The Sensory Coding of Warm Perception

Abstract

Highlights d Mice, like humans, perceive forepaw warming (R1 C) and discriminate warm from cool d Warm-activated and warm-silenced polymodal C-fibers both signal forepaw warming d Mice lacking the cool-sensitive ion channel TRPM8 are unable to perceive warm d The inability to perceive warm is associated with loss of warm-silenced C-fibers

Neuronal hyperexcitability is a DLK-dependent trigger of herpes simplex virus reactivation that can be induced by IL-1

“…Although there is no direct evidence as yet for neuronal excitability inducing reactivation in an in vivo model, a commonly used trigger for HSV reactivation, axotomy, can directly induce hyperexcitability and also result in IL-1β release from satellite glial cells ( Hanani and Spray, 2020 ). Thermal stress is used as an in vivo trigger of HSV reactivation ( Sawtell and Thompson, 1992 ), which can also cause increased neuronal firing of nociceptor sensory neurons ( Paricio-Montesinos et al, 2020 ). IL-6, which is also a known-inducer of neuronal hyperexcitability ( Vezzani and Viviani, 2015 ), has been linked to heat stress-induced HSV reactivation ( Noisakran et al, 1998 ).…”

TRPV1 is crucial for thermal homeostasis in the mouse by heat loss behaviors under warm ambient temperature

“…TRPV1 is not important for peripheral warm sensation; TRPV1 KO mice reveal normal heat avoidance between 40-50 °C by two-plate preference tests 22 and normal warm sensation between 32~42 °C by goal-directed thermal perception task 23 . Moreover, triple KO animals of TRPV1, TRPM2, TRPM3 could learn to report warming stimuli of 32~42 °C and sense small increase of warming stimuli 23 . Central injection of TRPV1 agonist is well known to induce hypothermia 19,29,30,37 .…”

“…Thus, both peripheral and central TRPV1 have been well known to be concerned with thermal homeostasis by lowering body temperature. But, the evidence that TRPV1 lacks the importance for peripheral warm sensation [21][22][23] rise questions what is the function of TRPV1 upon increase of acute ambient temperature. In the present study, core body temperature was significantly higher in TRPV1 KO mice than in WT mice upon exposure to 35.0 °C.…”

“…The ablation of TRPV1-expressing somatosensory neurons, but not TRPV1 gene, impairs avoidance to extrem heat in two-plate preference tests 22 . Moreover, TRPV1 KO mice and triple KO animals of TRPV1, TRPM2, TRPM3 are dispensable for warm sensation in a goal-directed thermal perception task 23 . Although TRPV1 has been shown to be obviously involved in body temperature regulation by pharmacological studies, the evidence that TRPV1 lacks the importance for peripheral warm sensation leads to the question whether TRPV1 is really necessary for thermal homeostasis in response to warm stimulation.…”

Keratinocytes are required for normal cold and heat sensation

“…Mus musculus and Rattus novegicus are members of the Muridae family that inhabit similar climates (Feng and Himsworth, 2014;Latham and Mason, 2004) and maintain similar core and skin temperatures. Both species exhibit similar reflexive and thermotactic behaviors when exposed to cold stimuli or environments, and ex vivo skin-nerve recordings have identified spontaneously active, low-threshold cool fibers and quiescent, high-threshold cold fibers (Joong Woo Leem et al, 1993;Koltzenburg et al, 1997;Paricio-Montesinos et al, 2020) in both species. To our knowledge, direct comparisons of behavioral and physiological cold responses between mouse and rat do not exist, but if completed, may reveal nuanced species differences that could be keratinocyte-mediated.…”