Excitatory transmission in the basolateral amygdala.
Excitatory transmission in the basolateral amygdala.
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DOI：
10.1152/jn.1991.66.3.999
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发表时间：
1991-09
影响因子：
2.5
通讯作者：
D. Rainnie;E. Asprodini;P. Shinnick‐Gallagher
中科院分区：
文献类型：
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作者：
D. Rainnie;E. Asprodini;P. Shinnick‐Gallagher
1. 从杏仁核基底外侧核（BLA）的神经元获得的细胞内电流钳记录用于表征通过刺激终纹（ST）或外侧杏仁核（LA）引发的突触后电位。利用非n-甲基-d -天冬氨酸（non-NMDA）拮抗剂6-氰-7-硝基-喹啉-2,3-二酮（CNQX）和NMDA拮抗剂(DL)-2-氨基-5-磷酸戊酸（APV）分析了谷氨酸受体亚型对兴奋性突触后电位（EPSPs）的贡献。2. 通过对瞬态电流注入的膜响应测定的BLA神经元的基本膜特性表明，在平均静息膜电位（RMP; -67.2 mV）时，输入电阻（RN）和膜充电时间常数（tau）接近最大值，且这两个值都随着膜超极化而降低，提示突触效能的内在调节。3. 对ST或LA刺激的反应包括EPSP，然后是快速抑制突触后电位（f-IPSP），或者是快速和随后的慢速ipsp （s-IPSP）。EPSP在本质上是分级的，随着刺激强度的增加，振幅增加，并且在注入直流电流后膜超极化。自发EPSP也可以作为离散事件或EPSP/IPSP波形进行观察。4. 在生理Mg2+浓度（1.2 mM）下，在平均RMP下，EPSP由双重、快速和缓慢的谷氨酸能成分组成。快速EPSP （f-EPSP）具有kainate/ ququalate受体激活的特征，即EPSP随着膜超极化而振幅增加，对NMDA受体拮抗剂APV（50微米）不敏感，并被非NMDA受体拮抗剂CNQX（10微米）阻断。相反，慢速epsp （s-EPSP）振幅随着膜超极化而下降，对CNQX不敏感（10微米），并被APV阻断（50微米），表明NMDA受体激活介导。5. 在CNQX存在的情况下（10微米），ST刺激诱发apv敏感的s-EPSP。相比之下，LA刺激诱发了f- epsp，随后加入双库兰（BMI； 30微米）阻断了f-IPSP，显示出apv敏感的s-EPSP在时间上重叠。这些数据表明，EPSP的振幅和持续时间部分是由伴随IPSP引起的膜电导分流决定的。6. CNQX或APV在BLA神经元中的超融合引起膜超极化，并阻断自发epsp和ipsp，提示这些化合物可能阻断细胞核内强直性兴奋性氨基酸（EAA）的释放，并在细胞核内发生一定程度的前馈抑制。（摘要删节为400字）
1. Intracellular current-clamp recordings obtained from neurons of the basolateral nucleus of the amygdala (BLA) were used to characterize postsynaptic potentials elicited through stimulation of the stria terminalis (ST) or the lateral amygdala (LA). The contribution of glutamatergic receptor subtypes to excitatory postsynaptic potentials (EPSPs) were analyzed by the use of the non N-methyl-D-aspartate (non-NMDA) antagonist, 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), and the NMDA antagonist, (DL)-2-amino-5-phosphonovaleric acid (APV). 2. Basic membrane properties of BLA neurons determined from membrane responses to transient current injection showed that at the mean resting membrane potential (RMP; -67.2 mV) the input resistance (RN) and time constant for membrane charging (tau) were near maximal, and that both values were reduced with membrane hyperpolarization, suggesting an intrinsic regulation of synaptic efficacy. 3. Responses to stimulation of the ST or LA consisted of an EPSP followed by either a fast inhibitory postsynaptic potential (f-IPSP) only, or by a fast- and subsequent slow-IPSP (s-IPSP). The EPSP was graded in nature, increasing in amplitude with increased stimulus intensity, and with membrane hyperpolarization after DC current injection. Spontaneous EPSPs were also observed either as discrete events or as EPSP/IPSP waveforms. 4. In physiological Mg2+ concentrations (1.2 mM), at the mean RMP, the EPSP consisted of dual, fast and slow, glutamatergic components. The fast-EPSP (f-EPSP) possessed characteristics of kainate/quisqualate receptor activation, namely, the EPSP increased in amplitude with membrane hyperpolarization, was insensitive to the NMDA receptor antagonist, APV (50 microM), and was blocked by the non-NMDA receptor antagonist, CNQX (10 microM). In contrast, the slow-EPSP (s-EPSP) decreased in amplitude with membrane hyperpolarization, was insensitive to CNQX (10 microM), and was blocked by APV (50 microM), indicating mediation by NMDA receptor activation. 5. In the presence of CNQX (10 microM), ST stimulation evoked an APV-sensitive s-EPSP. In contrast, LA stimulation evoked a f-IPSP, which when blocked by subsequent addition of bicuculline methiodide (BMI; 30 microM) revealed a temporally overlapping APV-sensitive s-EPSP. These data suggest that EPSP amplitude and duration are determined, in part, by the shunting of membrane conductance caused by a concomitant IPSP. 6. Superfusion of either CNQX or APV in BLA neurons caused membrane hyperpolarization and blockade of spontaneous EPSPs and IPSPs, suggesting that these compounds may act to block tonic excitatory amino acid (EAA) release within the nucleus, and that a degree of feed-forward inhibition occurs within the nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)