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2017 | 77 | Suppl.1 |
Tytuł artykułu

Changes of genes expression in the nucleus accumbens during neuropathic pain in mouse brain

Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
INTRODUCTION: The nucleus accumbens (NAc), which is known to be an important component of the mesolimbic dopaminergic reward system also plays a role in pain, however the molecular mechanisms of this involvement are not known. In the present study we explored molecular pathways involved in the neuropathic pain. Understanding of this process would allow us brain mapping and find biomarkers for pain transmission. AIM(S): The aim of this study was to investigate the alterations in genes expression after CCI in the NAc. METHOD(S): Neuropathic pain was induced by applying a Chronic Constriction Injury (CCI) model in C57BL/6J mice. Two behavioral tests for neuropathic pain were used: the von Frey’s test and the cold plate test. In our biochemical researches we used qRT-PCR. RESULTS: We found that nerve injury produced a significant increase in the expression of opioid genes (PDYN, PENK), opioid kappa and delta receptors genes (KOR, DOR) and calcium/calmodulin - dependent protein kinase kinase 1 (CAMKK1) in the nucleus accumbens. Furthermore, we observed that neuropathic pain augmented the expression of stress – and inflammatory response genes coding for the glucocorticoid receptor (GR), FK506 binding protein5 (FKBP5), and interleukins IL1 beta and IL6 in the nucleus accumbens. Moreover, elevated levels of GFAP (astrocyte marker) but not C1q (microglia marker) mRNAs were detected. CONCLUSIONS: Our results demonstrate that CCI produces lasting biochemical changes in the NAc.Taking into account the well-known roles of opioid systems in pain transmission and emotional processes, the observed changes in the expression of the opioid propeptides and receptors genes may contribute to changes in pain sensitivity and in affective response to nociceptive stimulation. Furhermore, increased expression of GFAP, GR, FKBP5, Il6 and Il1beta genes suggests that cellular stress and inflammatory processes are involved in this type of pain not only on the level of the spinal cord but also in the brain. FINANCIAL SUPPORT: Research supported by HEALTH-F2-2013-602891 NEUROPAIN.
Słowa kluczowe
Wydawca
-
Rocznik
Tom
77
Numer
Opis fizyczny
p.100
Twórcy
  • Department of Molecular Neuropharmacology, Institute of Pharmacology Polish Academy of Sciences, Cracow, Poland
  • Department of Molecular Neuropharmacology, Institute of Pharmacology Polish Academy of Sciences, Cracow, Poland
autor
  • Department of Molecular Neuropharmacology, Institute of Pharmacology Polish Academy of Sciences, Cracow, Poland
autor
  • Department of Pharmacology of Pain, Institute of Pharmacology Polish Academy of Sciences, Cracow, Poland
autor
  • Department of Pharmacology of Pain, Institute of Pharmacology Polish Academy of Sciences, Cracow, Poland
  • Department of Pharmacology of Pain, Institute of Pharmacology Polish Academy of Sciences, Cracow, Poland
  • Department of Molecular Neuropharmacology, Institute of Pharmacology Polish Academy of Sciences, Cracow, Poland
Bibliografia
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.agro-70446c73-4b39-40cd-a0ad-ed9fa97b77ac
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