expressed specifically in mature astrocytes. A well‐studied component of a complex response termed reactive astrogliosis that occurs after various types of CNS injury is the increased production of astrocytic processes filled with GFAP‐containing IFs. While increased expression of GFAP during reactive astrogliosis has been well established at the protein level, little is known about whether or not changes in GFAP mRNA levels occur after CNS injury. In the present study we used in situ hybridization methods, to examine, this issue. A 35S labeled mouse GFAP cDNA probe was used for in situ hybridizations of sections of the brain stem obtained 2, 7, and 14 days after unilateral transections of the corticospinal tract in the caudal medulla. Film as well as emulsion autoradiography showed a dramatic increase in GFAP mRNA labeling associated with the degenerating corticospinal tract. GFAP mRNA levels were already dramatically increased in the injured corticospinal tract by 2 days post axotomy and remained elevated at 14 days. Interestingly, in addition to the robust increase in GFAP mRNA levels specifically associated with the degenerating tract, a diffuse increase in GFAP mRNA labeling was observed throughout the grey matter of the brain stem at 2 days post‐axotomy, but not after this time. Immunoblotting and immunocytochemical experiments verified that the increased GFAP mRNA levels in the degenerating corticospinal system were accompanied by an increased expression of, the protein. These results demonstrate that an increase in GFAP mRNA levels occurs during Wallerian degeneration in the CNS and suggest that increased expression of the GFAP gene is a major contributor to CNS scarring that results after direct traumatic injury.
Verapamil regulation of Na‐K pump levels in rat skeletal myotubes: Role of spontaneous activity and Na channels
Authors: Brodie C. , Sampson S. R. 
Published: January 2005

AbstractThe effects of low and high doses of verapamil on expression of Na‐K pump and Na channels in cultured rat skeletal muscle were studied and compared. Myotubes were treated for 3 Jays with either 20 or 100 μM verapamil, and measurements were made of transmembrane resting potential, spontaneous action potential freguency, and specific binding of [3 H]ouabain and [3 H]saxitoxin upregulated both Na‐K pumps and Na channels, whereas high verapamil down regulated the former and upregulated the latter. Changes in channel levels preceded those in pump levels. Spontaneous contractile activity could be observed during treatment with low but not high verapamil. Simultaneous treatment with verapamil and elevated external K+ reversed the effect of low verapamil on Na‐K pumps, was without effect on high verapamil‐induced changes in pump levels, and potentiated the effects of both concentrations of verapamil on Na channel levels. Scatchard analysis showed that verapamil caused changes in Bmax without altering Kd. The verapamil‐induced changes in both Na‐K pumps and Na channels were blocked by inhibition of protein and RNA synthesis. We conclude that the differences in effects on Na‐K pumps obtained with the two doses are due to the different effects on spontaneous activity and associated changes in intracellular Na concentration.
Endogenous opioid‐immunoreactive neurons of the ventromedial hypothalamic nucleus concentrate estrogen in male and female rats
Authors: Akesson T. R. , Micevych P. E. 
Published: January 2005

AbstractEstrogen stimulates expression of proenkephalin mRNA in neurons of the hypothalamic ventromedial nucleus, and evidence is accumulating that synaptic release of one of the peptide end products, met‐en‐kephalin, influences events that regulate reproductive behavior. To address the question of whether estrogen acts directly on neurons that synthesize met‐en‐kephalin or indirectly through a separate neuronal population, we combined estrogen autoradiography with endogenous opioid peptide (EOP) immunohistochemistry. In agreement with previous studies, the ventrolateral subdivision of the hypothalamic ventromedial nucleus was densely packed with EOP‐immunoreactive cells. In males, 48% of the estrogen‐concentrating cells of the ventrolateral subdivision of the hypothalamic ventromedial nucleus contained EOP, and, in females, 27% of the estrogen‐concentrating cells contained EOP. These findings indicate that estrogen acts directly on neurons that express EOP and suggest a mechanism that underlies sexually differentiated reproductive behavior.
Quantitative autoradiographic study of L‐glutamate binding sites in normal and atrophic human cerebellum
Authors: Hatziefthimiou A. , Mitsacos A. , Mitsaki E. , Plaitakis A. , Kouvelas E. D. 
Published: January 2005

AbstractIn the present work the distribution of L‐glutamate binding sites in the different layers of human cerebellum of normal individuals and of seven patients who died with olivopontocerebellar atrophy (OPCA) was examined with the technique of quantitative autora‐diography. Specific L‐[3H]glutamate binding was higher in the molecular than in the granule cell layer of normal cerebellar tissue. A significant decrease of L‐[3H]glutamate specific binding was observed in me molecular layer of ail OPCA tissues. In the granule cell layer L‐[3H]glumate binding was decreased only in two patients who suffered from late‐onset sporadic OPCA and in one patient who suffered from a form of OPCA inherited in a dominant manner.Quisqualate‐sensitive binding sites were the most abundant binding sites in the molecular layer of normal cerebella, whereas N‐methyl‐D‐aspartic acid (NMDA)‐sensitive binding sites were the most abundant type in the granule cell layer. A significant decrease of quisqualate‐sensitive and an increase in NMDA‐sensitive binding sites were observed in the molecular layer of OPCA cerebellar tissues. No significant changes were observed in the granule cell layer of these tissues.
Expression and induction of intercellular adhesion molecules (ICAMs) and major histocompatibility complex (MHC) antigens on cultured murine oligodendrocytes and astrocytes
Authors: Satoh J. , Kim S. U. , Kastrukoff L. F. , Takei F. 
Published: January 2005

