ISSN:0360-4012    

DOI:10.1002/jnr.490170202

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractSynthesis of the mouse myelin basic proteins (MBPs) was studied in reticulocyte lysates programmed with brain mRNA in the presence or absence of brain factors. Addition of brain factors to the lysates increased the incorporation of [35S] methionine into total TCA‐precipitable protein by a factor of 6–9, and the majority of this stimulation was found to be due to initiation factors. Although brain factors increased total protein synthesis, the percentage of MBP synthesis was reduced from 4.3% of the total counts incorporated (in the absence of brain factors) to 1.4% (in their presence). Increasing the concentration of brain mRNA in the lysates also reduced the relative levels of MBP synthesis. These results suggested the MBP mRNAs, as a group, were less efficiently initiated than most brain mRNAs. An analysis of the nucleotide sequence flanking the initiator codon of the MBP mRNAs indicates the presence of a second AUG codon 5 bases upstream, immediately followed by a termination codon, which may provide a structural explanation for the poorer initiation efficiency of the MBP mRNAs. Further analysis of the synthesis of the individual MBPs in the presence or absence of inhibitors of initiation (7‐methylguanosine triphosphate and aurintricarboxylic acid) and elongation (anisomycin and emetine) indicated that the 14‐kD MBP mRNA was less efficiently translated than the other MBP mRNAs. Synthesis of the 14‐kD MBP was more strongly inhibited by the initiation inhibitors than the other MBP mRNAs, and synthesis of the 14‐kD MBP was increased relative to the other MBPs in the presence of elongation inhibitors. These results are consistent with the notion that the 14‐kD MBP mRNA is initiated less efficiently than the ot

ISSN:0360-4012    

DOI:10.1002/jnr.490170203

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractRecent evidence has demonstrated the presence of nerve growth factor (NGF) in areas of the central nervous system characterized by cholinergic innervation. We report that a unique population of rat basal forebrain magnocellular neurons that project to the cortex and hippocampus are immunoreactive to a monoclonal antibody to the NGF receptor. Removal of target contact results in a time‐dependent loss or shrinkage of cells in the basal forebrain that stain for NGF receptor and acetylcholinesterase, suggesting that under normal conditions, basal forebrain cholinergic neurons utilize NGF for trophic suppor

ISSN:0360-4012    

DOI:10.1002/jnr.490170204

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractPolycation‐binding neurite‐promoting factor (PNPF) from skeletal muscle of bovine fetuses has been compared to mouse tumor laminin by an immunological approach. Antiserum prepared against PNPF blocked the neurite‐promoting activity in a dose‐dependent manner. The anti‐PNPF antiserum bound to Mr = 200,000‐;195,000 bands as well as several components of higher molecular weight, as detected in immunoblots of reduced PNPF. The anti‐PNPF antiserum did not inhibit the neurite‐promoting activity of mouse laminin, although it did bind to native laminin. Antilaminin antiserum bound to PNFP and identified the same Mr = 200,000−195,000 bands and two other higher‐molecular‐weight bands, as did the anti‐PNPF antiserum. The activity of PNPF was confirmed to be sensitive to treatment with heparitinase. It is concluded that PNPF from bovine fetal muscle contains a complex of heparan sulfate and high‐molecular‐weight components, particularly of Mr = 200,000‐195,000, which share antigenic determinants with mouse laminin. However antilaminin antiserum fails to inhibit the activity of PNPF, suggesting that the active site, and/or adjacent regions, of PNPF are antigenically different from the neurite‐promoting site

ISSN:0360-4012    

DOI:10.1002/jnr.490170205

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractConsiderable evidence is mounting to support the concept of a modulatory role for the brain and neuroendocrine system on the immune response. This neuroimmunomodulation occurs in part through the interaction of specific neurosubstances with receptors on lymphocytes and monocytes. Nerve growth factor (NGF) is a neuronotrophic factor necessary for the development and maintenance of sympathetic and embryonic sensory neurons. This trophic effect is initiated through binding of NGF at specific cell surface receptor sites on NGF‐responsive cells. Several recent studies suggest that NGF may interact with cells of the immune system and may play a role in the regulation of some immunologic reactions. In this study we report on the presence of specific receptors for NGF on the surface of mononuclear cells from rat spleens. The NGF‐binding sites are of the low‐affinity type with Kd's in the 10−9M range. These receptors migrate on SDS‐PAGE as two molecular species of approximately 190 and 125 kilodaltons. Our findings of receptors for NGF on lymphocytes and accessory cells support other evidence that NGF may influence immunoreactivit

ISSN:0360-4012    

DOI:10.1002/jnr.490170206

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractIncubation of C6‐BU1glioma cells in the presence of isoproterenol and Ro20‐1724—a potent cAMP phosphodiesterase inhibitor—results in a transient increase in intracellular cAMP levels, followed by a rapid efflux of cyclic AMP from the cells into the media. Two distinct types of morphological changes could be seen: (1) rounded cell bodies with multipolar processes and beadings after 30 minutes of incubation—this period coincides with a 70–80‐fold increase in intracellular cAMP levels, and (2) elongated cell bodies with extended bipolar processes after 24–48 hours. By this time the intracellular cAMP concentration drpped to a low level, which was only three‐ to four fold higher than that in control. The transient increase in intracellular cAMP concentration results in retardation of cell growth, diminished uptake of3H‐2‐deoxyglucose, and abolition of enhanced synthesis of cyclic

