k 2007

An immunohistochemical staining for p-38 as a marker for satellite cells mediating indirect reactions of the dorsal root ganglia to nerve injury

DUBOVÝ, Petr, Ilona KLUSÁKOVÁ, Ivana SVÍŽENSKÁ a Radim JANČÁLEK

Základní údaje

Originální název

An immunohistochemical staining for p-38 as a marker for satellite cells mediating indirect reactions of the dorsal root ganglia to nerve injury

Název česky

Imunohistochemická lokalizace p38 jako markru sat.buněk zprostředkujících nepřímé reakce spinálních ganglií na poškození nervu

Autoři

DUBOVÝ, Petr, Ilona KLUSÁKOVÁ, Ivana SVÍŽENSKÁ a Radim JANČÁLEK

Vydání

European Glial Cell Meeting, 2007

Další údaje

Jazyk

angličtina

Typ výsledku

Prezentace na konferencích

Obor

30000 3. Medical and Health Sciences

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Odkazy

Organizační jednotka

Lékařská fakulta

ISBN

1740-925X

Klíčová slova anglicky

transforming factor; nerve injury; neuropathic pain

Příznaky

Mezinárodní význam
Změněno: 21. 1. 2008 09:06, MUDr. Ilona Klusáková, Ph.D.

Anotace

V originále

Nerve injury induces neuropathic pain and activation of p38 mitogen-activated protein kinase (p38) in different populations of DRG neurons and spinal cord microglia. We have investigated an immunohistochemical location of activated p38 protein in the C7-C8 and L4-L5 dorsal root ganglia (DRG) of naive rats and those operated for unilateral L4-L5 spinal nerve ligature (SNL), sciatic nerve ligature (ScNL), and sciatic nerve transection (ScNT). In contrast to published results an enhanced p38-IF was found not only in DRG neurons but also in the satellite cells (SC), particularly after ScNL and ScNT for 1, 2, and 4 weeks. An increased p38-IF was observed in the SC of contralateral L4-5 DRG and those of cervical segments in comparison to very low p38-IF in the cells of ipsilateral L4-5 DRG. In contrast, small and medium-sized neurons displayed increased p38-IF only in the ipsilateral L4-5 DRG. A week SNL induced elevated p38-IF in the cervical DRG neurons, but reduced p38-IF in the ipsi- and contralateral L4-5 DRG. The DRG neurons related to SNL displayed an increased p38-IF until 2 weeks. An increased p38-IF in the SC was observed in DRG not associated with damaged nerve. Our results suggested a nerve damage signaling that spreads in the nervous system to induce expression of the critical p38 mitogen-activated protein kinase. In addition, our results indicate that the signaling in the DRG not associated with injured nerve may be mediated by satellite glial cells.

Česky

Poškození nervu indukuje neuropathickou bolest a activuje p38 mitogen-aktivovanou protein kinázu (p38) v určité populaci neuronů spinálních ganglií a v mikroglii míchy. Sledovali jsem imunohistochemickou lokalizaci aktivovaného p38 proteinu v v C7-C8 a L4-L5 spinálních gangliích intaktních a operovaných potkanů pro unilaterální ligaturu L4-L5 spinálního nervu SNL) a sedacího nervu (ScNL) a po transekci sedacího nervu(ScNT). In contrast to published results an enhanced p38-IF was found not only in DRG neurons but also in the satellite cells (SC), particularly after ScNL and ScNT for 1, 2, and 4 weeks. An increased p38-IF was observed in the SC of contralateral L4-5 DRG and those of cervical segments in comparison to very low p38-IF in the cells of ipsilateral L4-5 DRG. In contrast, small and medium-sized neurons displayed increased p38-IF only in the ipsilateral L4-5 DRG. A week SNL induced elevated p38-IF in the cervical DRG neurons, but reduced p38-IF in the ipsi- and contralateral L4-5 DRG. The DRG neurons related to SNL displayed an increased p38-IF until 2 weeks. An increased p38-IF in the SC was observed in DRG not associated with damaged nerve. Our results suggested a nerve damage signaling that spreads in the nervous system to induce expression of the critical p38 mitogen-activated protein kinase. In addition, our results indicate that the signaling in the DRG not associated with injured nerve may be mediated by satellite glial cells.

Návaznosti

MSM0021622404, záměr
Název: Vnitřní organizace a neurobiologické mechanismy funkčních systémů CNS
Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Vnitřní organizace a neurobiologické mechanismy funkčních systémů CNS