Kimiaki Katanosaka

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Unaccustomed strenuous exercise that includes lengthening contraction (LC) often causes delayed-onset muscle soreness (DOMS), a kind of muscular mechanical hyperalgesia. The substances that induce this phenomenon are largely unknown. Peculiarly, DOMS is not perceived during and shortly after exercise, but rather is first perceived after approximately 1 d.(More)
Bradykinin (BK), a major inflammatory mediator, excites and sensitizes nociceptor neurons/fibers, thus evoking pain and hyperalgesia. The cellular signaling mechanisms underlying these actions have remained unsolved, especially in regard to the identity of channels that mediate acute excitation. Here, to clarify the contribution of transient receptor(More)
Transient receptor potential V3 (TRPV3) and TRPV4 are heat-activated cation channels expressed in keratinocytes. It has been proposed that heat-activation of TRPV3 and/or TRPV4 in the skin may release diffusible molecules which would then activate termini of neighboring dorsal root ganglion (DRG) neurons. Here we show that adenosine triphosphate (ATP) is(More)
Immunosuppressant drug FK506, which is widely used for the treatment of atopic dermatitis, has multiple actions on the nervous system. In order to elucidate the mechanisms underlying transient burning sensation elicited by topical application of FK506 to the skin of atopic patients, we investigated if FK506 directly activates sensory neurons and fibers, or(More)
Unaccustomed strenuous exercise that includes lengthening contraction (LC) often causes tenderness and movement related pain after some delay (delayed-onset muscle soreness, DOMS). We previously demonstrated that nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) are up-regulated in exercised muscle through up-regulation of(More)
Bradykinin is an endogenous nonapeptide known to induce pain and hyperalgesia to heat and mechanical stimulation. Correspondingly, it excites nociceptors in various tissues and sensitizes them to heat, whereas sensitizing effect on the mechanical response of nociceptors is not well established. Protein kinase C and TRPV1 contribute to the sensitizing(More)
Ischaemia, inflammation, and exercise lead to tissue acidosis, which induces pain and mechanical hyperalgesia. Corresponding to this, enhanced thin-fibre afferent responses to mechanical stimulation have been recorded in vitro at low pH. However, knowledge about how this sensitization by low pH occurs is lacking. In this study, we found that all three types(More)
The heart has a dynamic compensatory mechanism for haemodynamic stress. However, the molecular details of how mechanical forces are transduced in the heart are unclear. Here we show that the transient receptor potential, vanilloid family type 2 (TRPV2) cation channel is critical for the maintenance of cardiac structure and function. Within 4 days of(More)
Immature Drosophila rhodopsin is N-glycosylated, but undergoes complete deglycosylation during the process of protein maturation. In order to elucidate the site of glycosylation and its role in rhodopsin synthesis, we investigated the in vitro and in vivo synthesis of rhodopsin whose putative N-glycosylation sites (Asn-20 and Asn-196) were replaced by(More)
Adenosine triphosphate (ATP) is well known to be released from injured or inflamed tissues, and to excite/sensitize nociceptors in response to heat and mechanical stimulation. To determine whether muscle releases ATP when it is compressed, we measured ATP release from the extensor digitorum longus muscle (EDL). In addition, we investigated whether there is(More)