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  • 1
    Electronic Resource
    Electronic Resource
    Behavioral abnormalities and apoptotic changes in neurons in mice brain following a single administration of allylnitrile (1999)
    Springer
    Archives of toxicology 73 (1999), S. 22-32 
    Details
    ISSN: 1432-0738
    Keywords: Key words Allylnitrile ; Apoptosis ; Behavioral abnormalities ; Habenula ; Mice brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A single dose of allylnitrile in mice might induce persistent behavioral abnormalities, of which the mechanism is not yet known. The present study was undertaken to explore the relationship between behavioral abnormalities and pathological changes in the brain of mice following exposure to allylnitrile. Exposure to allylnitrile (63, 84, and 112 mg/kg, p.o.) resulted in dose-dependent changes in behavioral abnormalities, including increased locomotor activity, circling, retropulsion, head twitching, and alteration in reflexive behavior, which appeared at day 2 postdosing and were persistent throughout the experimental period (60 days) at the higher dose levels. Allylnitrile produced neuronal retraction including hyperchromasia of the nuclei in the raphe nuclei, cerebral cortex, hypothalamus, hippocampal CA1 and dentate gyrus later than 30 days. No gliosis was observed in these regions. Not all but a significant number of neurons in the hippocampal CA1, medial habenula and raphe nuclei were immunoreactive to CPP32 (Caspase-3) even at day 2. These neurons were also positive to Hoechst 33258 staining, indicating allylnitrile caused apoptotic changes in specific neurons when neuronal behaviors became apparent. These apoptotic changes were persistent even in the area without neuronal contraction such as medial habenula. However, almost all neurons in these areas were also positive to terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL). It is conceivable that allylnitrile caused apoptotic changes in neurons but did not always lead them to cell death immediately. Moreover, even when neuronal contraction resulted in retention of behavioral abnormalities, onset of these abnormalities seems to be associated with the impairment in the habenulo-raphe relay due to activation of apoptotic cascade in neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002040050582
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Differences in enhancing effects of zolpidem and benzodiazepine drugs on recurrent inhibition in rat hippocampal slices (1997)
    Springer
    Psychopharmacology 131 (1997), S. 394-398 
    Details
    ISSN: 1432-2072
    Keywords: Key words Zolpidem ; Benzodiazepine ; Hypnotic ; Recurrent inhibition ; GABA ; Hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been reported that the clinical and electroencephalographic profiles of zolpidem, a non-benzodiazepine drug which binds preferentially to the ω1 benzodiazepine recognition sites located within the GABAA receptor complex, are different from those of benzodiazepine drugs, which bind non-selectively to the ω1 and ω2 sites. In order to clarify the electrophysiological mechanism underlying the unique profile of zolpidem, the present study compared the enhancing effects of zolpidem and two benzodiazepine drugs, triazolam and diazepam, on recurrent inhibition. This inhibition was expressed as suppression of the orthodromically induced population spikes by the preceding antidromic stimulation of the alveus in the CA1 region of rat hippocampal slices. The rank order of potency for enhancing recurrent inhibition was triazolam 〉 diazepam 〉 zolpidem. From the present results and previously reported findings that zolpidem has a lower affinity for the ω2 sites than diazepam while both have the same affinity for the ω1 sites, we concluded that the hippocampal recurrent inhibition appears to be enhanced mainly by activation of the ω2 sites, but not by that of the ω1 sites. Furthermore, the lower potency of zolpidem for enhancing recurrent inhibition may underlie its unique profile in terms of its clinical and electroencephalographic effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050308
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Abnormal functional connectivity in Alzheimer’s disease: intrahemispheric EEG coherence during rest and photic stimulation (1998)
    Springer
    European archives of psychiatry and clinical neuroscience 248 (1998), S. 203-208 
    Details
    ISSN: 1433-8491
    Keywords: Key words Alzheimer’s disease ; Coherence analysis ; Photic stimulation ; EEG ; Functional connectivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Electroencephalography (EEG) coherence provides a measure of functional correlations between two EEG signals. The present study was conducted to examine intrahemispheric EEG coherence at rest and during photic stimulation (PS; 5, 10 and 15 Hz) in ten unmedicated patients with presenile dementia of the Alzheimer type (AD; mean age at onset 56 years). In the resting EEG, the AD patients had significantly lower coherence than gender- and age-matched control subjects in the alpha-1, alpha-2 and beta-1 frequency bands. The EEG analysis during PS also showed that the patients had significantly lower coherence in the frequency corresponding to PS at 10 and 15 Hz. In this study, the changes in coherence from the resting state to the stimulus condition (i.e. PS-related coherence reactivity) were examined. The patients were found to show significantly smaller coherence reactivity to PS at 5 and 15 Hz. These findings suggest that, in addition to the resting state, AD patients have an impairment of intrahemispheric functional connectivity during PS. They also suggest that AD shows a failure of PS-related functional reorganization.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004060050038
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    Paper (German National Licenses)
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