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  • 1
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Light-induced phase shifts of circadian rhythmic locomotor activity are associated with the expression of c-Jun, JunB, c-Fos and FosB transcription factors in the rat suprachiasmatic nucleus, as shown in the present study. In order to explore the importance of c-Fos and JunB, the predominantly expressed AP-1 proteins for the phase-shifting effects of light, we blocked the expression of c-Fos and JunB in the suprachiasmatic nucleus of male rats, housed under constant darkness, by intracerebroventricular application of 2 μ1 of 1 mM antisense phosphorothioate oligodeoxynucleotides (ASO) specifically directed against c-fos and JunB mRNA. A light pulse (300 lux for 1 h) at circadian time 15 induced a significant phase shift (by 125 ± 15 min) of the circadian locomotor activity rhythm, whereas application of AS0 6 h before the light pulse completely prevented this phase shift. Application of control nonsense oligodeoxynucleotides had no effect. ASO strongly reduced the light-induced expression of c-Fos and JunB proteins. In contrast, light pulses with or without the control nonsense oligodeoxynucleotides evoked strong nuclear c-Fos and JunB immunoreactivity in the rat suprachiasmatic nucleus. These results demonstrate for the first time that inducible transcription factors such as c-Fos and JunB are an essential part of fundamental biological processes in the adult mammalian nervous system, e.g. of light-induced phase shifts of the circadian pacemaker.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 6 (1994), S. 0 
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Peripheral noxious stimulation leads to a rapid and transient expression of c-fos, c-jun and other immediate-early genes (IEGs) in the spinal cord. However, the role of IEG encoded transcription factors in plasticity of spinal neurons remains speculative. In the present study we have shown that superfusion of rat spinal cord with antisense oligodeoxynucleotides complementary to c-fos mRNA suppresses heat-induced c-Fos protein expression without affecting other members of the Fos and Jun family, thus providing a technique to determine the function of IEGs in vivo.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1044-7431
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0533
    Keywords: Focal ischemia ; Immediate early genes ; Immunohistochemistry ; Spreading depression ; N-methyl-d-aspartate antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary FOS and JUN proteins are transcription factors thought to be involved in coupling neuronal excitation to target gene expression. Cortical infarction of consistent size and location was produced by irradiating the rat brain with Xenon light through the intact skull for 20 min following systemic injection of the photo-sensitizing dye, rose bengal. To investigate the time course and distribution pattern of five cellular ummediate early gene (IEG)-encoded proteins after focal ischemia, the expression of c-FOS, FOS B, c-JUN, JUN B and JUN D was studied immunocytochemically in sham-operated control animals and at different postischemic time intervals up to 24 h. A separate group of animals was pretreated with the non-competitive N-methyl-d-aspartate (NMDA) antagonist MK-801. Photochemically induced focal ischemia caused a rapid induction of FOS and JUN proteins in the entire ipsilateral cortex apart from the ischemic focus. Immunoreactivity in the ipsilateral subcortical gray and white matter and in the entire contralateral hemisphere was indistinguishable from control animals. Individual IEG-encoded proteins were sequentially induced with increased levels of immunoreactivity persisting for different time periods up to 24 h. c-FOS, FOS B, c-JUN and JUN B exhibited a characteristic distribution pattern as reflected by different staining intensities in individual cortical layers. The rapid IEG induction in the entire ipsilateral sensorimotor and limbic structure-associated cortices after photochemically induced infarction most likely reflects spreading depression caused by ischemia and mediated by NMDA receptors. This conclusion is supported by the finding that MK-801 pretreatment completely prevented the postischemic induction of FOS proteins and markedly attenuated the levels of JUN immunoreactivity in all cortical regions except in the peri-infarct area.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    European archives of oto-rhino-laryngology and head & neck 252 (1995), S. 287-291 
    ISSN: 1434-4726
    Keywords: Auditory deprivation ; c-fos labeled neurons Cochlear nucleus ; Inferior colliculus ; Cell maturation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract As an animal model for inborn hearing loss rat pups were reared in a sound-proof chamber from birth until age 21 days. In addition, pinnae were bilaterally sutured closed to reduce any influence of ambient sound. At the end of the sound deprivation, outer ear channals were reopened. Since previous studies failed to show any difference in the number or morphology of neurons in the auditory pathway in bilaterally sound-deprived animals, expression of c-fos protein was used as a functional marker to map trans-synaptic information transfer in the auditory pathway with cellular resolution. At day 21 sound-deprived rats and untreated controls were stimulated with pure tones of 8kHz for 5min at different sound pressure levels. Acoustic stimulation induced c-fos in both parts of the cochlear nucleus, superior olivary complex and inferior colliculus. Compared to untreated rats, deprivation reduced the number of c-fos labeled neurons in the dorsal and ventral part of the cochlear nucleus and inferior colliculus by 58% and 30%, respectively, following low sound pressure levels (90dB). In contrast, high sound pressure levels (120dB) increased the number of c-fos labeled neurons in these areas and evoked only minor differences in the number of labeled neurons in both untreated and sound-deprived rats.
    Type of Medium: Electronic Resource
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