期刊
JOURNAL OF NEUROSCIENCE
卷 25, 期 35, 页码 7986-7992出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2393-05.2005
关键词
bradykinin; spinal cord; pain; synaptic transmission; glutamate; neuromodulator
资金
- NINDS NIH HHS [R01 NS039518, R01 NS038253, NS039518, K08 NS044139, R37 NS039518, R01 NS040698] Funding Source: Medline
Bradykinin, an inflammatory mediator, sensitizes nociceptor peripheral terminals reducing pain threshold. We now show that the B-2 kinin receptor is expressed in rat dorsal horn neurons and that bradykinin, a B-2-specific agonist, augments AMPA- and NMDA-induced, and primary afferent-evoked EPSCs, and increases the frequency and amplitude of miniature EPSCs in superficial dorsal horn neurons in vitro. Administration of bradykinin to the spinal cord in vivo produces, moreover, an NMDA-dependent hyperalgesia. We also demonstrate that nociceptive inputs result in the production of bradykinin in the spinal cord and that an intrathecal B-2-selective antagonist suppresses behavioral manifestations of central sensitization, an activity-dependent increase in glutamatergic synaptic efficacy. Primary afferent-evoked central sensitization is, in addition, reduced in B-2 receptor knock-out mice. We conclude that bradykinin is released in the spinal cord in response to nociceptor inputs and acts as a synaptic neuromodulator, potentiating glutamatergic synaptic transmission to produce pain hypersensitivity.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据