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  • 1
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: We examined endothelin (ET) receptors in the hippocampus CA1 subfields of stroke-prone spontaneously hypertensive rats subjected to a 10-min bilateral carotid occlusion and reperfusion. When delayed neuronal death had occurred in the pyramidal cell layer at 7 days after transient forebrain ischemia, the quantitative receptor autoradiographic method we used revealed a dramatic increase in number of 125I-ET-1 binding sites in the hippocampus CA1 subfields. The highest number of de novo binding sites appeared in the area corresponding anatomically to the pyramidal cell layer with neuronal death. These binding sites were characteristically the ETB receptor. The de novo 125I-ET-1 binding was mainly present on microglia aggregating with a high density in the damaged pyramidal cell layer. As ET-1- and ET-3-like immunoreactivities were highly expressed within astrocytes in damaged neural tissue, the possibility that microglia with the ETB receptor are activated to participate in the pathophysiology of ischemia-related neural tissue damage by astrocytic ET-1 and ET-3 produced in response to transient forebrain ischemia would have to be considered.
    Materialart: Digitale Medien
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  • 2
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: The present study was designed to evaluate the role of γ-aminobutyric acid (GABA) in the secretory function of cultured chromaffin cells using the method of realtime monitoring. GABA evoked the secretion of catecholamines (CA) from adrenal chromaffin cells in a dose-dependent manner. Bicuculline 10-−5M inhibited the stimulatory action of GABA. Diazepam 5 × 10-−6 and 2.5 × 10-−5M facilitated the secretory response evoked by 7 × 10-−5M GABA by 22% and 96%, respectively, which was antagonized by Ro 15–1788. This finding suggests that GABA-benzodiazepine receptor coupling can function in the secretion of CA from the adrenal chromaffin cells in a manner similar to that observed in the brain. GABA-evoked release of CA was reduced by 1 μM nifedipine to 16% of control, suggesting the involvement of voltage-sensitive Ca2+ channels in the mechanisms of the CA-releasing action of GABA in these cells. From these findings, the involvement of GABAergic mechanisms in the regulation of adrenal medullary function can be proposed.
    Materialart: Digitale Medien
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  • 3
    ISSN: 1471-4159
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: Abstract: Modulation of the γ-aminobutyric acidB (GABAB) receptor-mediated response by protein kinase C (PKC) was examined with regard to inhibition by stimulation of the GABAB receptor of stimulation-evoked release of noradrenaline (NA) from slices of cerebellar cortex and of acetylcholine (ACh) from strips of ileum. 12-O-Tetradecanoylphorbol 13-acetate (TPA) potentiated the high K+-evoked Ca2+-dependent release of NA and ACh, but not the ouabain-evoked release, even in the presence of external Ca2+. The potentiating effect was antagonized by sphingosine, thereby suggesting that PKC participates in the exocytotic-vesicular release of neurotransmitters, but does not do so in case of a nonvesicular release. GABA inhibited the high K+-evoked release of NA and ACh, but not the ouabain-evoked Ca2+-independent release. The effect of GABA was mimicked by baclofen and was antagonized by phaclofen, thereby suggesting that stimulation of the GABAB receptor inhibits the vesicular but not the nonvesicular release of neurotransmitters. TPA suppressed the GABAB receptor-mediated inhibition of high K+-evoked release of NA and ACh. The effect of TPA was antagonized by sphingosine. These results indicate that stimulation of the GABAB receptor inhibits the stimulation-evoked Ca2+-dependent release of neurotransmitters and that activation of PKC suppresses the GABAB receptor-mediated response.
