bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transected axons of adult hypothalamo‐neurohypophysial neurons regenerate along tanycytic processes
Authors: Chauvet N. , Parmentier M. L. , Alonso G. 
Published: January 2005

AbstractIn the intact hypothalamo‐neurohypophysial system, oxytocinergic or vasopressinergic neurons project their axons throughout the internal layer of the median eminence towards the blood vessels of the hypophysial neural lobe. When transected at the level of the median eminence, these axons undergo massive sprouting towards the external layer of the organ and the underlying perivascular region containing hy'pophysial portal vessels. The present study was designed to explore the possible roles of median eminence glial cells in such a reorganization of transected neurohypophysial axons. The relationships between regenerating axons and glial cells were studied by laser scanning confocal microscopy and electron microscopy on vibratome sections immunostained with specific antibodies against neurohypophysial peptides and/or against glial markers. All along the intact median eminence, two main types of glial cells were identified: (1) tanycytes immunoreactive to vimentin and slightly immunoreactive to glial fibrillary acidic protein, and (2) classical astrocytes immunoreactive to glial fibrillary acidic protein but vimentin‐negative. In the intact median eminence, neurohypophysial axons were associated with astrocytic processes located in the internal layer. After a lesion of the hypophysial stalk, peptidergic regenerating axonal sprouts were found to project massively towards the external layer and to penetrate the underlying perivascular region in close association with tanycytic‐like processes immunoreactive to both vimentin and to glial fibrillary acidic protein. In contrast, regenerating sprouts were absent from those regions of the lesioned median eminence containing astrocytic processes immunoreactive to glial fibrillary acidic protein but vimentin‐negative. When fixed lesioned median eminences were treated by placing crystals of the lipophilic dye Dil on their ventricular surface, regenerating axons were found to be closely associated with Dil‐labelled tanycytic‐like end feet terminating in the external layer, and with connected thin processes projecting through the external vascular region. These data indicate that in the median eminence of the adult rat, lesioned neurohypophysial axons regenerate in close association with tanycytic processes. © 1995 Wiley‐Liss, Inc.
Myelin vesicles: What we know and what we do not know
Authors: Sedzik J. , Blaurock A. E. 
Published: January 2005

AbstractIn the following review, we address difficulties that have arisen when attempting to convert the myelin multilayers into vesicles. The emphasis is on CNS myelin of adult mammals although both central nervous system (CNS) and peripheral nervous system (PNS) myelin are considered. The ability to prepare vesicle of myelin membrane has yet not been feasible. We hope to clarify some aspect of this problem and offer some possible approaches. Special attention is paid to myelin swelling phenomena because these indicate ways in which the myelin multilayer can break down. Images of isolated myelin are reviewed with special attention to the ways in which the multilayer actually breaks down. Attempts at reproducing a procedure for vesiculating myelin are summarized, and a critique is given to account for the inability to reproduce the published results. Finally, novel approaches for vesiculating myelin are proposed, which are based on well‐characterized swelling phenomena. © 1995 Wiley‐Liss, Inc.
Oxidative damage to proteins and lipids of CNS myelin produced by in vitro generated reactive oxygen species
Authors: Bongarzone E. R. , Pasquini J. M. , Soto E. F. 
Published: January 2005

AbstractPurified myelin isolated from 70‐day‐old rats was submitted to nonenzymatic peroxidative systems containing 100 μM FeC13.6H2O,100 μM ascorbic acid, and 100 μM CuSO4.6H2O 10 mM H2O2 in order to investigate the extent of damage produced by reactive oxygen species (ROS). Iron and copper catalyzing systems were selected because of the known importance of these metals in producing free radical chain reactions in biological membranes (Halliwell and Gutteridge: “Free Radicals in Biology and Medicine,” Oxford: Clarendon Press, 1989). Our findings, show that (1) although after 1 hour of peroxidation, an important level of thiobarbituric acid‐reactive substances (TBARS) was detected, polyunsaturated fatty acids (20:2; 20:4; 22:4 and 22:6) were markedly affected only after 14 hours of incubation; (2) protein thiol groups were very sensitive to the attack of ROS generated by copper but resistant to iron‐generated ROS; (3) aggregation of myelin proteins produced by peroxidation could be prevented by sulfhydryl (SH)‐reducing agents, and (4) as a consequence of these modifications, compact myelin suffered disruption of its intraperiodic line. In conclusion, our results demonstrate that this unique membrane of the central nervous system (CNS) is highly vulnerable to oxidative stress and that this susceptibility to oxidative damage could be prevented, at least partially, by the use of SH‐protective molecules. © 1995 Wiley‐Liss, Inc.
β‐Amyloid precursor protein is modified with O‐linked N‐acetylglucosamine
Authors: Griffith L. S. , Mathes M. , Schmitz B. 
Published: January 2005

