棉酚对大鼠血睾屏障的影响

用30mg/kg体重的醋酸棉酚喂大白鼠,从服药的第3周,即发现曲细精管的电位差由34℃时的对照值4.75±1.39mV降为 3.63±0.79mV,并且失去了电位差-温度之间的线性关系.服药至第5周时,硝酸镧可透入基底膜,进入上皮内和部分支持细胞紧密连接结构;服药8周后,硝酸镧可透过支持细胞的紧密连接结构,同时该区排列变为不规则.提示棉酚可导致血睾屏障功能障碍,从而破坏精子发育环境,这可能是棉酚抑制精子生成的主要原因之一。     

ELECTROPHYSIOLOGICAL EVIDENCE FOR HYPERALGESIA IN THE PERIPHERAL NEUROPATHY

A peripheral neuropathy was produced in adult rats by placing loosely constrained ligature around the common sciatic nerve. At the ligature region of the nerve, demyelination developed. The postoperative behavior of these rats indicated that hyperalgesia and allodynia were produced. The electrical activity pattern of the damaged fibers was remarkably different from those of normal nerves: there were some abnormal spontaneous afferent firings from the injured fibers; multi-impulse responses of C-fiber to single shock was recorded; a lasting firing was elicited after the injured region was gently pressed or by oil drops at 40℃; an antidromic electric stimulus to the injured region, stimulations of L, sympathetic ganglion or systemic administration of noradrenalin, all caused an increase in on-goingspontaneous discharges of the injured fibers or brought the silent fibers into firing. Stimulation of the dorsal roots of the sciatic nerve produced no effect on their activities or caused a pause of the on-goi     

外周神经损伤引起痛觉过敏的神经生理学机制

本文是在坐骨神经髓鞘膜脱落,继而诱发相关肢体感受野痛觉过敏和感觉异常的外周神经病理模型上,记录到各类神经传入纤维自发高频或诱发的阵发性异常电活动。神经受伤区受到轻微的机械触压或温度改变的刺激都可诱发长时间的放电活动;中枢端的逆行性电刺激,交感神经链的刺激以及静脉注射去甲肾上腺素都可诱发出新的放电或增加自发的异常放电频率;电刺激受伤神经的背根成分则不影响或抑制放电;α受体阻断剂可消除异常放电。揭示交感神经的去甲肾上腺素释放是外周神经损伤后痛觉过敏和感觉异常的外周原因。     

Inhibitory Effect of Anisodamine on the Neuropathic Hyperalgesia Following Peripheral Nerve Injury(Ⅱ)

A peripheral neuropathy with hyperalgesia and allodynia was produced by loosely tying constrictive ligature around the left sciatic nerve of rats, i.v. injection of anisodamine 20mg/Kg abolished both neuropathic hyperalgesia responses to noxious radiant heat and ectopic discharges generated from the injured region of the nerve. Anisodanime applied either systemically or locally to the damaged area of the nerve not only ceased the spontaneous ectopic discharges recorded from A_β to C fibers but also blocked the afferent ectopic discharge elicited by K~+ channel blocker, noradrenaline, Ca~(2+) or antidromic stimulation of sciatic nerve proximal to the injured nerve area. The experiments indicated that anisodamine probably possessed a calcium channel blocker-like activity and produced selective block of the new channels in the injured area. It is suggested that anisodamine may be a candidate therapeutic agent in relieving hyperalgesia and allodynia following nerve injury.     

延脑下部单胺类神经元及其神经介质对脊髓痛敏神经元活动的影响

在70个猫的脊髓背角痛敏神经元和5个脊髓交感节前神经元上,观察到:1.外源性地电泳去甲肾上腺素(NA),可以明显地抑制痛敏神经元的诱发或自发放电.刺激延脑下部的去甲肾上腺能Al核团,或注射NA的释放剂苯丙胺,或针刺“足三里”都可获得与电泳NA相类似的结果;2.5-羟色胺(5-HT)对痛敏神经元的诱发性痛放电有抑制作用,其作用类似NA,但常能增强其自发放电;3.脊髓交感节前神经元对上述因素的反应也类同于痛敏神经元;4.电泳NA,刺激Al核团,注射苯丙胺或刺激深部肌肉组织均可兴奋痛抑制神经元的活动.提示下脑干的去甲肾上腺能神经核团,可能是构成脊髓痛反射活动的下行性负反馈通路的重要驿站.     

