Prolonged exposure to bradykinin and prostaglandin E2 increases TRPV1 mRNA but does not alter TRPV1 and TRPV1b protein expression in cultured rat primary sensory neurons

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• 作者：Shilpa Mistry^a ; ¹ ; Cleoper C Paule^a ; ¹ ; Angelika Varga^a ; Andy Photiou^b ; Agnes Jenes^a ; ^c ; Antonio Avelino^d ; ^e ; Laki Buluwela^b ; Istvan Nagy^a ; ^{i.nagy@imperial.ac.uk" class="auth_mail}
• 关键词：Pain ; Inflammation ; Dorsal root ganglion ; Capsaicin
• 刊名：Neuroscience Letters
• 出版年：3 April, 2014
• 年：2014
• 卷：564
• 期：Complete
• 页码：89-93
• 全文大小：541 K

文摘

Sensitisation of the capsaicin receptor, transient receptor potential vanilloid type 1 (TRPV1) ion channel in nociceptive primary sensory neurons (PSN) underlies the development of inflammatory heat hyperalgesia. Removal of the negative-dominant splice variant of the TRPV1 molecule, TRPV1b from TRPV1/TRPV1b heterotetrameric channels, which should be associated with changes in the expression of TRPV1 and TRPV1b transcripts and proteins, has been suggested to contribute to that sensitisation. Respective reverse-transcriptase polymerase chain reaction (RT-PCR) and Western-blotting revealed that both TRPV1 and TRPV1b mRNA, and their encoded proteins are expressed in rat cultured PSN. Sequencing of the RT-PCR products showed that TRPV1b mRNA lacks the entire exon 7. Further, growing PSN for 2 days in the presence of 10 渭M bradykinin (BK) and 10 渭M prostaglandin E₂ (PGE₂) significantly increases TRPV1 responsiveness and TRPV1 mRNA expression, without producing any changes in TRPV1b mRNA, and TRPV1 and TRPV1b protein expression. These data challenge the hypothesis that alterations in the composition of the TRPV1 ion channel contributes to the sensitisation.