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  • 1995-1999  (3)
  • Cerebral ischemia  (1)
  • Ergonovine  (1)
  • Gepirone  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Histochemical study of Ca2+-ATPase activity in ischemic CA1 pyramidal neurons in the gerbil hippocampus (1995)
    Springer
    Acta neuropathologica 90 (1995), S. 448-453 
    Details
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Cell death ; Hippocampus ; Ca2+-ATPase ; Ultracytochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although cytosolic Ca2+ accumulation plays a pivotal role in delayed neuronal death, there have been no investigations on the role of the cellular Ca2+ export system in this novel phenomenon. To clarify the function of the Ca2+-pump in delayed neuronal death, the plasma membrane Ca2+-ATPase activity of CA1 pyramidal neurons was investigated ultracytochemically in normal and ischemic gerbil hippocampus. To correlate enzyme activity with delayed neuronal death, histochemical detection was performed at various recirculation times after 5 min of ischemia produced by occlusion of the bilateral carotid arteries. At 10 min after ischemia, CA1 pyramidal neurons showed weak Ca2+-ATPase activity. Although enzyme activity had almost fully recovered 2 h after ischemia, it was reduced again 6 h after ischemia. Thereafter, Ca2+-ATPase activity on the plasma membrance of CA1 pyramidal neurons decreased progressively, losing its localization on day 3. On day 4 following ischemia, reaction products were diffusely scattered throughout the whole cell body. Our results indicate that, after once having recovered from ischemic damage, severe disturbance of the membrane Ca2+ export system proceeds from the early stage of delayed neuronal death and disturbs the re-export of accumulated cytosolic Ca2+, which might contribute to delayed neuronal death. Occult disruption of Ca2+ homeostasis seems to occur from an extremely early stage of delayed neuronal death in CA1 pyramidal cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00294804
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Prolonged but not acute fluoxetine administration produces its inhibitory effect on hippocampal seizures in rats (1995)
    Springer
    Psychopharmacology 118 (1995), S. 305-309 
    Details
    ISSN: 1432-2072
    Keywords: Epilepsy ; Serotonin ; Fluoxetine ; Gepirone ; Long-term treatment ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study assessed the effects of acute as well as long-term administration of fluoxetine, a selective serotonin (5-HT) reuptake inhibitor with anti-depressant properties, on hippocampal (HIP) seizures elicited by electrical stimulation in rats. The fluoxetine effect on HIP seizures was also assessed following long-term treatment with gepirone, a 5-HT1A receptor agonist. Acute single administration of fluoxetine (1, 10 mg/kg; IP) was found to produce no significant effect on HIP seizure activity. Following daily IP administration of fluoxetine (10 mg/kg per day) or gepirone (10 mg/kg per day) for 21 days, animals were given a 7-day drug-free period and then challenged with an acute dose of 10 mg/kg fluoxetine. These treatment regimens resulted in a significantly increased afterdischarge threshold of HIP seizures in response to acute fluoxetine administration. The inhibitory effect of fluoxetine, however, was not present 4 weeks after long-term treatment with either fluoxetine or gepirone. The present results indicate that long-term treatment with these compounds enhances the antiepileptic effect of subsequent fluoxetine administration on the generation of HIP seizures. This effect is possibly related to the well-demonstrated evidence that fluoxetine and gepirone, on long-term treatment, facilitate net 5-HT neurotransmission through desensitization of presynaptic 5-HT autoreceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02245959
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Mechanisms of ergonovine-induced hyperconstriction of coronary artery after x-ray irradiation in pigs (1995)
    Springer
    Basic research in cardiology 90 (1995), S. 167-175 
    Details
    ISSN: 1435-1803
    Keywords: Ergonovine ; coronary hyperconstriction ; serotonin2 receptor ; endothelium-dependent relaxation ; x-ray irradiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mechanisms of ergonovine-induced coronary hyperconstriction were examined in vivo and in vitro in miniature pigs. To provoke coronary hyperconstriction, the endothelium of a segment of a major branch of the left coronary artery was denuded in 19 Göttingen miniature pigs (4 to 6 months of age). In Group I (n=12), the denuded site of the coronary artery was selectively irradiated with 15 Gy of x-ray twice, 3 and 4 months after endothelial denudation. The remaining 7 pigs were not irradiated (Group II). The vasoconstrictive effect of intracoronary administration of ergonivine (1 to 1000 μg) was examined angiographically 3 months (just before irradiation in group I) and 5 months after denudation in the two groups. After the angiographical study, the vessels were isolated and isometric tensions were measured in an organ chamber. In the in vivo studies, ergonovineinduced vasoconstriction at the denuded and x-ray irradiated site in Group I was significantly greater than that at the control site or that at the denuded site in Group II. Pretreatments with serotonin receptor blockers (ketanserin or methysergide) significantly attenuated ergonovine-induced hyperconstriction, while an alpha-adrenergic receptor blocker (prazosin) did not (% inhibition; ketanserin 74±9%, p〈0.01, methysergide 60±10%, p〈0.01, prazosin 9±5%, NS). In the in vitro studies, ergonivine produced significantly greater tension at the denuded and x-ray irradiated site (Group I) than at the control site or at the denuded site (Group II). Ergonovine-induced endotheliumdependent relaxation was impaired at the denuded site in both groups to a similar extent. These results suggest that ergonovine-induced hyperconstriction at the denuded and x-ray irradiated coronary artery resulted mainly from the hyperreactivity of medial smooth muscle mediated by serotonin2 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00789446
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    Paper (German National Licenses)
    Fulltext
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