AbstractExpression of intercellular adhesion molecule‐1 (ICAM‐1), ICAM‐2‐like molecule (Lgp55), and class I/II major histocompatibility complex (MHC) antigens (H‐2 and Ia) was investigated in cultures of mu‐rine Oligodendrocytes and astrocytes. Under unstim‐ulated conditions, low levels of ICAM‐1 expression were observed on astrocytes (<20%), but not on oligodendrocytes. Lgp55 was expressed intensely on oligodendrocytes (>90%) and to a lesser degree on astrocytes (>70%). A weak class I MHC (H‐2) im‐munoreactivity was identified on both Oligodendrocytes and astrocytes (50‐70%). Class II MHC (Ia) antigen was undetectable on both cell types.After 48‐hr exposure to immune mediators that include interferon‐γ (IFN‐γ), 500 U/ml, and supernatant from concanavalin A (Con A)‐activated spleen cells, ICAM‐1 expression was markedly increased on astrocytes (>80%), but not on Oligodendrocytes. Lgp55 expression on both cell types was not altered. Induction of H‐2 antigen expression by immune mediators was quite high on both cell types (>95%), while Ia antigen induction was low on astrocytes (<50%) and did not occur on Oligodendrocytes. Cell type‐specific expression and induction of ICAMs and MHC antigens by immune mediators may play roles in lymphocyte‐glial cell interactions at the sites of inflammation in the central nervous system (CNS).
Xenopus Oocytes as immunological vectors to produce monoclonal antibodies to rat brain antigens
Authors: Matute C. , Tigyi G. J. , Miledi Ricardo 
Published: January 2005

AbstractA novel approach was developed to raise a panel of monoclonal antibodies (mAb) against brain antigens using Xenopus oocytes as immunological vectors. Xenopus oocytes were injected to express proteins encoded by brain‐derived mRNA extracted from rat cerebral cortex. A crude membrane preparation from mRNA‐injected oocytes was then used to immunize mice previously rendered immunotolerant to native oocyte membranes. mAb reacting with cryostat cut sections from rat brain were selected and further characterized by immunohistological and immunobiochemical techniques. Several mAb recognized brain specific antigens, including some that were cell type specific and others that revealed a regional binding pattern. A particular group of antibodies recognized an epitope localized exclusively to the cerebellar pinceau terminals. Although some of the hybridomas found in this panel may be products of natural autoreactive lymphocytes, the presence of a specific immune response to mRNA expression products is discussed. These results indicate that mRNA injected oocytes are useful tools to raise mAb to study the molecular diversity of the nervous system.
Phosphorylation of brain (NA+,K+)‐ATPase alpha catalytic subimits in normal and epileptic cerebral cortex: II. Partial seizures in human epilepsy
Authors: Guillaume Daniel , Grisar T. , Delgado‐Escueta A. V. , Laschet J. , Bureau‐Heeren M. 
Published: January 2005

AbstractWe examined the activity and phosphorylation level of (Na+, K+)‐ATPase (E.C. 3.6.1.3) partially puri fied from normal and epileptic human cortices. Con trol patients (n = 11) were operated on for a non‐ epileptogenic deep brain lesion, while epileptic patients (n = 10) were operated on for temporal or frontal originating partial seizures, resistant to med ications or secondary to evolutive brain tumors. No differences in the specific activity of microsomal (Na+, K+)‐ATPase were observed between the two groups of patients. After partial purification of the enzyme followed by SDS‐polyacrylaniide, gel. electrophoresis, (Na+, K+)‐ATPase catalytic subunit had a decreased affinity for K+ in human epileptic cortex and lost its sensitivity to phenytoin dephosphorylation. Indirect evidence suggests that those abnormalities of (Na+, K+)‐ATPase in human epileptic cortex hold preferentially true for the alpha(–) enzymatic subunit. Those result indicate that, in human epileptic cortex, (Na+, K+) glial subtype is altered in its K+ regulation and phenytoin sensitivity and could be responsible for ictal transformation and seizure spread.
Modulation of retinal differentiation by oncogenes: Effect of the v‐src gene on expression of choline acetyltransferase and glutamine synthetase
Authors: Notter M. F. D. , del Cerro M. , Balduzzi P. C. 
Published: January 2005

AbstractExpression of the protooncogene c‐src in chick neural retina is developmentally regulated and associated with neural differentiation. In the present study, chick neural retina (NR) cell cultures from 7 day embryos were exposed to the exogenous src oncogene, the c‐src counterpart, to establish the effect of expression of v‐src on specific retinal cellular differentiation. NR cells from 7 day chick embryos were placed in monolayer or rotation culture and infected with Rous sarcoma virus (RSV) containing a single transforming gene. Other cultures were infected with a transforming defective mutant of RSV which still possesses mitogenic activity for NR cells. While control cultures showed typical neuronal and Muller cell morphologies at the light and electron microscopic level, NR cells infected with RSV exhibited dramatic morphological alterations in monolayer culture and cell aggregates. However, the mutant src gene induced mitosis without accompanying transforming properties. When aggregate cultures were treated with hydrocortisone to induce glutamine synthetase (GS) expression in Muller cells, control cultures showed the typical immunofluorescence pattern of GS staining, while RSV infected cultures showed no GS fluorescence. Cultures infected with mutant RSV showed some staining for GS. In contrast, choline acetyltransferase activity was shown to increase in both monolayer and aggregate cultures of retinal cells following v‐src expression. These data indicate that the presence of excess v‐src in differentiating cultures of NR inhibits the expression of some neural specific enzymes and enhances the presence of other specific proteins. Moreover, continually growing cultures of oncogene‐altered retinal cells may be useful as models to study gene expression in development of the nervous system.