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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: Neuropathic pain in human appears not to be opioid-resistant but only reduced sensitivity to systemic opioids is observed in this condition. We studied the contribution of central and peripheral mu-opioid receptors to the antinociception in rats with a spinal nerve ligation-induced neuropathy. Results of the present study indicate that both spinal and peripheral opioid receptors may contribute to the opioid-induced antinociception in the neuropathy. Further, mu-opioid peptide ligands (DAMGO and endomorphins) are more effective than opioid alkaloids in relieving of neuropathic pain. Moreover, reduction of the mu-opioid antinociceptive potency appears to be due to the fact that nerve injury reduced expression of mu-opioid receptors in the spinal ganglia. Identification of the molecular mechanisms involved may be of importance to the understanding of the molecular mechanism of opioid action in neuropathic pain, as well as to the development of better and more effective treatment of neuropathic pain in humans.
    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: 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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  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Influence of morphine self-administration on gene expression in the rat amygdala was studied using rat genome DNA arrays U34A from Affymetrix. Animals were trained to self-administer morphine, each having two ‘yoked’ control animals, receiving passive injections of either morphine or saline. After 40 sessions of self-administration, amygdalae were removed, total RNA was isolated and used to prepare probes for Genechip® arrays. The treatment was found to significantly change abundance of 29 transcripts. Analysis by means of reverse transcription real-time PCR showed significant changes in abundance of five transcripts: γ protein kinase C (PKC), upstream binding factor 2 (UBF2), lysozyme, noggin and heat shock protein 70 (hsp70). After 30 days of forced abstinence from morphine self-administration, abundance of hsp70 and lysozyme returned to basal levels. Changes in abundance of UBF2 persisted, and abundance of three additional genes, namely nuclear factor I/A, γ1 subunit of GABAA receptor and the neuronal calcium sensor 1, changed. Additionally, acute as well as chronic intraperitoneal morphine administration changed the abundance of PKC γ, γ1 subunit of GABAA and hsp70 genes.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 201 (1994), S. 222-227 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochemical and Biophysical Research Communications 85 (1978), S. 1119-1127 
    ISSN: 0006-291X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 6
    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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  • 7
    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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  • 8
    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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  • 9
    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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