摘要
外源性Ca^(2+)及Ca^(2+)通道阻断剂异搏定(verapamil)和硝酸镧(La(NO_?)_?)作用于神经脱髓鞘膜区,均可影响异常的神经冲动。5mmol/L Ca^(2+)不能使受损神经异常放电频率改变,10～20mmol/L Ca^(2+)总能引起兴奋效应,40mmol/L Ca^(2+)则可使异常电活动频率降低。静脉或局部应用异搏定不但可抑制受损神经自发性异常电活动,还可阻断四乙胺(TEA)诱发的电活动。La^(?)也可降低受损神经异常放电频率。而Ca^(2+)、异搏定及La^(?)作用于正常神经干,并不影响其正常传导与电活动。提示神经损伤区轴突膜上形成了Ca^(2+)通道,而来自损伤区的异常电活动与Ca^(2+)通道密切相关。
Peripheral nerve demyelination was produced in adult rats by placing looselyconstrictive ligatures around the comnon sciatic nerve. The postoperative behavior of these rats indicated that hyperalgesia, allodynia and possible spontaneous pain were produced. In the meantime, abnormal spontaneous afferent activities (ectopic firings)originating from the demyelinated region were recorded. Evidence showed that the application of Ga^(2+) and Ca^(2+) channel blockers modulated the abnormal activity of the injured nerve. Ga^(2+) facilitation was dependent on its concentration (in the range of 10～20mol/L), while 40mol/L Ca^(2+) always abolished firing. Verapamil, as well as La^(3+), applied locally or i. v. (for verapamil) not only strongly inhibited the spontaneous ectopic firings, but also blocked discharges elicited by tetraethylammonium. It is suggested that newly formed Ca^(2+) channels on the naked axolemma are largely responsible for the abnormal afferent activities following demyelination of the nerve.
出处
《中国医学科学院学报》
CAS
CSCD
北大核心
1992年第1期59-62,共4页
Acta Academiae Medicinae Sinicae
基金
卫生部重点课题基金
国家自然科学基金资助课题
关键词
神经传导
钙通道阻断剂
neural conduction
calcium channels
calcium channel blockers