AbstractThe β‐amyloid precursor protein (APP) has been implicated in the etiology of Alzheimer's disease (Kang et al.: Nature 325:733–736, 1987; Selkoe: Science 248:1058–1060, 1990; Selkoe: In Cowan et al. (eds): “Annual Review of Neuroscience.” Palo Alto, CA: Annual Reviews, Inc., pp 489–519, 1994) and numerous studies have shown that b̃‐amyloid is involved in amyloid plaque formation (Rumble et al.: N Engl J Med 320:1446–1452, 1989; Sisodia et al.: Science 248: 492–495, 1990). Evidence is presented that APP is modified with N‐acetylglucosamine linked to cytoplasmic serine or threonine residues (O‐GIcNAc). This is the first report of a plasma membrane protein modified with this carbohydrate. It has been postulated that this modification, which is ubiquitous in all organisms studied to date except bacteria (Haltiwanger et al.: Biochem Soc Trans 20:264–269, 1992; Dong et al.: J Biol Chem 268:16679–16687, 1993; Elliot et al.: J Neurosci 13:2424–2429, 1993; Kelly et al.: J Biol Chem 268:10416–10424, 1993), may function as an alternative to phosphorylation (Dong et al., 1993) and is involved in the multimerization of proteins (Haltiwanger et al., 1992; Dong et al., 1993). O‐GlcNAc occurs at “PEST” sequences (Rogers et al.: Science 234:364–368, 1986) and it has been suggested that this modification within such a sequence leads to increased proteolytic stability of the molecule (Dong et al., 1993). The importance of proteolytic cleavage (Kang et al., 1987; Selkoe, 1990, 1994), and the possible involvement of phosphorylation (Gandy et al.: Proc Natl Acad Sci USA 85:6218–6221, 1988; Gillespie et al.: Biochem Biophys Res Commun 187: 1285–1290, 1992; Suzuki et al.: J Neurosci 48:755–761, 1992; Suzuki et al.: EMBO J 13:1114–1122, 1994) in the regulation of APP processing suggest that this novel modification may somehow be involved in the biochemistry of APP. © 1995 Wiley‐Liss, Inc.
Inhibition of neurite outgrowth following intracellular delivery of anti‐GAP‐43 antibodies depends upon culture conditions and method of neurite induction
Authors: Shea T. B. , Benowitz L. I. 
Published: January 2005

AbstractNB2a/dl neuroblastoma cells acquire a neuronal phenotype in response to several differentiating agents, including dibutyryl cAMP (dbcAMP) and the withdrawal of serum. As shown previously, antibodies to the growth‐associated protein, GAP‐43, introduced intracellularly using a lipid carrier, blocked the differentiation induced by dbcAMP. Antibodies to GAP43, at a low concentration, also blocked neurite out‐growth induced by serum withdrawal when cells were grown on a relatively unadhesive substrate. On more adhesive substrates such as poly‐L‐lysine and laminin, however, anti‐GAP‐43 antibodies had less of an effect on neurite outgrowth. Previous studies have shown that the increased adhesivity of laminin allows a small but significant population of neurites to grow from serum‐deprived cells, even in the presence of the microtubule‐depolymerizing drug, colchicine. The outgrowth of this population of neurites was blocked by antibodies to GAP‐43. These results are in conformity with recent studies showing that the requirement for GAP‐43 in neuritogenesis may be related to membrane adhesiveness, and may contribute to an understanding of some of the apparent discrepancies in the literature concerning the involvement of GAP‐43 in neuronal differentiation. © 1995 Wiley‐Liss, Inc.
Adaptation of C6 glioma cells to serum‐free conditions leads to the expression of a mixed astrocyte‐oligodendrocyte phenotype and increased production of neurite‐promoting activity
Authors: Coyle D. E. 
Published: January 2005

