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About:
Glial cell type-specific changes in spinal dipeptidyl peptidase 4 expression and effects of its inhibitors in inflammatory and neuropatic pain
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covidontheweb.inria.fr
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Academic Article
research paper
schema:ScholarlyArticle
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Academic Article
research paper
schema:ScholarlyArticle
isDefinedBy
Covid-on-the-Web dataset
has title
Glial cell type-specific changes in spinal dipeptidyl peptidase 4 expression and effects of its inhibitors in inflammatory and neuropatic pain
Creator
Alpár, Alán
Balázsa, Tamás
Barta, Benjamin
Bölcskei, Kata
Fekete, Csaba
Gerber, Gábor
Helyes, Zsuzsanna
Király, Kornél
Kozsurek, Márk
Lukácsi, Erika
Pap, Károly
Puskár, Zita
Szabon, Judit
Tékus, Valéria
Tóth, Zsuzsanna
Source
Medline; PMC
abstract
Altered pain sensations such as hyperalgesia and allodynia are characteristic features of various pain states, and remain difficult to treat. We have shown previously that spinal application of dipeptidyl peptidase 4 (DPP4) inhibitors induces strong antihyperalgesic effect during inflammatory pain. In this study we observed low level of DPP4 mRNA in the rat spinal dorsal horn in physiological conditions, which did not change significantly either in carrageenan-induced inflammatory or partial nerve ligation-generated neuropathic states. In naïve animals, microglia and astrocytes expressed DPP4 protein with one and two orders of magnitude higher than neurons, respectively. DPP4 significantly increased in astrocytes during inflammation and in microglia in neuropathy. Intrathecal application of two DPP4 inhibitors tripeptide isoleucin-prolin-isoleucin (IPI) and the antidiabetic drug vildagliptin resulted in robust opioid-dependent antihyperalgesic effect during inflammation, and milder but significant opioid-independent antihyperalgesic action in the neuropathic model. The opioid-mediated antihyperalgesic effect of IPI was exclusively related to mu-opioid receptors, while vildagliptin affected mainly delta-receptor activity, although mu- and kappa-receptors were also involved. None of the inhibitors influenced allodynia. Our results suggest pathology and glia-type specific changes of DPP4 activity in the spinal cord, which contribute to the development and maintenance of hyperalgesia and interact with endogenous opioid systems.
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2018-02-22
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bibo:doi
10.1038/s41598-018-21799-8
bibo:pmid
29472575
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88d9d333b7b85d34405f27fc2e469cad48a1f8c4
schema:url
https://doi.org/10.1038/s41598-018-21799-8
resource representing a document's title
Glial cell type-specific changes in spinal dipeptidyl peptidase 4 expression and effects of its inhibitors in inflammatory and neuropatic pain
has PubMed Central identifier
PMC5823904
has PubMed identifier
29472575
schema:publication
Sci Rep
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covid:88d9d333b7b85d34405f27fc2e469cad48a1f8c4#body_text
is
schema:about
of
named entity 'DIPEPTIDYL PEPTIDASE 4'
named entity 'antidiabetic drug'
named entity 'change'
named entity 'strong'
named entity 'neuropathic'
named entity 'DPP4'
named entity 'neuropathic'
named entity 'activity'
named entity 'inflammatory'
named entity 'CELL TYPE'
named entity 'ITS'
named entity 'GLIAL CELL'
covid:arg/88d9d333b7b85d34405f27fc2e469cad48a1f8c4
named entity 'INHIBITORS'
named entity 'OPIOID'
named entity 'APPLICATION'
named entity 'BUT'
named entity 'EXPRESSED'
named entity 'INDEPENDENT'
named entity 'MRNA'
named entity 'RECEPTORS'
named entity 'INTRATHECAL'
named entity 'STUDY'
named entity 'ASTROCYTES'
named entity 'RELATED'
named entity 'DIFFICULT'
named entity 'DIPEPTIDYL PEPTIDASE 4'
named entity 'INFLAMMATORY PAIN'
named entity 'STATES'
named entity 'SYSTEMS'
named entity 'RESULTS'
named entity 'VARIOUS'
named entity 'PAIN SENSATIONS'
named entity 'MAINTENANCE'
named entity 'MAGNITUDE'
named entity 'PATHOLOGY'
named entity 'ALLODYNIA'
named entity 'CARRAGEENAN'
named entity 'ANTIDIABETIC DRUG'
named entity 'IPI'
named entity 'LOW LEVEL'
named entity 'GENERATED'
named entity 'INFLAMMATION'
named entity 'ROBUST'
named entity 'RAT'
named entity 'ANIMALS'
named entity 'GLIA'
named entity 'NEUROPATHY'
named entity 'SUGGEST'
named entity 'KAPPA'
named entity 'TREAT'
named entity 'RECEPTOR ACTIVITY'
named entity 'FEATURES'
named entity 'CHARACTERISTIC'
named entity 'OPEN'
named entity 'DPP4'
named entity 'EITHER'
named entity 'TRIPEPTIDE'
named entity 'TYPE'
named entity 'DEPENDENT'
named entity 'ENDOGENOUS OPIOID'
named entity 'OBSERVED'
named entity 'DORSAL HORN'
named entity 'MEDIATED'
named entity 'PARTIAL'
named entity 'AFFECTED'
named entity 'PREVIOUSLY'
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