De Bonnel G, De Montigny C
Eur J Pharmacol. 1983 Sep 16;93(1-2):45-54. doi: 10.1016/0014-2999(83)90029-8.
Low intravenous doses of two benzodiazepines, lorazepam and diazepam, antagonized the activation of dorsal hippocampus CA1 pyramidal neurons by kainate to a greater extent than the activations produced by glutamate and acetylcholine. A similar effect was obtained with microiontophoretic application of two water-soluble benzodiazepines, flurazepam and chlordiazepoxide. Chlorpromazine and phenobarbital did not exert any consistent effect on kainate-induced activation. RO 15-1788, a benzodiazepine antagonist, prevented the effect of lorazepam on kainate-induced activation. The regional selectivity of this effect was indicated by the failure of lorazepam to produce a sustained reduction of kainate action in the CA3 hippocampal region and in the cerebral cortex. This selective antagonism by benzodiazepines of the excitation of selected limbic neurons via 'kainate-sensitive' receptors might be related to their anxiolytic effect.
静脉注射低剂量的两种苯二氮䓬类药物，劳拉西泮和地西泮，对海人酸激活背侧海马CA1锥体神经元的拮抗作用，比谷氨酸和乙酰胆碱所产生的激活作用更强。通过微量离子电泳施加两种水溶性苯二氮䓬类药物，氟西泮和氯氮卓，也获得了类似的效果。氯丙嗪和苯巴比妥对海人酸诱导的激活作用没有产生任何一致的影响。苯二氮䓬类拮抗剂RO 15-1788可阻止劳拉西泮对海人酸诱导激活的作用。劳拉西泮未能在海马CA3区和大脑皮层持续降低海人酸的作用，这表明了这种作用的区域选择性。苯二氮䓬类药物通过“海人酸敏感”受体对选定边缘神经元兴奋的这种选择性拮抗作用，可能与其抗焦虑作用有关。