AbstractC6 cells were adapted to proliferate in defined culture medium to allow the study of long‐term effects of serum‐free growth conditions on their phenotypic antigen expression and production of neurite promoting factors (NPFs). Cultures were grown in either Ham's F‐12 or supplemented Opti‐MEM‐I containing 15% heat‐inactivated horse serum and 2.5% fetal calf serum (serum‐containing) or in supplemented OptiMEM‐I alone (serum‐free). Immunocytochemical and immunofluorescence techniques were used to determine the antigenic expression of A2B5, galactocerebroside (Ga1C), and glial fibrillary acidic protein (GFAP) in passage matched and sister cultures of serum and serum‐free grown C6 cells. When C6 cells were grown under serum‐containing conditions, two populations of cells were seen: young oligodendrocytes (A2B5+, GFAP‐, GalC+ ), and mixed astrocyte‐oligodendrocyte phenotype (A2B5+, GFAP‐, Ga1C+). After adaptation of the C6 cells to serumfree conditions over 2–3 passages, only one population of cells was observed, the mixed astrocyte‐oligodendrocyte phenotype. The serum‐free conditions also resulted in, greater staining of the C6 cells. Conditioned media from the two growth conditions were fractionated by ultrafiltration into two fractions: components >50 kDa and components of 10–50 kDa. The amount of neurite promoting activity seen between the two culture conditions resulted in a 3‐fold increase in NPF activity under serum‐free conditions in the >50 kDa fraction. The 10–50 kDa fraction only expressed NPF activity if obtained from the serumgrown C6 cells. This alteration in NPF activity appears to be the result of the phenotypical alteration of the C6 cells, and may suggest that the NPF activities from the two culture conditions may not be identical. © 1995 Wiley‐Liss, Inc.
Calbindin D28K‐containing neurons, and not HSP70‐expressing neurons, are more resistant to HIV‐1 envelope (gp120) toxicity in cortical cell cultures
Authors: Diop A. G. , Lesort M. , Esclaire F. , Dumas M. , Hugon J. 
Published: January 2005

AbstractHIV‐1‐associated cognitive/motor complex is one of the major neurological complications of AIDS and is associated with neuronal loss. Gp120, the HIV envelope protein, is toxic for neurons in cultures and produces a rise in intracytosolic calcium. This neurotoxicity is dose‐dependent and time‐dependent. We evaluated the selective gp120 toxicity in primary neuronal cultures for calbindin‐free and calbindin‐containing neurons with semi‐quantitative immunocytochemistry using an anti‐calbindin D28K monoclonal antibody. The number of immunolabelled neurons was inversely correlated to neuronal survival. In cultures exposed to gp120 (100 pM) for 24 hr the neuronal survival of initial platings was 19.7 ± 2.1% and the percentage of neuronal survival was 84.6 ± 4.9% in control cultures exposed to the vehicle. The corresponding percentages of immunolabelled neurons were 85.0 ± 2.1% in treated cultures and 23.6 ± 3.1% in control cultures (P < 0.001). The expression of heat shock proteins by heating cell cultures did not: protect neurons from gp120 toxicity. These results suggest that calbindin D28K‐containing neurons are more resistant to gp120‐toxicity in this cell culture system. © 1995 Wiley‐Liss, Inc.
Comparison of c‐jun, junB, and junD mRNA expression and protein in the rat dorsal root ganglia following sciatic nerve transection
Authors: De León M. , Nahin R. L. , Molina C. A. , De Léon D. D. , Ruda M. A. 
Published: January 2005

AbstractThe present study was designed to compare the expression of the Jun family of protooncogenes following nerve injury. Adult rats were anesthetized and the sciatic nerve transected. Dorsal root ganglia (DRG) at 1, 2, 3, and 7 days after nerve transection were collected, their total RNA extracted, and Northern blots performed using 32P‐labeled oligonucleotide probes. The constitutive expression of c‐jun mRNA was very low in DRG. Induction of c jun mRNA was observed by day 1 after nerve transection, with a sixfold peak at 3 stays and a twofold induction still present by day 7. The constitutive expression of junB mRNA was also low in the DRG, and sciatic nerve transection produced only a modest induction (1.7fold by day 3) in the DRG ipsilateral to the nerve cut. junD mRNA was constitutively expressed at high levels in the DRG, and its level of expression did not change after sciatic nerve transection. Immunocytochemistry studies demonstrated a pattern of c‐Jun, JunB, and JunD immunoreactivity (IR) associated with the cell nuclei of DRG neurons. c‐Jun IR was found at very low levels in the undamaged contralateral DRG neurons, but sciatic nerve transection dramatically increased the number of c‐Jun‐immunoreactive neurons. Dot blot immunoblotting assay confirmed that the DRG ipsilateral to the sciatic nerve cut contained a higher level of c‐Jun protein than the contralateral control DRG. Similar to c‐Jun IR, JunB IR was minimal in the undamaged contralateral DRAG. However, the DRG ipsilateral to the nerve transection did not show an increase in the number of immunoreactive neurons. JunD protein was expressed at high levels in the contralateral DRG, and this level of expression persisted after sciatic nerve transection in the ipsilateral DRG. DNA gel retardation assay experiments with an AP‐1 consensus sequence showed a single DNA‐protein complex. This complex was increased in ipsilateral as compared with contralateral DRG extracts. The amount of DNA protein complex was reduced byc‐Jun protein antiserum but was not altered when treated with a Fos antibody. We conclude that cjun, junB and junD mRNAs and proteins are differentially regulated in the DRG after sciatic nerve transection. © 1995 Wiley‐Liss, Inc.
Localization of mRNAs for adrenoleukodystrophy and the 70 kDa peroxisomal (PMP70) proteins in the rat brain during post‐natal development
Authors: Pollard H. , Moreau J. , Aubourg P. 
Published: January 2005

