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Molecular Pain

, 8:13

First Online: 24 February 2012Received: 27 August 2011Accepted: 24 February 2012

Abstract

BackgroundMinocycline prevents the development of neuropathic and inflammatory pain by inhibiting microglial activation and postsynaptic currents. But, how minocycline obviates acute visceral pain is unclear. The present study investigated whether minocycline had an any antinociceptive effect on acetic acid-induced acute abdominal pain after intraperitoneal i.p. administration of saline or minocycline 1 hour before acetic acid injection 1.0%, 250 μl, i.p



ResultsMinocycline 4, 10, or 40 mg-kg significantly decreased acetic acid-induced nociception 0-60 minutes post-injection and the enhancement in the number of c-Fos positive cells in the T5-L2 spinal cord induced by acetic acid injection. Also, the expression of spinal phosphorylated extracellular signal-regulated kinase p-ERK induced by acetic acid was reduced by minocycline pre-administration. Interestingly, intrathecal introduction of PD98059, an ERK upstream kinase inhibitor, markedly blocked the acetic acid-stimulated pain responses.

ConclusionsThese results demonstrate that minocycline effectively inhibits acetic acid-induced acute abdominal nociception via the inhibition of neuronal p-ERK expression in the spinal cord, and that minocycline may have therapeutic potential in suppressing acute abdominal pain.

KeywordsMinocycline Acute visceral pain c-Fos p-ERK Writhes Electronic supplementary materialThe online version of this article doi:10.1186-1744-8069-8-13 contains supplementary material, which is available to authorized users.

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Autor: Ik-Hyun Cho - Min Jung Lee - Minhee Jang - Nam Gil Gwak - Ka Yeon Lee - Hyuk-Sang Jung

Fuente: https://link.springer.com/







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