|1.||Ji, Yong-Hua: 11 articles (06/2015 - 10/2003)|
|2.||Jiang, Feng: 5 articles (06/2015 - 11/2010)|
|3.||Fu, Jin: 4 articles (06/2015 - 10/2013)|
|4.||Hua, Li-Ming: 4 articles (02/2014 - 11/2010)|
|5.||Jiao, Yun-Lu: 3 articles (06/2015 - 10/2013)|
|6.||Liu, Tong: 3 articles (06/2015 - 01/2006)|
|7.||Zhao, Rong: 3 articles (01/2015 - 12/2005)|
|8.||Feng, Yi-Jun: 2 articles (06/2015 - 01/2015)|
|9.||Tao, Jie: 2 articles (06/2015 - 01/2015)|
|10.||Ji, Yonghua: 2 articles (06/2015 - 10/2010)|
06/25/2015 - "Our results indicate that both 5-HT3AR signaling pathway and microglia are activated in the process of induction and maintenance of BmK I-induced pain nociception. "
06/25/2015 - "However, the underlying mechanism of 5-HT3R on BmK I-induced pain remains unclear. "
06/25/2015 - "Spinal 5-HT3AR contributes to BmK I-induced inflammatory pain in rats."
06/01/2015 - "In conclusion, our data clearly demonstrated that BmK I modulated Nav1.8 remarkably, suggesting BmK I as a valuable probe for studying Nav1.8. And Nav1.8 is an important target related to BmK I-evoked pain. "
06/25/2015 - "Subcutaneous injection of BmK I could be adopted to well establish a novel pain model. "
06/01/2009 - "These results demonstrated that BmK I could target rNav1.2a and induce the I(NaP) by preventing the development of slow inactivation and deactivation from the open-state, leading to the enhancement of membrane excitability, which may be involved in the BmK I-induced epilepsy."
01/01/2006 - "These results indicated that the rat hippocampus is a susceptible target for the proconvulsant effects of BmK I, and the induction of epileptic seizures may be ascribed to the modulation of BmK I on the inactivation of voltage-gated sodium channels distributing in the rat hippocampal neurons."
01/01/2006 - "The epileptic seizures induced by BmK I, a modulator of sodium channels."
01/01/2006 - "In the present study, the susceptibility to rat epileptic seizures induced by the intrahippocampal administration of BmK I, a modulator of sodium channels purified from the venom of Chinese scorpion, has been investigated. "
02/01/2014 - "Intrathecal administration of deforolimus, a specific inhibitor of mTOR, attenuated BmK I-induced pain responses (spontaneous flinching, paroxysmal pain-like behavior, and mechanical hypersensitivity). "
10/25/2013 - "The unilateral thermal and bilateral mechanical pain hypersensitivity of rat induced by BmK I was suppressed in a dose-dependent manner following pretreatment with SB203580 (a specific inhibitor of p-p38). "
01/01/2013 - "In addition, intrathecal (i.t.) injection of rapamycin - a specific inhibitor of mTOR - was observed to result in the reduction of spontaneous pain responses and the attenuation of unilateral thermal and bilateral mechanical hypersensitivity elicited by BmK I. Thus, these results indicate that the mTOR signaling pathway is mobilized in the induction and maintenance of pain-activated hypersensitivity. "
06/25/2015 - "Animal behavioral testing, RT-PCR and Western blotting were used to yield the following results: first, intraplantar (i.pl.) injection of BmK I (10 μg) induced elevated mRNA and protein levels of 5-HT3AR in bilateral L4-L5 spinal cord; Second, intrathecal (i.t.) injection of ondansetron (a specific antagonist of 5-HT3AR) reduced spontaneous pain responses, attenuated unilateral thermal and bilateral mechanical hypersensitivity elicited by BmK I; Microglia could be activated by BmK I (i.pl.) in both sides of L4-L5 spinal cord, and this effect was reversed by intrathecal pre-treatment with 5-HT3AR antagonist. "
10/25/2013 - "Intraplantar (i.pl.) injection of BmK I, a receptor site 3-specific modulator of voltage-gated sodium channels (VGSCs) from the venom of scorpion Buthus martensi Karsch (BmK), was shown to induce long-lasting and spontaneous nociceptive responses as demonstrated through experiments utilizing primary thermal and mirror-imaged mechanical hypersensitivity with different time course of development in rats. "
06/25/2015 - "Meanwhile, our results suggest that the neuronal 5-HT3AR may communicate with microglia indirectly via CX3CL1 which is involved in regulating the BmK I-induced hyperalgesia and sensitization. "
12/23/2005 - "It was further suggested that a combined effect of BmK I including inhibiting the inactivation of TTX-S and TTX-R channels, accelerating activation and decreasing the activation threshold of TTX-S channels, might produce a hyperexcitability of small DRG neurons, and thus contribute to the BmK I-induced hyperalgesia."
10/15/2010 - "BmK I, a site-3-specific modulator of VGSCs (voltage-gated sodium channels) from the Chinese scorpion Buthus martensi Karsch, can induce spontaneous nociception and hyperalgesia and generate epileptiform responses in rats, which is attributed to the modulation of VGSCs in the neural system. "
01/01/2015 - "BmK I, a site-3-specific modulator of voltage-gated sodium channels (VGSCs), causes pain and hyperalgesia in rats, while BmK IT2, a site-4-specific modulator of VGSCs, suppresses pain-related responses. "
|1.||Sodium Channels (Sodium Channel)
|4.||Scorpion Venoms (Scorpion Venom)
|9.||Messenger RNA (mRNA)
|10.||Morphine (MS Contin)