Houghton A K, Gorringe C M, Clarke R W
Department of Physiology and Environmental Science, University of Nottingham, Loughborough, Leics, U.K.
Neuroscience. 1995 Nov;69(1):241-8. doi: 10.1016/0306-4522(95)00242-b.
In the decerebrated and spinalized rabbit, reflexes evoked in the gastrocnemius medialis muscle nerve by electrical stimulation of teh sural nerve are suppressed after blockade of NK-tachykinin receptors. This observation suggests that endogenous tachykinins tonically enhance transmission between sural nerve afferents and gastrocnemius motoneurons. In the present study we have investigated some possible sources of this tachykininergic tone. Electrical stimulation of the sural nerve at 1 Hz, as used in our previous investigation, leads to increased gastrocnemius reflex responses with successive stimuli. We examined reflexes evoked by pairs of sural stimuli separated by intervals of 10-1000 ms, and found that responses to the second stimuli of such pairs were significantly enhanced at intervals from 50 to 500 ms. Treatment with the NK receptor antagonist CP-99,994 [(+)-(2S,3S)-3-(2-methoxybenzylamino)-2-phenylpiperidine; 1 mg/kg, i.v.] reduced gastrocnemius reflex responses per se, but did not alter the facilitatory effects of pairing sural stimuli. Subsequent treatment with the glutamate N-methyl-D-aspartate receptor blocker dizocilpine (0.5 mg/kg, i.v.) further reduced reflex responses and abolished paired-pulse facilitation. In a second set of experiments, rabbits were prepared so that reflexes could be studied with minimal surgical preparation of the hindlimb. Reflex responses recorded in this way were enhanced by treatment with CP-99,994 (up to 1 mg/kg, i.v.). Subsequent administration of the opioid receptor antagonist naloxone (1-10 microg/kg, i.v.) increased reflexes, as seen previously in surgically-prepared animals. These data show that tachkininergic modulation of spinal reflexes in the rabbit results from the nociceptive input arising from surgical preparation of the leg. In contrast, tonic opioidergic inhibition of reflexes is not substantially dependent on such input.
在去大脑和脊髓横断的兔中，电刺激腓肠神经在腓肠内侧肌神经诱发的反射，在阻断NK-速激肽受体后受到抑制。这一观察结果提示内源性速激肽持续增强腓肠神经传入纤维与腓肠肌运动神经元之间的传递。在本研究中，我们调查了这种速激肽能紧张性的一些可能来源。如我们先前研究中那样，以1Hz频率电刺激腓肠神经，会使连续刺激时腓肠肌反射反应增强。我们检查了间隔10 - 1000ms的成对腓肠神经刺激诱发的反射，发现对此类成对刺激中第二个刺激的反应在50至500ms的间隔时显著增强。用NK受体拮抗剂CP - 99,994 [（+） - （2S，3S） - 3 - （2 - 甲氧基苄基氨基） - 2 - 苯基哌啶；1mg/kg，静脉注射]处理本身会降低腓肠肌反射反应，但不改变成对腓肠神经刺激的易化作用。随后用谷氨酸N - 甲基 - D - 天冬氨酸受体阻断剂地佐环平（0.5mg/kg，静脉注射）处理进一步降低了反射反应并消除了双脉冲易化。在第二组实验中，制备兔以便能在对后肢进行最小限度手术准备的情况下研究反射。以这种方式记录的反射反应经CP - 99,994（高达1mg/kg，静脉注射）处理后增强。随后给予阿片受体拮抗剂纳洛酮（1 - 10μg/kg，静脉注射）使反射增强，如先前在手术制备的动物中所见。这些数据表明，兔脊髓反射的速激肽能调制源于腿部手术准备产生的伤害性传入。相反，反射的紧张性阿片能抑制在很大程度上不依赖于此类传入。