    Materialart: Digitale Medien
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  • 4
    ISSN: 1440-1681
    Quelle: Blackwell Publishing Journal Backfiles 1879-2005
    Thema: Medizin
    Notizen: 1. When delayed neuronal death occurred in the hippocampus CA1 pyramidal cell layer of stroke-prone spontaneously hypertensive rats (SHRSP) at 4 and 7 days after a 10 min bilateral carotid occlusion and reperfusion, intense endothelin-1 (ET-1)- and ET-3-like immunoreactivities became evident in astrocytes in the damaged hippocampus CA1 subfields.2. We also observed that microglia equipped with an ETb receptor aggregated within the CA1 pyramidal cell layer with neuronal death.3. There was a dramatic increase in nitric oxide synthase (NOS) activity in astrocytes and microglia in the damaged hippocampus CA1 subfields.4. Thus, the possibility that microglia with the ETb receptor are activated to produce NO, a neurotoxic factor, by astrocytic ET-1 and ET-3 produced in response to transient forebrain ischaemia would have to be considered.
    Materialart: Digitale Medien
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  • 5
    Digitale Medien
    Digitale Medien
    Springer
    Psychopharmacology 68 (1980), S. 7-13 
    ISSN: 1432-2072
    Schlagwort(e): Δ 9 ; Muricide ; Antidepressants ; Psychotropic drugs
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract The effects of psychotropic drugs on THC-induced long-lasting muricide were investigated in rats. Changes in open field activity (ambulation and rearing) of the rat werre concurrently assessed as an index of behavioral toxicity. Imipramine-like antidepressants, atropine, and antiparkinsonism drugs exhibited a selective inhibitory activity on muricide, whereas the effects of neuroleptics, pentobarbital, diazepam, and methamphetamine were nonspecific. It is also suggested that cholinergic, catecholaminergic, and serotonergic mechanisms are involved in THC-induced muricide. This type of induced muricide appears to be a useful experimental model particularly suitable for the evaluation of antidepressants in correlation with brain amine dynamics.
    Materialart: Digitale Medien
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  • 6
    ISSN: 1476-4687
    Quelle: Nature Archives 1869 - 2009
    Thema: Biologie , Chemie und Pharmazie , Medizin , Allgemeine Naturwissenschaft , Physik
    Notizen: [Auszug] We monitored the biological effect of homozygous disruption of the PrP gene in mice by observing 39 homozygous (PrP'1'), 90 heterozygous (PrP+l) and 46 wild-type (PrP+/+) mice over a long period. The PrPl mice grew normally and showed no behavioural abnormality for at least one ...
    Materialart: Digitale Medien
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  • 7
    Digitale Medien
    Digitale Medien
    Springer
    Cellular and molecular neurobiology 10 (1990), S. 539-552 
    ISSN: 1573-6830
    Schlagwort(e): neuropeptide Y (NPY) ; peptide YY (PYY) ; NPY receptor ; PYY receptor ; quantitative receptor autoradiography ; rat brain
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie
    Notizen: Summary 1. Specific binding sites for neuropeptide Y (NPY) and peptide YY (PYY) were investigated in rat brain areas using quantitative receptor autoradiography with125I-Bolton-Hunter NPY (125I-BH-NPY) and125I-PYY, radioligands for PP-fold family peptides receptors. 2. There were no differences between localization of125I-BH-NPY and125I-PYY binding sites in the rat brain. High densities of the binding sites were present in the anterior olfactory nucleus, lateral septal nucleus, stratum radiatum of the hippocampus, posteromedial cortical amygdaloid nucleus, and area postrema. 3. In cold ligand-saturation experiments done in the presence of increasing concentrations of unlabeled NPY and PYY,125I-BH-NPY and125I-PYY binding to the stratum radiatum of the hippocampus, layer I of the somatosensory frontoparietal cortex, molecular layer of the cerebellum, and area postrema was single and of a high affinity. There was a significant difference between the affinities of125I-BH-NPY (K d = 0.96 nM) and125I-PYY binding (K d = 0.05 nM) to the molecular layer of the cerebellum. The binding of the two radioligands to the other areas examined had the same affinities. 4. When comparing the potency of unlabeled rat pancreatic polypeptide (rPP), a family peptide of NPY and PYY, to inhibit the binding to the areas examined, rPP displaced125I-BH-NPY and125I-PYY binding to the area postrema more potently than it did the binding to the stratum radiatum of the hippocampus, layer I of the somatosensory frontoparietal cortex, and molecular layer of the cerebellum. 5. Thus, the quantitative receptor autoradiographic method with125 I-BH-NPY and125I-PYY revealed differences in binding characteristics of specific NPY and PYY binding sites in different areas of the rat brain. The results provide further evidence for the existence of multiple NPY-PYY receptors in the central nervous system.
