浏览全部资源
扫码关注微信
中国中医研究院针灸研究所
纸质出版日期:1986
移动端阅览
朱丽霞, 黎春元, 吉长福, 等. 脊髓r-氨基丁酸参与针刺镇痛[J]. 针刺研究, 1986,(2):126-131.
JNVOLVFMENT OF GABA IN ACUPUNCTURE ANALGESIA[J]. Acupuncture research, 1986, (2): 126-131.
r-氨基丁酸(GABA)是广泛分布于中枢神经系统内的抑制性神经递质
其在针刺镇痛中的作用早已为人们注视
但所获结果很不一致。有报道说明电针镇痛时脑内GABA增多
而细胞外 GABA含量的增多与针刺镇痛有关
但范少光等研究结果是脑内GABA能系统具有对抗针刺镇痛作用
可能与给药部位、途径及方法以及测痛方法等不同有关
并说明GABA的作用是复杂的
有待进一步研究。脊髓背角胶状质含有GABA能中间神经元
可与初级传入末梢形成轴-轴突触
也可与伤害感受种经元形成轴-树突触
脊髓水平的GABA可能在痛觉调制与针刺It is well known that many GABA-ergic interneurons are located in substantia gelatinosa and synaptically connect with the primary afferent terminals and projecting neurons
and they may play an important role in pain modulation. In the present study
the role of the α-aminobutyric acid (GABA) in the inhibition of spinal transmission of nociceptive info- rmation produced by acupuncture was observed by using iontophoretic bi- cuculline
an antagonist of GABA
at dorsal horn neurons of rats. Iontophoretic GABA-induced inhibitory effects on spontaenous disch- arges and nociceptive responses were partially reversed by iontophoretic bicuculline with ejecting current of 60 nA and 180 nA respectively. However
the inhibitory after-effect lasting for 20 minutes on the nociceptive responses of dorsal horn neurons produced by acupuncture app- lied at bilateral acupoints for 5 minutes couldn't be antagonized by ion- tophoretic bicuculline with current of 120-180 nA(n=10
P>0.05). In another series of experiments
immediately (15ms) after cessation of acupuncture for
500 ms the nociceptive response was reduced to 77.5% of the control value
while the inhibitory effect of acupuncture on the nociceptive response did not occur if the bicuculline had been administe- red iontophoretically. It means that the immediate inhibitory effects of acupuncture can be almost completely blocked by iontophoretic bicuculline. It is of statistically significance (n=10
P<0.001). It is referred that GABA may be involved in the spinal segmental inhibition produced by acupuncture.
0
浏览量
0
下载量
12
CNKI被引量
关联资源
相关文章
相关作者
相关机构