Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Histaminergic H2 Action Protects Hippocampal CA1 Neurons by Prolonging the Onset of the Anoxic Depolarization in Gerbils (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 67 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The central histaminergic action on ischemia-induced neuronal damage was examined by evaluating the histological outcome and the direct current (DC) potential shift in the hippocampal CA1 region in gerbils. An intracerebroventricular administration of histamine (10–100 nmol) improved the delayed ischemic damage in hippocampal CA1 pyramidal cells produced by 3 min of transient forebrain ischemia. A high dose (75 nmol) of mepyramine, an H1 antagonist, aggravated ischemia-induced neuronal damage, but not a low dose (0.75 nmol). Administration of cimetidine (4 nmol) and ranitidine (3 nmol), H2 antagonists, aggravated the neuronal damage. An injection of histamine (100 nmol) prolonged the onset time of the ischemia-induced sudden shift in the extracellular DC potential (anoxic depolarization; AD) to 133% of that in control animals. Administration of mepyramine (75 nmol) did not markedly change the AD, whereas injections of cimetidine (40 nmol) and ranitidine (3 nmol) reduced the onset latency to 47 and 45%, respectively. These findings suggest that the central H2 action serves to protect neurons by delaying the onset of AD in gerbils.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.67062613.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Transient Increase of Cyclic AMP Induced by Glutamate in Cultured Neurons from Rat Spinal Cord (1995)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 65 (1995), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: We demonstrated that glutamate increased the cyclic AMP level in cultured neurons from rat spinal cord. A bath application of glutamate (300 µM) elicited a rapid increase of the cyclic AMP concentration reaching a level three times as high as the basal level in ∼3 min, and its content then decreased to the control level in 15 min. The increase was not observed in a Ca2+-free medium and was inhibited by an antagonist of NMDA receptors or a voltage-sensitive Ca2+ channel blocker. Preincubation with W7 also inhibited the glutamate-evoked cyclic AMP increase. NMDA, aspartate, and high-K+ conditions also induced a cyclic AMP increase; however, a decreasing phase did not follow. The decreasing phase was observed when (2S,1′S,2′S)-2-(carboxycyclopropyl)-glycine, a potent agonist for metabotropic glutamate receptors, was combined with NMDA. These results suggest that the cyclic AMP increase is mediated by a Ca2+ influx via both NMDA receptors and voltage-sensitive Ca2+ channels followed by an activation of the Ca2+/calmodulin system, and the decreasing phase observed in the case of glutamate exposure is due to the activation of the metabotropic glutamate receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1995.65041816.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    CNS-specific prostacyclin ligands as neuronal survival-promoting factors in the brain (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Prostacyclin (PGI2) is a critical regulator of the cardiovascular system, via dilatation of vascular smooth muscle and inhibition of platelet aggregation (Moncada, S. 1982, Br. J. Pharmacol., 76, 3). Our previous studies demonstrated that a novel subtype of PGI2 receptor, which is clearly distinct from a peripheral subtype in terms of ligand specificity, is expressed in the rostral region of the brain, e.g. cerebral cortex, hippocampus, thalamus and striatum, and that (15r)-16-m-17,18,19,20-tetranorisocarbacyclin (15r-TIC) and 15-deoxy-16-m-17,18,19,20-tetranorisocarbacyclin (15-deoxy-TIC) specifically bind to the central nervous system (CNS)-specific PGI2 receptor. Here, we report that these CNS-specific PGI2 receptor ligands, including PGI2 itself, prevented the neuronal death. They prevented apoptotic cell death of hippocampal neurons induced by high (50%) oxygen atmosphere, xanthine + xanthine oxidase, and serum deprivation. IC50s for neuronal death were ∼ 30 and 300 nm for 15-deoxy-TIC and 15r-TIC, respectively, which well correlated with the binding potency for the CNS-specific PGI2 receptor. 6-Keto-PGF1α (a stable metabolite of PGI2), peripheral nervous system-specific PGI2 ligands and other prostaglandins (PGs) than PGI2 did not show such neuroprotective effects. In vivo, 15r-TIC protected CA1 pyramidal neurons against ischaemic damage in gerbils. These results indicate that CNS-specific PGI2 ligands have neuronal survival-promoting activity both in vitro and in vivo, and may represent a new type of therapeutic drug for neurodegeneration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00791.