    Materialart: Digitale Medien
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  • 8
    ISSN: 1573-6830
    Schlagwort(e): endotheline-3 ; dopamine release ; intracellular Ca2+ concentration ; inositol 1,4,5-trisphosphate ; striatal slices
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie
    Notizen: Summary 1. Real-time monitoring of dopamine (DA) release from rat striatal slices demonstrated that endothelin (ET)-3 (0.1–10μM) produced a biphasic DA release consisting of transient and sustained components. When extracellular Ca2+ was removed, the sustained but not transient response remarkably decreased. 2. ET-3 (1–10μM) stimulated an increase in the intracellular Ca2+ concentration ([Ca2+]i), which also consisted of two components. The external Ca2+ depletion inhibited primarily the sustained component of the Ca2+ response to ET-3. 3. ET-3 increased inositol 1,4,5-trisphosphate (IP3) concentrations in striatal slices. This response peaked at 10 to 20 sec and returned to the basal level 2 min after stimulation, an event which was in good accord with a prompt and transient phase of both cytosolic Ca2+ activity and DA release evoked by ET-3. 4. Thus, ET-3 produces a transient and a sustained release of DA from striatal slices by stimulating intracellular Ca2+ mobilization via IP3 formation and extracellular Ca2+ influx, respectively.
    Materialart: Digitale Medien
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  • 9
    ISSN: 1573-6830
    Schlagwort(e): nitric oxide synthase ; NADPH-diaphorase ; striatum ; middle cerebral artery occlusion ; astrocytes ; microglia ; endothelial cells ; rat ; histochemistry
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie
    Notizen: Summary 1. The time course of nitric oxide synthase (NOS) activity in neuronal, endothelial, and glial cells in the rat striatum after middle cerebral artery (MCA) occlusion and reperfusion was examined using a histochemical NADPH-diaphorase staining method. 2. In sham-operated rats, neuronal cells of the striatum exhibited strong NADPH-diaphorase activities. When rats were subjected to MCA occlusion for 1 hr, neuronal damage, including neurons with positive NADPH-diaphorase activities, appeared in the striatum at 3 hr after and extended to all areas of the striatum 3–4 days after reperfusion. 3. NADPH-diaphorase activities in the endothelial cells increased in the damaged part of striatum from 3 hr after, peaked at 1–2 days after MCA occlusion/reperfusion, then gradually decreased. 4. In parallel with the development of neuronal damage, some astrocytes and a high proportion of microglia/macrophages located in the perisite and in the center of the damaged striatum, respectively, exhibited a moderate to high level of NADPH-diaphorase activities. Most of these activities disappeared at 4 days after MCA occlusion. 5. These findings provided evidence that an inappropriate activation of NOS in endothelial cells and microglia/macrophages, in response to MCA occlusion/reperfusion, is closely associated with initiation and progression of ischemic neuronal injury in the striatum.
    Materialart: Digitale Medien
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  • 10
    ISSN: 1573-6830
    Schlagwort(e): nitric oxide ; noradrenaline ; C6 glioma cells ; direct electrochemical monitoring
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie
    Notizen: Abstract 1. Nitric oxide (NO) production in C6 glioma cells was directly monitored in real time by electrochemical detection with a NO-specific biosensor. 2. We present here the first direct evidence that noradrenaline elicits long-lasting NO production in C6 cells pretreated with lipopolysaccharide and interferon-γ, an effect blocked by N G-monomethyl-L-arginine, a NO synthase inhibitor. 3. This direct electrochemical measurement of glia-derived NO should facilitate our understanding of the kinetics of glial signaling in glia-glia and glia-neuron networks in the brain.
    Materialart: Digitale Medien
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