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
    Apoptotic cell death in experimental rabies in suckling mice (1998)
    Springer
    Acta neuropathologica 95 (1998), S. 159-164 
    Details
    ISSN: 1432-0533
    Keywords: Key words Apoptosis ; Encephalitis ; Rabies ; Pathogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A fatal encephalomyelitis developed after intracerebral inoculation of 6-day-old ICR mice with the challenge virus standard (CVS) strain of fixed rabies virus. The brains of CVS-infected mice showed widespread morphologic changes of apoptosis, which were particularly prominent in pyramidal neurons of the hippocampus and in the cerebral cortex. Evidence of oligonucleosomal DNA fragmentation was sought in situ using the TUNEL method. TUNEL staining was observed in many neurons, and rabies virus antigen was usually demonstrated with immunoperoxidase staining in similar regions. Neurons in the dentate gyrus of the hippocampus demonstrated expression of viral antigen, apoptotic changes, and positive TUNEL staining. This region normally demonstrates little infection in CVS-infected adult mice. Double labeling of neurons with TUNEL and viral antigen indicated that infected neurons actually underwent apoptosis. Increased immunoreactivity against the Bax protein was demonstrated compared to uninfected mice. Purkinje cells expressed viral antigen, but did not show significant morphologic changes of apoptosis or TUNEL staining. In contrast, neurons in the external granular layer of the cerebellum did not express viral antigen, but demonstrated greater morphologic changes of apoptosis and positive TUNEL staining than uninfected controls. Apoptotic cell death likely plays an important role in the pathogenesis of rabies virus infection in suckling mice. There was evidence of more apoptosis in the brains of suckling mice than in those of adult mice and this finding explains the greater neurovirulence of rabies virus in younger mice. Rabies virus likely induces apoptosis in vivo by both direct and indirect mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050781
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Pathogenesis of experimental rabies in mice: an immunohistochemical study (1989)
    Springer
    Acta neuropathologica 78 (1989), S. 159-165 
    Details
    ISSN: 1432-0533
    Keywords: Encephalitis ; Encephalomyelitis ; Immunohistochemistry ; Pathogenesis ; Rabies
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The spread of rabies virus in the central nervous system of mice was examined after hindlimb footpad and intracerebral inoculation of the CVS strain of fixed rabies virus. All mice developed paralytic rabies. After intracerebral inoculation there was early simultaneous infection of neurons in the cerebral cortex and pyramidal neurons of the hippocampus, and later there was spread to the cerebellum. After high-dose intracerebral inoculation there was early infection ependymal cells lining the lateral ventricles and neurons adjacent to the central canal of the spinal cord, suggesting that rabies virus entry into the CNS occurs, at least in part, by a cerebrospinal fluid pathway. The sequence of involvement was different after hindlimb footpad inoculation. Infection became established in the cerebellum on day 5, in the cerebral cortex on day 6, and in the hippocampus on day 8. CA3 was initially affected, CA1 became infected 2 days later, and there was much less involvement of the dentate gyrus. Hippocampal infection occurred late relative to the rest of the brain after peripheral inoculation, but not after intracerebral inoculation. The hippocampus is not a good location for the detection of early brain infection after peripheral inoculation, although it may be involved when a natural rabies vector has the ability to transmit infection. These findings also raise questions about the mechanisms for the limbic dysfunction observed in clinical rabies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688204
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Apoptotic cell death is an important cause of neuronal injury in experimental Venezuelan equine encephalitis virus infection of mice (1997)
    Springer
    Acta neuropathologica 93 (1997), S. 349-353 
    Details
    ISSN: 1432-0533
    Keywords: Key words Apoptosis ; Arbovirus ; Encephalitis ; Pathogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mice develop a fatal encephalomyelitis after infection with the Trinidad donkey strain of Venezuelan equine encephalitis (VEE) virus. Adult mice were inoculated intraperitoneally with VEE virus and the brains were examined at different time points. Morphological changes were assessed by histological staining. VEE virus antigen was detected with immunoperoxidase staining, and DNA fragmentation was evaluated in situ using the terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) method. VEE antigen was found in many areas of the brain and it was prominent in neurons. There were mild associated inflammatory changes. DNA fragmentation was demonstrated in many of these areas using TUNEL. In areas with TUNEL staining, morphological neuronal changes ranged from nuclear chromatin condensations to nuclear and cellular fragmentation, which are characteristic of apoptosis. There is strong morphological and biochemical evidence of apoptotic cell death in this experimental model of VEE virus infection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050626
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Effect of the benzodiazepine receptor agonist, zolpidem, on palatable fluid consumption in the rat (1993)
    Springer
    Psychopharmacology 111 (1993), S. 185-189 
    Details
    ISSN: 1432-2072
    Keywords: Fluid consumption ; Zolpidem ; Diazepam ; FG 8205 ; Benzodiazepines ; Rats ; Habituation ; Neophobia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two experiments examined the effect of the benzodiazepine receptor agonist, zolpidem, on palatable fluid intake in water-deprived rats. In the first experiment, pretreatment with 3.0 or 10.0 mg/kg zolpidem IP was found to increase consumption of a novel glucose drink (3% d-glucose and 0.1% sodium saccharine w/v in water). The increase in fluid consumption induced with zolpidem was comparable to the increases observed with diazepam and the benzodiazepine partial agonist, FG 8205. Experiment 2 demonstrated that this zolpidem-induced increase in drinking could be observed in both naive rats and in rats that had been habituated to the glucose drink and the testing environment: pretreatment with 3.0 mg/kg PO of zolpidem was found to increase fluid consumption in rats that had received either 0 or 8 days pre-exposure to the testing conditions. Contrary to earlier reports, these results support the conclusion that zolpidem, like other benzodiazepine agonists, can directly modulate ingestive behaviour.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02245521
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    State-dependent effects of atypical benzodiazepine-receptor agonists (1995)
    Springer
    Psychopharmacology 119 (1995), S. 399-404 
    Details
    ISSN: 1432-2072
    Keywords: Rat ; State-dependency ; Diazepam ; FG 8205 ; Zolpidem ; Agonist ; Partial agonist ; Benzodiazepine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The state-dependent effect of the BZ-receptor agonist diazepam (1.25–10 mg/kg), the partial agonist FG 8205 (0.5–4.0 mg/kg) and the BZ1-receptor agonist zolpidem (0.25–2 mg/kg) were investigated in rats. During daily sessions, animals were trained to acquire FR10 lever pressing for food reinforcement whilst under the influence of the agonists, using an operant technique. Forty-eight hours after the final training session under drug, their performance of the FR10 was evaluated during a test session, carried out following vehicle administration only. Neither diazepam, nor FG 8205 impaired acquisition of the task. In the group treated with 2 mg/kg zolpidem, six out of eight rats failed to learn within 20 sessions, but the smaller doses were without effect on acquisition. When drug treatment was withdrawn, there was evidence that all three of the agonists tested produced state-dependency. This was apparent in the form of longer latencies to obtain reinforcement and decreased lever pressing rates. The significance of these findings are discussed in the context of the relationship between the state-dependent effects of BZ-receptor agonists and their other properties, and the receptor subtypes which might underly these effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02245855
    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...