Li H, Rogawski M A
Neuronal Excitability Section, Epilepsy Research Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1408, USA.
Neuropharmacology. 1998 Oct-Nov;37(10-11):1279-86. doi: 10.1016/s0028-3908(98)00109-9.
A non-NMDA and non-AMPA receptor mediated excitatory synaptic response was identified in intracellularly recorded basolateral amygdala (BLA) neurons in an in vitro slice preparation. Synaptic potentials were evoked by stimulation of either the external capsule (EC) or basal amygdala (BA). NMDA and GABA(A) receptors were blocked by inclusion of 100 microM (+/-)-2-amino-5-phosphonopentanoic acid and 10 microM bicuculline in the perfusion solution. The AMPA receptor-selective allosteric antagonists GYKI 52466 (50 microM) and GYKI 53655 (50 microM) partially suppressed depolarizing synaptic responses evoked by single shock EC stimulation, but fully blocked synaptic responses evoked by BA stimulation. In recordings carried out in the presence of the AMPA receptor antagonists, EC stimulation with pulse trains (5-8 pulses at 50-100 Hz) evoked a large increase in the amplitude of synaptic responses. The AMPA receptor-independent component of the train-induced synaptic response had a null potential near 0 mV. Such AMPA receptor-independent, train-evoked synaptic responses were largely blocked by the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM; 85 +/- 4%). In addition, the responses were blocked by the GluR5-selective kainate receptor antagonist LY293558 (10 microM; 95 +/- 2%). These results indicate that a component of the EC (but not the BA) synaptic response is mediated by kainate receptors containing the GluR5 subunit.
在体外脑片制备中，对细胞内记录的基底外侧杏仁核（BLA）神经元进行研究时，发现了一种非NMDA和非AMPA受体介导的兴奋性突触反应。通过刺激外囊（EC）或基底杏仁核（BA）诱发突触电位。在灌流液中加入100μM（±）-2-氨基-5-膦酰基戊酸和10μM荷包牡丹碱，可阻断NMDA和GABA（A）受体。AMPA受体选择性变构拮抗剂GYKI 52466（50μM）和GYKI 53655（50μM）部分抑制了单次电击EC刺激诱发的去极化突触反应，但完全阻断了BA刺激诱发的突触反应。在存在AMPA受体拮抗剂的记录中，用脉冲串（50 - 100Hz，5 - 8个脉冲）刺激EC会使突触反应幅度大幅增加。串刺激诱发的突触反应中不依赖AMPA受体的成分在0mV附近具有零电位。这种不依赖AMPA受体的串刺激诱发的突触反应在很大程度上被AMPA/海人藻酸受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮（20μM；85±4%）阻断。此外，这些反应也被GluR5选择性海人藻酸受体拮抗剂LY293558（10μM；95±2%）阻断。这些结果表明，EC（而非BA）突触反应的一个成分是由含有GluR5亚基的海人藻酸受体介导的。
