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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 85 (2003), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Recent studies have pointed to the role of peripheral receptors in chronic pain process. They are located on nerve fibers, which project to dorsal root ganglion (DRG). We demonstrated using RT PCR method that peripheral nerve injury caused a reduction in a number of mu-opioid receptors in DRG. We also checked the peripheral effects of opioid (morphine, DAMGO, EM-1, EM-2) and ORL-1 (nociceptin) receptor agonists. Our findings show that intraplantarly administered agonists were effective in antagonizing allodynia. Peripheral mu-opioid and ORL1 receptors mediate the observed effects as was evidenced by treatment with naloxone methiodide, which is only peripherally active. The present results demonstrated that opioids after peripheral treatment, in spite of decreased expression of mu-opioid receptor mRNA in DRG, are effective and their peripheral use may eliminate central unwanted side-effects.Acknowledgement:   Supported by EU grant (No. QLRT-2001-02919).
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 85 (2003), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Neuroimmune interactions are discussed to drive neuropathic pain. We used the Bennett model to correlate pain and cellular expression profiles of the complement factors C1q and C1q-associated serine proteases C1r/C1s in lumbar spinal cord. At 2 days C1q mRNA levels increased ipsilateral to the lesion, and peaked at 8 days when allodynia and severe walking problems were present. During regeneration walking problems disappeared together with C1q mRNA levels. C1q biosynthesis was restricted to microglia. Surprisingly, C1s/C1r biosynthesis was not increased after injury suggesting a role for C1q different from classical complement activation. Sustained C1q expression in spinal microglia after lesion in conjunction with pain behavior indicates that microglial C1q may be causally involved in the development and maintenance of neuropathic pain.Acknowledgements:  Supported by BMBF01GG9818, SFB297, DFGWE910/8-3, KBN3P05C00623.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 85 (2003), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Melanocortin peptides have been reported to influence opiate tolerance, but the neuronal basis underlying these actions is unknown. We studied the contribution of melanocortin (MC4R) receptors to morphine effects. The MC4R mRNA level in the amygdala was decreased after acute morphine treatment and increased in rats tolerant to morphine as evidenced by quantitative real-time PCR method. Moreover, the intra-amygdalar microinjection of antagonist of MC4R attenuated morphine tolerance. Expression of the spinal MC4R after sciatic nerve injury was decreased in the early phase of neuropathy and slightly decreased 2–3 weeks after injury. These findings suggest that the altered melanocortin receptor function may contribute to the development of morphine-induced effects. Thus, the melanocortin receptors may be a target for development of better and more effective drugs for the therapy of chronic pain.Acknowledgement:  Supported by KBN grant for the statutory activity.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1435-1463
    Keywords: Glutamate receptors mRNA ; kainate ; pilocarpine ; limbic seizures ; hippocampus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The expression of mRNA coding for AMPA selective glutamate (Glu) R2 receptor and kainate selective GluR5 receptor was studied in the rat hippocampal formation in two animal models of limbic seizures evoked by systemic administration of pilocarpine (400 mg/kg ip) or kainate (15 mg/kg ip). As shown by an in situ hybridization study, pilocarpine decreased the GluR2 flip mRNA level in CA1 and CA3 areas of the hippocampus after 3h and kainate after 24 h, e.g. at the time preceding neuronal degeneration. No changes in the GluR2 flop or GluR5 mRNA level were found in those regions. In the dentate gyrus, resistant to neurodegeneration, pilocarpine and kainate differentialy affected the expression of GluR2 and GluR5 mRNAs. After 72 h pilocarpine, but not kainate, increased the GluR2 flop mRNA level and decreased the flip one, which suggests attenuation of the GluR2 sensitivity. On the other hand, kainate, elevated the GluR2 flip and GluR5 mRNA level in the dentate gyrus after 72 h. All in all the above data suggest that changes in the GluR2 gene expression may play some role in the neuronal damage to vulnerable areas (CA1, CA3). However, differences in the kainate- and pilocarpine-induced changes in the dentate gyrus at the late time points indicate that alterations in the stoichiometry of GluR2 forms or GluR5 gene expression in this brain region are not a common causal factor responsible for delayed neuronal hyperexcitability.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1435-1463
    Keywords: Keywords: Pilocarpine ; kainate ; seizures ; thyrotropin-releasing hormone ; mRNA ; hippocampus ; rat.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The expression of mRNA coding for prepro-thyrotropin releasing hormone (preproTRH) was estimated in the rat brain in two animal models of limbic seizures, evoked by systemic administration of pilocarpine (400 mg/kg ip) or kainate (12 mg/kg ip). As shown by an in situ hybridization study, after 24 h both pilocarpine- and kainate-induced seizures profoundly increased the preproTRH mRNA level in the dentate gyrus. After 72 h, the preproTRH mRNA level was back to control values. Kainate-treated rats showed an elevated level of TRH in the hippocampus, septum, frontal and occipital cortex after 24 and 72 h, whereas in the striatum and amygdala the TRH level was raised after 72 h only. In the hypothalamus, TRH levels was lowered after 3 and 24 h, and returned to the control after 72 h. Pilocarpine-induced seizures also elevated the TRH level after 72 h in the majority of the above structures, except for the hypothalamus and amygdala where no changes were found at any time point. A radioreceptor assay showed that kainate decreased the Bmax value of TRH receptors in the striatum and hippocampus after 3 and 24 h, respectively, and had no effect on the Kd values. In contrast, pilocarpine-induced seizures lowered the Bmax of TRH receptors in the striatum, hippocampus and piriform cortex after 72 h only, and decreased Kd values in the striatum, amygdala and frontal cortex. These data showed that pilocarpine- and kainate-induced seizures enhanced likewise preproTRH mRNA in the dentate gyrus; on the other hand, they differed with respect to time- and structure-related changes in TRH tissue levels and TRH receptors. These differences may have functional significance in TRH-dependent control mechanism of the seizure activity in these two models of limbic epilepsy.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Regulatory Peptides 54 (1994), S. 233-235 
    ISSN: 0167-0115
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Regulatory Peptides 53 (1994), S. S209-S210 
    ISSN: 0167-0115
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1435-1463
    Keywords: Galanin ; galanin fragments ; behavior ; analgesia ; rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Behavioral effect of galanin and its fragments, galanin1–15 and galanin16–29 (200 ng, 1 and 5 μg), after intracerebroventricular (i.c.v.) administration was studied in rats. The number of crossings and pippings and the time of locomotion (an open field test) showed a similar sedative action of galanin and galanin16–29, with no significant effect of galanin1–15. Galanin and its fragments, injected in doses of 200 ng, 1 and 5 μg, did not affect nociception, as measured by a tail-flick and paw pressure test. Galanin and galanin1–15, but not galanin16–29 (5 μg i.c.v.), injected together with morphine (2.5 μg i.c.v.), significantly potentiated the analgetic effect of morphine assessed by a paw pressure test; a similar tendency was also observed in a tail-flick test. Galanin and its two fragments injected in doses of 200 ng, 1 and 5 μg, did not change the effect of morphine given in a dose of 1 μg. These data suggest that galanin, having no effect when given alone, potentiate the analgetic effect of morphine. The fact that the N-terminal fragment of galanin acts like a natural peptide suggests a receptor mediated action. In conclusion, the analgesic effect of morphine was potentiated by galanin and its N-terminal fragment galanin1–15. On the other hand, behavioral study showed a similar sedative action of galanin and C-terminal fragment galanin16–29. This suggests that the N- and C-terminal fragments of galanin are differentially involved in behavioral effects of the peptide.
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