The Relationship Between New Ion Channels and Ectopic Discharges From a Region of Nerve Injury

Changes in ectopic discharges from axons in an injured nerve were examined while agents that interact with ion channels were applied to the site of the nerve injury. Tetraethylammonium (TEA) greatly facilitated spontaneous ectopic discharges or evoked ectopic firing in previously silent axons.Tetrodotoxin, an Na~+ channel blocker,completely blocked spontaneous discharges.Verapamil, La3~+, and Mn2~+, agents that interact with Ca2~+ channels,blocked spontaneous discharges and depressed the responses evoked by TEA, noradrenaline and high concentration of K~+.Increasing Ca2~+ levels facilitated ectopic discharges and this effect was blocked by La3~+ and Mn2~+. Normal axons (from uninjured nerves) were insensitive to all the effects seen in the axons from the injured nerve.These results suggest that following nerve injury the membrane of the regenerating sprout contains new ion channels, particularly Ca2~+ channels, anti that these channels are responsible for the generation of ectopic discharges.     

EFFECT OF GOSSYPOL ON THE POTENTIAL DIFFERENCE OF RAT SEMINIFEROUS TUBULES

The p.d. of the rat seminiferous tubules was 4.75±1.39 mV (lumen negative) at 35℃ and varied linearly with temperatures from 26 to 40℃.A depolarization of the seminiferous tubules was found in the rats administered with gossypol at the dosage of 30 mg/kg body weight for 3 weeks, the p.d. lowered to 3.63±0.79 mV at 35℃ and was independent of the changes of seminiferous tubules temperature. In the 5-week-gossypol-treatment group, the tracer penetrated not only the myoid cell layer, but also went beyond the tight junction complexes between Sertoli cells. The lanthanum appeared in the cleft surrounding spermatogonia. In the 8-week-gossypol-treatment group, the lanthanum was found in the adluminal compartment.It indicates that gossypol can cause a dysfunction of the Sertoli cells and blood-testis barrier and disturb a good physiological environment for the developing spermatecytes.     

神经损伤区新生离子通道与异常电活动的关系

本文报道在因慢性压迫而引起损伤并产生异常传入放电的神经纤维上,应用几种离子通道药物局部作用于神经损伤区或全身注射,观察受伤神经纤维传入电活动的变化。实验表明,在神经损伤后而产生异常传入电活动的背景上,K~+通道的阻断剂四乙胺(TEA)使异常放电频率明显增加;Na~+通道阻断剂河豚毒素(TTX)浸润神经损伤区使异常放电活动消失;Ca~(2+)通道阻断剂异搏定,或影响Ca~(2+)通道的Mn~(2+),La~(3+)离子,不但抑制自发的异常电活动,而且可阻止TEA,去甲肾上腺素(NA)或K~+在损伤区诱发的异常放电。相反,增加神经损伤区的Ca~(2+)浓度使放电增加。这些离子通道药物对神经损伤区的异常放电的易化或抑制作用与对正常传入神经纤维电活动的不敏感性迥然不同,提示神经损伤后发生的异常传入电活动与损伤区的轴突膜上新生离子通道有关,其中可能有新生的Ca~(2+)通道,并参与异常放电的产生。     

山茛菪碱对外周神经病理性痛觉过敏的抑制作用

在坐骨神经损伤诱发同侧后肢病理性痛觉异常的大鼠上,观察山莨菪碱对痛觉过敏行为和神经异位电活动的影响,发现山莨菪碱具有明显对抗痛觉异常的作用,腹腔一次注射可持续4天抑制痛觉过敏并转变痛觉过敏为痛觉迟钝;神经受伤区局部应用或静脉注射山莨菪碱不但可使Aβ至C类纤维的自发异位传入放电消失,还可阻止局部应用K~+通道阻断剂,去甲肾上腺素(NA),Ca~(2+)或对神经损伤区逆行性电刺激而诱发的异位传入性放电。实验证明,山莨菪碱的这种抗痛觉过敏作用主要是通过类似Ca~(2+)通道阻断剂性质并选择性地作用于神经损伤区的新生离子通道上。提示山莨菪碱可能作为缓解神经损伤性的痛觉过敏和感觉异常的药物。