Yuka Terada
Kindai University
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Yuka Terada.
Journal of Neuroscience Research | 2015
Yuka Terada; Mayuko Fujimura; Sachiyo Nishimura; Maho Tsubota; Fumiko Sekiguchi; Atsufumi Kawabata
Hydrogen sulfide (H2S), formed by multiple enzymes, including cystathionine‐γ‐lyase (CSE), targets Cav3.2 T‐type Ca2+ channels (T channels) and transient receptor potential ankyrin‐1 (TRPA1), facilitating somatic pain. Pancreatitis‐related pain also appears to involve activation of T channels by H2S formed by the upregulated CSE. Therefore, this study investigates the roles of the Cav3.2 isoform and/or TRPA1 in pancreatic nociception in the absence and presence of pancreatitis. In anesthetized mice, AP18, a TRPA1 inhibitor, abolished the Fos expression in the spinal dorsal horn caused by injection of a TRPA1 agonist into the pancreatic duct. As did mibefradil, a T‐channel inhibitor, in our previous report, AP18 prevented the Fos expression following ductal NaHS, an H2S donor. In the mice with cerulein‐induced acute pancreatitis, the referred hyperalgesia was suppressed by NNC 55‐0396 (NNC), a selective T‐channel inhibitor; zinc chloride; or ascorbic acid, known to inhibit Cav3.2 selectively among three T‐channel isoforms; and knockdown of Cav3.2. In contrast, AP18 and knockdown of TRPA1 had no significant effect on the cerulein‐induced referred hyperalgesia, although they significantly potentiated the antihyperalgesic effect of NNC at a subeffective dose. TRPA1 but not Cav3.2 in the dorsal root ganglia was downregulated at a protein level in mice with cerulein‐induced pancreatitis. The data indicate that TRPA1 and Cav3.2 mediate the exogenous H2S‐induced pancreatic nociception in naïve mice and suggest that, in the mice with pancreatitis, Cav3.2 targeted by H2S primarily participates in the pancreatic pain, whereas TRPA1 is downregulated and plays a secondary role in pancreatic nociceptive signaling.
Handbook of experimental pharmacology | 2015
Yuka Terada; Atsufumi Kawabata
Hydrogen sulfide (H2S) formed by multiple enzymes including cystathionine-γ-lyase (CSE) targets Cav3.2 T-type Ca2+ channels (T-channels) and transient receptor potential ankyrin-1 (TRPA1). Intraplantar and intracolonic administration of H2S donors promotes somatic and visceral pain, respectively, via activation of Cav3.2 and TRPA1 in rats and/or mice. Injection of H2S donors into the plantar tissues, pancreatic duct, colonic lumen, or bladder causes T-channel-dependent excitation of nociceptors, determined as phosphorylation of ERK or expression of Fos in the spinal dorsal horn. Electrophysiological studies demonstrate that exogenous and/or endogenous H2S facilitates membrane currents through T-channels in NG108-15 cells and isolated mouse dorsal root ganglion (DRG) neurons that abundantly express Cav3.2 and also in Cav3.2-transfected HEK293 cells. In mice with cerulein-induced pancreatitis and cyclophosphamide-induced cystitis, visceral pain and/or referred hyperalgesia are inhibited by CSE inhibitors and by pharmacological blockade or genetic silencing of Cav3.2, and CSE protein is upregulated in the pancreas and bladder. In rats with neuropathy induced by L5 spinal nerve cutting or by repeated administration of paclitaxel, an anticancer drug, the neuropathic hyperalgesia is reversed by inhibitors of CSE or T-channels and by silencing of Cav3.2. Upregulation of Cav3.2 protein in DRG is detectable in the former, but not in the latter, neuropathic pain models. Thus, H2S appears to function as a nociceptive messenger by facilitating functions of Cav3.2 and TRPA1, and the enhanced function of the CSE/H2S/Cav3.2 pathway is considered to be involved in the pancreatitis- and cystitis-related pain and in neuropathic pain.
Pharmacology | 2017
Yuka Terada; Maho Tsubota; Hiiragi Sugo; Kohei Wakitani; Fumiko Sekiguchi; Kyoichi Wada; Mitsutaka Takada; Akira Oita; Atsufumi Kawabata
Transient receptor potential vanilloid-1 (TRPV1) expressed in nociceptors is directly phosphorylated and activated by protein kinase C, and involved in the signaling of pancreatic pain. On the other hand, Cav3.2 T-type Ca2+ channels expressed in nociceptors are functionally upregulated by phosphorylation with protein kinase A and also play a role in pancreatitis-related pain. Calcineurin, a phosphatase, negatively regulates various channel functions including TRPV1, and calcineurin inhibitor-induced pain syndrome by tacrolimus, a calcineurin inhibitor, used as an immunosuppressant, has been a clinical problem. We thus examined the effect of tacrolimus on pancreatitis-related pain in mice. Repeated treatment with cerulein caused referred hyperalgesia accompanying acute pancreatitis, which was unaffected by tacrolimus. Pancreatitis-related symptoms disappeared in 24 h, whereas the referred hyperalgesia recurred following the administration of tacrolimus, which was abolished by the blockers of TRPV1 but not T-type Ca2+ channels. Thus, tacrolimus appears to cause the TRPV1-dependent relapse of pancreatitis-related pain, suggesting the involvement of calcineurin in the termination of pancreatic pain.
Journal of Pharmacological Sciences | 2013
Yuka Terada; Mayuko Fujimura; Sachiyo Nishimura; Maho Tsubota; Fumiko Sekiguchi; Hiroyuki Nishikawa; Atsufumi Kawabata
Journal of Neuroimmune Pharmacology | 2017
Yuhei Irie; Maho Tsubota; Hiroyasu Ishikura; Fumiko Sekiguchi; Yuka Terada; Toshifumi Tsujiuchi; Keyue Liu; Masahiro Nishibori; Atsufumi Kawabata
principles and practice of constraint programming | 2017
Yuka Terada; Kyoichi Wada; Sachi Matsuda; Takeshi Kuwahara; Atsufumi Kawabata; Mitsutaka Takada; Takuya Watanabe; Seiko Nakajima; Takuma Sato; Osamu Seguchi; Masanobu Yanase; Norihide Fukushima; Takeshi Nakatani
principles and practice of constraint programming | 2018
Maya Takayoshi; Kyoichi Wada; Yuka Terada; Sachi Matsuda; Kazuki Nakagita; Akira Oita; Mitsutaka Takada; Aki Shionoiri; Haruki Sunami; Seiko Nakajima; Kensuke Kuroda; Takuma Sato; Osamu Seguchi; Masanobu Yanase; Norihide Fukushima
principles and practice of constraint programming | 2018
Kazuki Nakagita; Kyoichi Wada; Yuka Terada; Sachi Matsuda; Nobue Terakawa; Akira Oita; Mitsutaka Takada
European Journal of Drug Metabolism and Pharmacokinetics | 2018
Takaya Uno; Kyoichi Wada; Sachi Matsuda; Yuka Terada; Akira Oita; Atsushi Kawase; Mitsutaka Takada
European Journal of Clinical Pharmacology | 2018
Takaya Uno; Kyoichi Wada; Sachi Matsuda; Yuka Terada; Nobue Terakawa; Akira Oita; Satoshi Yokoyama; Atsushi Kawase; Kouichi Hosomi; Mitsutaka Takada