ISSN:0360-4012    

DOI:10.1002/jnr.490170207

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractDopamine (DA) terminals in rat corpus stratum and frontal cortex possess muscarinic receptors that mediate enhancement of the depolarization‐evoked release of the catecholamine. The effects of the membrane‐permeating cyclic guanosine monophosphate (cyclic GMP) analog 8‐Br‐cyclic GMP and of the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX) on the muscarinic‐induced increase of DA release were investigated in striatal synaptosomes prelabeled with [3H]DA and exposed in superfusion to 15 mM KCl and to acetylcholine (ACh). Preincubation of synaptosomes with 8‐Br‐cyclic GMP (10‐200 μM) or with IBMX (200 μM) prevented the ACh‐induced enhancement of [3H]DA release, without affecting the K+‐evoked release of the [3H]amine. No significant decrease of the ACh effect was observed when 8‐Brcyclic GMP or IBMX were added concomitantly with ACh to the superfusion medium. The data suggest that stimulation of presynaptic muscarinic receptors on DA terminals may produce enhancement of3HDA release through a decrease of the intraterm

ISSN:0360-4012    

DOI:10.1002/jnr.490170208

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractThe intracellular distribution of acetylcholinesterase (AChE) was determined in adult rat anterior gracilis muscles. Echothiophate iodide (ECHO), a water‐soluble cholinesterase inhibitor, was applied to muscles in situ to eliminate extracellular and/or extracellularly oriented enzyme. Control and ECHO‐treated muscles were either cut into 1‐mm segments and assayed for AChE activity or cytochemically stained for AChE. Subsequent analysis by light and electron microscopy showed that the AChE stain inside myofibers was highly localized and clearly visible only in the zone immediately underlying the point of nerve‐muscle contact. Biochemical assay of muscle segments showed intracellular AChE to be most highly concentrated in regions containing large numbers of endplates (approximately twice the activity of endplate‐free areas). Since such “endplate‐rich” segments are in fact mostly extra‐synaptic tissue, we conclude that intracellular AChE of adult rat gracilis myofibers, although present along the length of the cell, is more than two times as concentrated in sub‐synaptic areas as compared to extra‐synaptic areas. This result must be carefully considered when attempting to identify “endplate‐specific” AChE activity of mammalian muscle, and further points to the importance of neural influences on

ISSN:0360-4012    

DOI:10.1002/jnr.490170209

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractThe question whether the benzodiazepine receptor site in astrocytes or in neurons might be identical to the adenosine uptake site was studied by determining pharmacological profiles, inhibition types, and the effects of benzodiazepine antagonsts in primary cultures of either astrocytes or neurons. Fourteen different benzodiazepines and five different adenosine uptake inhibitors displaced [3H] diazepam and inhibited adenosine uptake in both astrocytes and neurons. However, the rank orders (determined as IC50values) with which these two parameters were affected were profoundly different, indicating dissimilarities between these two sites. For several of the compounds a difference in inhibition type (competitive vs. noncompetitive) was observed between the benzodiazepine‐binding site and the adenosine uptake site in astrocytes and/or neurons, which further corroborated the conclusion of a difference between the benzodiazepine‐binding site and the adenosine uptake site. Finally, the neuronal benzodiazepine antagonists RO 15‐1788 and CGS‐8216 and the astrocytic benzodiazepine antagonist PK 11195, which reverse the action of benzodiazepines, were not able to reverse inhibition of adenosine uptake by diazepam but exerted an inhibitory effect of th

ISSN:0360-4012    

DOI:10.1002/jnr.490170210

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY

摘要:

AbstractThe levels of brain acidic phospholipids (poly‐PI, PI, PA, and PS), DG, and FFA and their acyl group profiles were determined after induction of ischemia in gerbils by ligation of the common carotid arteries and decapitation. Ischemia induced by both procedures resulted in a significant decrease in poly‐PI (20% for 1‐min decapitation and 1‐min ligation). Except for a 16% increase in PI in the 5‐min decapitation group, no apparent change was found in other phospholipids after either ischemic condition. The level of DG was increased one‐ and threefold after 1 and 5 min, respectively, of decapitative ischemic treatment. Ligation of the carotid arteries for 1 min resulted also in a onefold increase in the DG level. The decapitative model resulted in a one‐ and fivefold increase in FFA level (with respect to 1 and 5 min, respectively), whereas ligation for 1 min resulted in an increase of 42% of the FFA. The acyl groups of poly‐PI and PI in the control gerbil brain are enriched in 18:0 and 20:4, but those of DG, FFA, and PA have a higher proportion of 16:0 besides 18:0 and 20:4. However, a preferential increase in the proportion of 18:0 and 20:4 was shown for the DG and FFA in both types of ischemic treatments. It is concluded from the results that both models of ischemic treatment elicit a similar decrease in poly‐PI and increase in DG, but differ in the amount of FFA release. The higher level of FFA release in the decapitative model suggests that other biochemical mechanisms may be activated to cause the a

ISSN:0360-4012    

DOI:10.1002/jnr.490170211

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1987

数据来源: WILEY