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    IBUDILAST REDUCES INTRACELLULAR CALCIUM ELEVATION INDUCED BY IN VITRO ISCHAEMIA IN GERBIL HIPPOCAMPAL SLICES (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. A microfluorometry was carried out to investigate the effect of 3-isobutyryl-2-isopropylpyrazolo[1,5-a]pyridine (ibudilast) on changes in levels of intracellular calcium concentration ([Ca2+]i) induced by in vitro ischaemia in the CA1 field of gerbil hippocampal slices.2. When slices, loaded with a calcium ion sensitive dye (rhod-2) were exposed to a glucose-free physiological medium equilibrated with a 95% N2/5% CO2 gas mixture (standard in vitro ischaemia), a large [Ca2+]i elevation was detected approximately 5 min after the beginning of in vitro ischaemia.3. When slices were perfused with the in vitro ischaemic medium containing 43 μmol/L ibudilast, a [Ca2+]i elevation was still observed; however, the extent of the increase in [Ca2+]i was significantly depressed in all subregions of the hippocampal slices.4. The extent of this inhibitory effect of ibudilast on the in vitro ischaemia-induced [Ca2+]i elevation was in a similar range as those of Ca2+ blockers, including (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cycloheptan-5,10-imine maleate (MK-801), flunarizine and dantrolene.5. Similar [Ca2+]i increases in the CA1 field were induced by a Ca2+-free in vitro ischaemia, a high concentration of KCl or by specific agonists for glutamate receptor subtypes (N-methyl-d-aspartate (NMDA), (s)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and kainate); these increases were also depressed with 43 μmol/L ibudilast present in the perfusion medium.6. These results indicate that ibudilast may act by depressing the Ca2+ accumulation during and shortly after ischaemia, a possible pharmacological action of ibudilast that leads to the amelioration of ischaemic injury in the central nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb02830.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    IBUDILAST PROTECTS AGAINST NEURONAL DAMAGE INDUCED BY GLUTAMATE IN CULTURED HIPPOCAMPAL NEURONS (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 23 (1996), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effect of ibudilast, a drug that has been clinically used for asthma and the improvement of cerebrovascular disorders, was examined on glutamate neurotoxicity in cultured neurons from rat hippocampus.2. The extent of neuronal damage induced by exposure of the neurons to glutamate for 5 min was estimated by the activity of lactate dehydrogenase (LDH) released from degenerated neurons into the medium during a 24 h postexposure period. When ibudilast was added into all pre-incubation, exposure and postexposure media, the extent of neuronal damage decreased to approximately half that of control at an ibudilast concentration of 43 μmol/L.3. The neuroprotective effects of ibudilast were dose-dependent. Sufficient protection was detected even when ibudilast was added only into the postexposure medium.4. The extent of 45Ca2+ influx during glutamate exposure was slightly reduced by the addition of ibudilast. Intracellular cAMP, as measured by radioimmunoassay, was increased by neuronal exposure to glutamate and then decreased after the removal of glutamate; however in the presence of ibudilast, AMP was maintained at the high level.5. These results suggest that protection against glutamate neurotoxicity by ibudilast is not only attributable to the inhibition of phenomena that occur during glutamate exposure, such as Ca2+ influx, but also to some beneficial metabolic changes that are induced by a sustained high level of intracellular cAMP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1996.tb02772.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    The role of remaining presynaptic terminals in the hippocampal CA1 after selective neuronal death: ischemia-induced glutamate efflux (1995)
    Springer
    Acta neuropathologica 91 (1995), S. 41-46 
    Details
    ISSN: 1432-0533
    Keywords: Key words Glutamate ; Ischemia ; Microdialysis ; Hippocampus ; Cell death
