Zobrazeno 1 - 10
of 30
pro vyhledávání: '"Ko Zushida"'
Autor:
Premal Shah, Charles Hevi, Gleb P. Shumyatsky, John S. Favate, Stephanie E. Sillivan, Courtney A. Miller, Ileana Fuentes, Steve Buyske, Noriko K. Goldsmith, Eric R. Kandel, Akinori Nishi, Ko Zushida, Yoshikazu Morishita, Shusaku Uchida
Fear extinction is an adaptive behavioral process critical for organism’s survival, but deficiency in extinction may lead to PTSD. While the amygdala and its neural circuits are critical for fear extinction, the molecular identity and organizationa
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::7aec694fe94708898adc4d72b35eac6c
https://doi.org/10.1101/2020.12.31.424996
https://doi.org/10.1101/2020.12.31.424996
Autor:
Guillaume Martel, Charles Hevi, Alexandra Wong, Ko Zushida, Shusaku Uchida, Gleb P Shumyatsky
Publikováno v:
PLoS ONE, Vol 7, Iss 2, p e30942 (2012)
Extinction is an integral part of normal healthy fear responses, while it is compromised in several fear-related mental conditions in humans, such as post-traumatic stress disorder (PTSD). Although much research has recently been focused on fear exti
Externí odkaz:
https://doaj.org/article/94fed4053aae4cd4a1554078f7af802a
Autor:
Ko Zushida, Tomohiro Kabuta, Kazuyuki Yamada, Keiji Wada, Masayuki Sekiguchi, Mikako Sakurai, Satoshi Nagamine
Publikováno v:
European Journal of Neuroscience. 27:691-701
Overexpression of ubiquitin C-terminal hydrolase L1 (UCH-L1) in mice rescues amyloid beta-protein-induced decreases in synaptic plasticity and memory. However, the physiological role of UCH-L1 in the brain is not fully understood. In the present stud
Publikováno v:
The Journal of Neuroscience. 27:158-166
Contextual fear memory is attenuated by the re-exposure of mice to the context without aversive stimulus. This phenomenon is called extinction. Here, we report that a potentiator of AMPA receptors, 4-[2-(phenylsulfonylamino)ethylthio]-2,6-difluorophe
Publikováno v:
European Journal of Pharmacology. 453:209-215
The antinociceptive effects of pinacidil, an adenosine triphosphate (ATP)-sensitive K(+)i (K(ATP)) channel opener, were examined using the tail-flick test in non-diabetic and diabetic mice. Pinacidil i.c.v. produced dose-dependent antinociception in
Publikováno v:
Brain Research. 948:17-23
We examined the effect of diabetes on the fenvalerate-induced nociceptive response in mice. The intrathecal (i.t.) or intraplantar (i.pl.) injection of fenvalerate, a sodium channel activator, induced a characteristic behavioral syndrome mainly consi
Publikováno v:
European Journal of Pharmacology. 416:95-99
We examined the role of cholecystokinin in the reduction of endomorphin-2-induced antinociception in diabetic mice. Endomorphin-1 (1–10 μg, i.c.v.) and endomorphin-2 (3–30 μg, i.c.v.) dose dependently inhibited the tail-flick response in non-di
Publikováno v:
Japanese Journal of Pharmacology. 86:336-341
The intrathecal injection of fenvalerate, a sodium channel activator, at doses of 0.01 to 3 microg, dose-dependently induced the duration of a characteristic behavioral syndrome mainly consisting of reciprocal hind limb scratching directed towards ca
Publikováno v:
Life Sciences. 68:91-97
The antinociceptive effect of vitamin K2 (menatetrenone) in mice was examined using tail-flick and formalin test. Menatetrenone at doses of 10, 50 and 100 mg/kg, i.p. produced a dose-dependent and significant inhibition of the tail-flick response in
Publikováno v:
European Journal of Pharmacology. 391:91-96
The antinociceptive effects of endomorphin-1 and endomorphin-2, endogenous mu-opioid receptor agonists, were examined using the tail-flick test in non-diabetic and diabetic mice. Endomorphin-1, at doses of 1 to 10 microg, i.c.v., and endomorphin-2, a