Neonatal capsaicin treatment in rats affects TRPV1-related noxious heat sensation and circadian body temperature rhythm

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MeSH: Animals ; Animals, Newborn ; Body Temperature/drug effects* ; Capsaicin/pharmacology* ; Circadian Rhythm/drug effects* ; Circadian Rhythm/genetics ; Circadian Rhythm Signaling Peptides and Proteins/genetics ; Circadian Rhythm Signaling Peptides and Proteins/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Female ; Ganglia, Spinal/drug effects ; Gene Expression Regulation, Developmental/drug effects* ; Heat Shock Transcription Factors ; Hot Temperature ; Male ; Motor Activity/drug effects ; Nociception/drug effects* ; Pain Measurement/drug effects ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Statistics, Nonparametric ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism* ; Transcription Factors/genetics ; Transcription Factors/metabolism

Keywords: Circadian body temperature ; Clock gene network disorder ; Neonatal capsaicin treatment ; Noxious heat desensitization ; Rat ; TRPV1

Abstract: The transient receptor potential vanilloid 1 (TRPV1) is a cation channel that serves as a polymodal detector of noxious stimuli such as capsaicin. Therefore, capsaicin treatment has been used to investigate the physiological function of TRPV1. Here, we report physiological changes induced by treating neonatal rats with capsaicin. Capsaicin (50 mg/kg) (cap-treated) or vehicle (vehicle-treated) was systemically administered to newborn SD rat pups within 48 h after birth. TRPV1 expression, intake volume of capsaicin water, and noxious heat sensation were measured 6 weeks after capsaicin treatment. Circadian body temperature and locomotion were recorded by biotelemetry. Expression of Per1, Per2, Bmal1 and Hsf1 (clock genes) was also investigated. Neonatal capsaicin treatment not only decreased TRPV1 expression but also induced desensitization to noxious heat stimuli. Circadian body temperature of cap-treated rats increased significantly compared with that of vehicle-treated rats. Additionally, the amplitude of the circadian body temperature was reversed in cap-treated rats. Expression of the hypothalamic Hsf1 and liver Per2 clock genes followed a similar trend. Therefore, we suggest that these findings will be useful in studying various physiological mechanisms related to TRPV1.