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Bilateral quantitative changes of laminin-1 in the dorsal and ventral roots following unilateral chronic constriction injury of sciatic nerve - An immunofluorescence tissue array

Název česky Bilaterální kvantitativní změny lamininu 1 v dorzálních a ventrálních kořenech po unilaterální chronické konstrikci sciatického nervu - Imunofluorescenční analýza tkáně
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DUBOVÝ Petr DAVID Marek HRADILOVÁ SVÍŽENSKÁ Ivana KLUSÁKOVÁ Ilona

Rok publikování 2009
Druh Konferenční abstrakty
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
Popis Bilateral changes of immunofluorescence for laminin-1 (lam-1) were investigated in the rat spinal nerve roots (L4-L5) following neuropathic pain induction by unilateral sciatic nerve ligature. Induction of neuropathic pain was confirmed in experimental animals by behavioral tests of mechanical allodynia and thermal hyperalgesia. Dorsal and ventral roots of naive rats displayed lam-1 immunostaining in the basal laminae on outer surface of Schwann cell/axon units, perineurial sheaths and blood vessels. Significantly higher brightness of immunofluorescence for lam-1 was observed in the ventral than dorsal roots removed from naive rats as well as those operated on sciatic nerve ligature and surviving for 1 or 3 days. Chronic constriction injury of sciatic nerve for 7 and 14 days results in reduction of different levels of immunofluorescence brightness between dorsal and ventral roots. In comparison to naive and sham-operated animals, apparent bilateral decrease of immunofluorescence brightness for lam-1 was found in both dorsal and ventral roots 7 days after unilateral nerve injury. Although the pattern of lam-1 alterations in both ipsi- and contralateral roots was similar, changes of immunofluorescence were more evident in ipsilateral than contralateral roots. The results indicate that quantitative changes of immunofluorescence for lam-1 are present bilaterally in proximal segments of peripheral nerve far from unilateral chronic constriction injury inducing neuropathic pain. This suggests a possible mechanism for misbalance alongside the afferent and motor axons, the involvement of which in neuropathic pain induction is assumed.
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