AbstractAdrenoleukodystrophy (ALD) is a genetic demyelinating disorder caused by the mutation of a gene encoding a 75‐kDa peroxisomal protein (ALDP) that belongs to the superfamily of ATP binding casette (ABC) transporters. The PMP 70 gene codes for another peroxisomal ABC transporter that shows 38.5% amino acid identity with ALDP. ALDP and PMP70 have the structure of huff transporter and Could possibly heterodimerize to form a full transporter within the peroxisomal membrane. Using in situ hybridization histochemistry in rat brain, we demonstrate that ALD and PMP70 mRNAs have different spatial and temporal expression during postnatal development. Whereas expression of PMP 70 mRNA was low at birth and culminates between the 2nd and 3rd week in hippocampus and cerebellum, maximum expression of ALDP was found at birth in all brain areas and decreased thereafter. The absence of coordinated expression of ALD and PMP70 genes suggests therefore that ALD and PMP70 proteins are unlikely to function as exclusive and obligatory partners in the brain. © 1995 Wiley‐Liss, Inc.
Regional and temporal profiles of c‐fos and nerve growth factor mRNA expression in rat brain after lateral cortical impact injury
Authors: Yang K. , Mu X. S. , Xue J. J. , Perez‐Polo J. R. , Hayes R. L. 
Published: January 2005

AbstractLesion‐induced increases in NGF mRNA are thought to be mediated by c fos gene expression. Conversely, NGF induction of c‐fos expression has been reported following administration of exogenous NGF. However, the relationship between c‐fos and NGF gene expression after traumatic injury to the intact brain is not known. Thus, we applied in situ hybridization and semiquantitative reverse transcription‐polymerase chain reaction (RT‐PCR) methods to determine temporal profiles of c‐fos and NGF mRNA expression in rat brains after controlled impact to the exposed cortex. Using alternate sections from the same rat brains, in situ hybridization studies showed that in neocortex, c‐fos mRNA transiently increased at 30 min, 1 hr, and 3 hr after injury, while there were no increases of NGF mRNA at these postinjury time points. In the hippocampus, in situ hybridization showed that c‐fos mRNA increased at 30 min, 1 hr and 3 hr postinjury, while NGF mRNA increased at 1 hr, 3 hr but not at 30 min after injury. RT‐PCR studies in hippocampus confirmed that c‐fos mRNA increased as early as 5 min after injury, peaked at 30 min postinjury, and remained elevated 5 hr postinjury. Levels of hippocampal NGF mRNA expression increased by 1 hr after injury and plateaued until 3 and 5 hr postinjury. These data are consistent with the possible regulatory role of endogenous c‐fos on NGF expression following traumatic brain injury. © 1995 Wiley‐Liss, Inc.
Identifying agonistic and antagonistic mechanisms operative at the GABA receptor
Authors: Galvez‐Ruano E. , Aprison M. H. , Robertson D. H. , Lipkowitz K. B. 
Published: January 2005

