Gabriel S, Grützmann R, Lemke M, Gabriel H J, Henklein P, Davidowa H
Department of Neurophysiology, Institute of Physiology, Humboldt University Berlin, Berlin, Germany.
Brain Res Bull. 1996;39(6):381-9. doi: 10.1016/0361-9230(96)00030-5.
The interaction of sulfated cholecystokinin (CCK-8S) with excitatory amino acids (EAA) was studied on single units of the dorsal lateral geniculate nucleus (dLGN), the dentate gyrus, and the hippocampal CA3 region in rats anaesthetized with urethane. lontophoretic co-administration of small, individually ineffective currents of CCK-8S and kainic acid or N-methyl-D-aspartate repeatedly elicited an increase of the discharge rate in nearly all geniculate and half of the dentate neurons but not in those of the CA3 region. The effect could be reduced by the CCKB receptor antagonist PD 135,158 more often than by the CCKA antagonist KL 1001. The increased firing due to co-administration of CCK and kainate could also be suppressed by the non-NMDA antagonist CNQX but not by the NMDA antagonists CPP or AP-5, which were otherwise able to prevent the neuron from responding to co-administration of CCK and NMDA. It is suggested that in distinct brain regions the effectivity of the "low level" EAA transmission may be enhanced by small amounts of CCK-8S. This is thought to be mediated by a coactivation of CCK and EEA receptors.
在用乌拉坦麻醉的大鼠的背外侧膝状核（dLGN）、齿状回和海马CA3区的单个神经元上，研究了硫酸化胆囊收缩素（CCK-8S）与兴奋性氨基酸（EAA）的相互作用。通过离子电泳联合给予小剂量、单独无效的CCK-8S和 kainic 酸或 N-甲基-D-天冬氨酸的电流，几乎在所有膝状神经元和一半的齿状神经元中反复引起放电率增加，但在CA3区神经元中未出现这种情况。CCKB受体拮抗剂PD 135,158比CCKA拮抗剂KL 1001更常能降低这种效应。联合给予CCK和kainate引起的放电增加也能被非NMDA拮抗剂CNQX抑制，但不能被NMDA拮抗剂CPP或AP-5抑制，否则它们能够阻止神经元对联合给予CCK和NMDA的反应。提示在不同脑区，少量CCK-8S可能增强“低水平”EAA传递的有效性。这被认为是由CCK和EEA受体的共同激活介导的。