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Following selective neuronal death, numerous presynaptic terminals maintain their structural integrity in the brain region. The role that these remaining presynaptic terminals play in the brain region showing selective neuronal death is not known. In the present study, we investigated the possibility that brief transient ischemia induces an excessive release of glutamate from the remaining presynaptic terminals, which then spreads by diffusion. The glutamate could act as an excitotoxin and be a pathogenic factor in the local injured brain region. Transient ischemia of 3.5 min duration was used in the gerbil as a pretreatment to obtain hippocampal CA1 in which most of postsynaptic neurons were eliminated but numerous presynaptic terminals remained normal. At 10–14 days after the pretreatment, brain microdialysis experiments were performed in vivo in the CA1 to measure the levels of extracellular glutamate induced by 5 min ischemia. Prior to 5 min ischemia the basal concentration of glutamate in the CA1 was the same as that observed in gerbils that had been subjected to sham pretreatment. During 5 min ischemia, no significant increase in glutamate was induced in the CA1 which showed selective neuronal death. However, a massive increase in glutamate was induced in the CA1 of the sham-pretreated gerbils. These results suggest that the remaining presynaptic terminals are unlikely to play a pathogenic role in the CA1 after selective neuronal death has occurred.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050390
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    In vitro ischemia-induced intracellular Ca2+ elevation in cerebellar slices: a comparative study with the values found in hippocampal slices (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 2-7 
    Details
    ISSN: 1432-0533
    Keywords: Calcium ; Ischemia ; Cerebellum ; Purkinje cell ; Microfluorometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Changes in levels of intracellular calcium ion ([Ca2+]i) induced by in vitro ischemic conditions in gerbil cerebellar and hippocampal slices were investigated using a calcium imaging system and electron microscopy. When the cerebellar slice was perfused with a glucose-free physiological medium equilibrated with a 95% N2/5% CO2 gas mixture (in vitro ischemic medium), a large [Ca2+]i elevation was region-specifically induced in the molecular laver of the cerebellar cortex (a dendritic field of Purkinje cells). When the hippocampal slice was perfused with in vitro ischemic medium, a large [Ca2+]i elevation was region-specifically induced in CA1 field of the hippocampal slices. Electron microscopic examinations showed that the large [Ca2+]i elevations occurred in Purkinje cells and CA1 pyramidal neurons. To isolate Ca2+ release from intracellular Ca2+ store sites, the slices were perfused with Ca2+-free in vitro ischemic medium. the increases in [Ca2+]i in both cerebellar and hippocampal slices were significantly lower than those observed in the slices perfused with the Ca2+-containing in vitro ischemic medium. However, the suppression of the [Ca2+]i-elevation in the molecular layer of the cerebellar slices was smaller than that in the CA1 field of the hippocampal slices. These results reinforce the hypothesis that calcium plays a pivotal role in the development of ischemia-induced neuronal death, and suggest that Ca2+ release from intracellular Ca2+ store sites may play an important role in the ischemia-induced [Ca2+]i elevation in Purkinje cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294252
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    A possible mechanism for the hypoxia-hypoglycemia-induced release of excitatory amino acids from cultured hippocampal astrocytes (1995)
    Springer
    Neurochemical research 20 (1995), S. 737-743 
    Details
    ISSN: 1573-6903
    Keywords: Aspartate ; glutamate ; ischemic brain injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to elucidate the mechanism of release of excitatory amino acid (EAA) induced by hypoxiahypoglycemia (in vitro ischemia) from cultured hippocampal astrocytes, we compared the EAA release by in vitro ischemia with those by other treatments. The EAA release induced by in vitro ischemia treatment was rapid and reversible. The amount of released aspartate was comparable to that of glutamate, although the endogenous content of aspartate was one sixth that of glutamate. High-K (100 mM) treatment and the addition of 5 mM NaCN induced a rapid EAA release and the glutamate release was much greater than aspartate. Addition of 5 mM iodoacetate, a glycolysis inhibitor, induced a slow EAA release, and the amount of released aspartate was much higher than that of glutamate. On the other hand, the in vitro ischemia treatment and the addition of 5 mM NaCN induced only 20% reduction in ATP content for initial 5 min, whereas the addition of 5 mM iodiacetate induced a marked reduction. Our data suggest that ischemia-induced EAA release from astrocytes is a complex process in which local energy failure, inhibition of glycolysis, and depolarization of the cell membrane are involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01705543
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...