Shul'gina G I
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.
Neurosci Behav Physiol. 1998 May-Jun;28(3):278-84. doi: 10.1007/BF02462957.
Administration of sodium nitrite (an NO-generating preparation) doses of 11 mg/kg to rabbits was followed by motor disinhibition, with increases in myogram amplitudes in responses to nonreinforced flashes presented on a background of continuous illumination which served as a conditioned inhibitory stimulus; these changes appeared 1-1.5 h after administration and lasted throughout the 4-h observation period. After sodium nitrite doses of 5.5 mg/kg, responses to conditioned inhibition showed only a tendency to motor disinhibition. These results can be explained in terms of the ability of sodium nitrite to inhibit the function of GABAergic receptors, as development of internal inhibition is accompanied by increased inhibitory hyperpolarization processes in which the GABAergic mediator system is involved. The lower and higher sodium nitrite doses produced no increases in myogram amplitudes in responses to combinations of flashes of light and pain reinforcement, as occurred when these stimuli were presented to controls.
给兔子注射剂量为11毫克/千克的亚硝酸钠(一种产生一氧化氮的制剂)后,出现运动抑制,在持续光照背景下(作为条件性抑制刺激)对非强化闪光的反应中,肌电图振幅增加;这些变化在给药后1 - 1.5小时出现,并在整个4小时的观察期内持续。注射剂量为5.5毫克/千克的亚硝酸钠后,对条件性抑制的反应仅表现出运动抑制的趋势。这些结果可以用亚硝酸钠抑制γ-氨基丁酸能受体功能来解释,因为内抑制的发展伴随着抑制性超极化过程的增加,而γ-氨基丁酸能介质系统参与其中。与给予对照组这些刺激时的情况不同,较低和较高剂量的亚硝酸钠并未使对光闪光和疼痛强化组合的反应中肌电图振幅增加。