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