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Endotoxin causes calcitonin gene-related peptide release from isolated spinal cord in rat

Xian Wang

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Abstract

In the present study, it was determined whether endotoxin (ETX) could directly trigger the release of calcitonin gene-related peptide (CGRP) from isolated rat spinal cord containing the central ends of sensory nerves. The results showed that both ETX and its major toxic component lipid A caused a concentration-dependent release of CGRP. The ETX-evoked CGRP release was blocked by ETX inhibitor and tetrodotoxin, a selective sodium channel blocker. Capsaicin depletes the neurotransmitter of sensory nerve, and capsazepine is an antagonist of capsaicin. Both capsaicin and capsazepine significantly inhibited ETX-induced CGRP release. The data suggest that ETX, mediated by lipid A, may stimulate the capsaicin-sensitive nerve terminals and trigger CGRP release in rat spinal cord.

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What this paper is about

In the present study, it was determined whether endotoxin (ETX) could directly trigger the release of calcitonin gene-related peptide (CGRP) from isolated rat spinal cord containing the central ends of sensory nerves. The results showed that both ETX and its major toxic component lipid A caused a concentration-dependent release of CGRP. The ETX-evoked CGRP release was blocked by ETX inhibitor and tetrodotoxin, a selective sodium channel blocker. Capsaicin depletes the neurotransmitter of sensory nerve, and capsazepine is an antagonist of capsaicin. Both capsaicin and capsazepine significantly inhibited ETX-induced CGRP release. The data suggest that ETX, mediated by lipid A, may stimulate the capsaicin-sensitive nerve terminals and trigger CGRP release in rat spinal cord.

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Available abstract

In the present study, it was determined whether endotoxin (ETX) could directly trigger the release of calcitonin gene-related peptide (CGRP) from isolated rat spinal cord containing the central ends of sensory nerves. The results showed that both ETX and its major toxic component lipid A caused a concentration-dependent release of CGRP. The ETX-evoked CGRP release was blocked by ETX inhibitor and tetrodotoxin, a selective sodium channel blocker. Capsaicin depletes the neurotransmitter of sensory nerve, and capsazepine is an antagonist of capsaicin. Both capsaicin and capsazepine significantly inhibited ETX-induced CGRP release. The data suggest that ETX, mediated by lipid A, may stimulate the capsaicin-sensitive nerve terminals and trigger CGRP release in rat spinal cord.

Key concepts: Capsazepine, Capsaicin, Calcitonin gene-related peptide, Chemistry, TRPV1, Spinal cord, Pharmacology, Antagonist

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