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TRPV3 and TRPV4 ion channels are not major contributors to mouse heat sensation

DOI: 10.1186/1744-8069-7-37

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TRPV3 knockout mice on the C57BL6 background exhibited no obvious alterations in thermal preference behavior. On the 129S6 background, absence of TRPV3 resulted in a more restrictive range of occupancy centered around cooler floor temperatures. TRPV3 knockout mice showed no deficits in acute heat nociception on either background. Mice deficient in both TRPV3 and TRPV4 on a C57BL6 background showed thermal preference behavior similar to wild-type controls on the thermal gradient, and little or no change in acute heat nociception or inflammatory heat hyperalgesia. Masking of TRPV1 by the TRPV1 antagonist JNJ-17203212 did not reveal differences between C57BL6 animals deficient in TRPV3 and TRPV4, compared to their wild-type counterparts.Our results support the notion that TRPV3 and TRPV4 likely make limited and strain-dependent contributions to innocuous warm temperature perception or noxious heat sensation, even when TRPV1 is masked. These findings imply the existence of other significant mechanisms for heat perception.TRPV1 is a non-selective cation channel that can be activated by heat (at > ~42°C) or a wide range of chemical agonists such as capsaicin and acid [1]. TRPV1 is highly expressed in small diameter primary sensory neurons. Mice deficient for TRPV1 show blunted noxious heat perception in tests of acute heat nociception and inflammatory heat hyperalgesia [2]. Although these responses are impaired, mice devoid of TRPV1 are still able to respond to heat. For example, although TRPV1 knockout mice exhibit a 4-fold longer tail withdrawal latency at 50°C, they still withdraw their tails in response to hot water. In one TRPV1 knockout line, behavioral deficits were reported in thermal hyperalgesia but not in acute heat nociception [3]. Moreover, thermal selection behavior on a thermal gradient is normal in the absence of TRPV1 [4]. Significant residual responses to heat have also been observed in skin-nerve explants derived from TRPV1 knockout mice [2,5,6]. Thus,


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