THIS ARTICLE HAS BEEN RETRACTED Activation of capsaicin-sensitive primary sensory neurones induces anandamide production and release

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Errata

This article is corrected by:

  1. Errata: Retraction Volume 119, Issue 4, 890, Article first published online: 21 September 2011

Address correspondence and reprint requests to Istvan Nagy, MD, PhD, Department of Anaesthetics and Intensive Care, Imperial College, Faculty of Medicine, Chelsea and Westminster Hospital, Room G3.30, 369 Fulham Road, London SW10 9NH, UK. E-mail: i.nagy@ic.ac.uk

Abstract

The inhibitory cannabinoid 1 receptor and the excitatory vanilloid receptor 1, both of which are responsive to the endogenous ligand anandamide, are co-expressed on a subpopulation of primary sensory neurones. We report that activation of the cannabinoid 1 receptor/vanilloid receptor 1-co-expressing primary sensory neurones induces the production and release of anandamide. Application of capsaicin (3 nm−1 µm) to cultured primary sensory neurones evoked calcitonin gene-related peptide release, which was significantly increased by the selective cannabinoid 1 receptor antagonist, SR141716A (200 nm). Mass spectrometric analyses of the extracellular solution revealed that exposure to capsaicin (10 nm or 100 nm) enhanced the anandamide concentration of the medium from less then 0.05 pmol/µL to more then 2 pmol/µL. Depolarization of the neurones with 50 mm KCl also enhanced the anandamide content of the buffer. Both the capsaicin- and KCl-induced anandamide release depended on extracellular Ca2+. Prolonged treatment of the cultures with capsaicin (10 µm) reduced both the capsaicin- and KCl-induced anandamide release. These findings indicate that activation of capsaicin-sensitive primary sensory neurones evokes anandamide production and release, and that anandamide might be a key endogenous regulator of the excitability of these neurones.

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