AbstractBased on our molecular modeling investigations of the glycinergic receptor, we expanded our studies to similarly investigate the GABAergic receptor. New data suggest there may exist a slightly different agonistic mechanism for the molecules described herein as compared to glycine. The origin of this is undoubtedly the fact that, while glycine has a positive and two negative binding sites, it is significantly shorter than GABA and the other GABA agonists. Clearly, discovery of more glycine agonists is needed to further clarify this point. Moreover, we find a remarkedly different antagonistic mechanism exists for this phylogenetically newer inhibitory system in the central ncrvous system (CNS) than recently reported for strychnine and eight weaker glycine antagonists. We used GABA and six agonists (muscimol, dihydromuscimol, TRIP, isoguvacine, trans‐3‐aminocyclopentane‐1‐carboxylic acid, piperidine‐4‐sulfonic acid) and five antagonists (bicuculline‐Nl5‐rnethobromide, R5135, pitrazepin, iso‐THAZ and securinine) to derive our conclusions. We found that each of the agonists have three clearly defined atoms that can serve as attachment points at the GABAA receptor site. One of the three attachment atoms includes a carbonyl or carboxylate oxygen. The role of the carbonyl or carboxylate atom is very important. First, we theorize that a rapid two‐point attachment occurs (one from the positive end and one from one of the other two negative atoms on the ligand) at the recognition site in the receptor where GABA or a GABAergic agonistt binds. The positive end of the agonist perhaps associates through hydrogen bonding to a β‐carboxyl group in one of the aspartate molecules in the poly. peptide. The negative attachment points perhaps bind through hydrogen bonding to arginine molecules in this polypeptide. The second negative site in the agonist immediately triggers a conformational change by pulling together the aforementioned groups by electrostatic attraction, and hence opening the chloride channel. We propose the carbonyl oxygen is partly responsible for triggering the opening by formation of a double hydrogen bond to arginine. We postulate that this attraction is the first step inducing the conformational change. In the case of the GABA antagonists investigated, a fourth attachment site was not found. In fact only two sites have been identified similar to the group II glycine antagonists. Our data support a hypothesis for GABAergic antagonist activity which suggests that the antagonist simply binds to the recognition site and blocks the neurotransmitter, GABA, from entering this site thereby preventing the opening of the chloride channel; it just stays closed. This mechanism is different from the mechanism proposed for the large number of Group I glycine antagonists (Aprison et al.: J Neurosci Res 41:259‐269, 1995). © 1995 Wiley‐Liss, Inc.
Efficient and sustained transgene expression in mature rat oligodendrocytes in primary culture
Authors: Guo Z. , Yang N.‐S. , Jiao S. , Sun J. , Cheng L. , Wolff J. A. , Duncan I. D. 
Published: January 2005

AbstractIn order to evaluate the characteristics and efficiency of gene transfer in primary cultures of oligodendrocytes, four different techniques including particle bombardment (Accell® gene gun), cationic liposomemediated transfection (lipofection), calcium phosphate co‐precipitation and retroviral infection were compared using the LacZ and luciferase reporter genes. Highly purified postnatal adult rat oligodendrocytes were obtained by sequential immunopanning, plated in culture, and transfected using various reporter and promoter genes. The most efficient expression of LacZ and luciferase genes was found with particle mediated gene delivery. The transgene expression level obtained with gene gun delivery was at least two‐ to 100‐fold greater than three other tested gene transfer methods. Comparison of the relative strength of four viral and two cellular promoters in these primary oligodendrocytes cultures demonstrated that the CMV promoter was the strongest. Using a human growth hormone (hGH) reporter gene, a long‐term transgene expression pattern in primary oligodendrocytes was demonstrated to be sustained in culture for the entire experimental period (4 weeks) after particle‐mediated gene transfer. These results demonstrate that expression of a foreign gene can be effectively achieved ins primary cultures of adult oligodendrocytes, especially by using the particle bombardment method. The results also suggest that the current ex vivo gene transfer system may be used to manipulate oligodendrocytes for future application in gene therapy studies. © 1996 Wiley‐Liss, Inc.
Individual manifestations of Parkinson's disease after ten or more years of levodopa
Authors: Klawans Harold L. 
Published: January 2005

AbstractTwenty‐five consecutive patients with Parkinson's disease, who had been on levodopa for 10 or more years, were studied. Over the 12.9 years of treatment, the average Northwestern Disability Score had increased from 9.6 to 18.9. By this measure, 24 of 25 patients were worse, and one was unchanged. The progression of disability did not involve all pretreatment parkinsonian features equally in any of the patients studied. Instead a distinctive pattern of deterioration was seen: postural reflexes worsened in 24/25, speech in 24/25, and gait in 22/25. In contrast, rigidity was improved or unchanged in 17/25, tremor was improved or unchanged in 17/17, while handwriting was improved or unchanged in 21/22. Finger dexterity which was improved in 5/25, unchanged in 15/25, and worse in 5/25 which seemed to be between these two extremes. These observations demonstrate that some signs of parkinsonism can remain quite responsive to levodopa for more than 10 years while at the same time other manifestations of the disease are no longer as responsive to this form of treatment.
Clonidine in the treatment of essential tremor
Authors: Koller William , Herbster Gregory , Cone Sandra 
Published: January 2005

AbstractThe effect of clonidine treatment (average dose 0.4 mg/day) was investigated in 10 patients with essential tremor in a double‐blind placebo‐controlled design. Tremor amplitude and frequency were recorded with an accelerometer. Tremor was not significantly altered by clonidine therapy. Side effects were common. It is concluded that clonidine is not effective treatment for essential tremor.