Inhibitory transmission in the basolateral amygdala.
Inhibitory transmission in the basolateral amygdala.
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DOI：
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发表时间：
1991
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.采用细胞内记录技术，记录杏仁核基底外侧核（BLA）神经元的突触抑制性突触后电位（IPSPs）。双极电极定位在终纹（ST）或杏仁核（LA）被用来引起突触反应的频率为0.25赫兹。2.两种具有IPSP成分的突触波形可以通过任一通路的电刺激来诱发：双相、兴奋性突触后电位（EPSP）、快IPSP（f-IPSP）波形和多相、EPSP、f-IPSP和随后的慢IPSP（s-IPSP）波形。任一波形的表达取决于刺激的部位。ST刺激诱发了类似数量的双相（45%）和多相（50%）突触反应。与此相反，刺激LA途径诱发主要（80%）多相突触反应。3. ST刺激引起的f-和s-IPSP的振幅在谷氨酸能的N-甲基-D-天冬氨酸（NMDA）拮抗剂（DL）-2-氨基-5-膦酰基戊酸（APV，50 μ M）存在下均降低，并被谷氨酸能的非NMDA拮抗剂6-氰基-7-硝基喹喔啉-2，3-二酮（CNQX，10 μ M）消除。与此相反，CNQX-抗性f-IPSP诱发LA刺激和取消随后加入荷包牡丹碱甲碘（BMI），γ-氨基丁酸（GABAA）受体拮抗剂，表明直接抑制BLA神经元的GABA能LA中间神经元。s-IPSPs和f-IPSPs对多巴胺能拮抗剂的敏感性表明存在对BLA神经元的前馈抑制。4. f-IPSP具有由与Cl-通道相连的GABAA受体介导的电位特征，即-70 mV的逆转电位、-60 mV时记录的膜电阻下降（13.5 M Ω）、BMI的阻断作用以及戊巴比妥钠（NaPB）的增强作用。5. s-IPSP与4.5 M Ω的电阻降低、-95 mV的逆转电位相关，并被2-羟基-萨氯芬（100 μ M）可逆性抑制（约66%），表明GABAB受体活化。6.与f-IPSP相关的大电阻变化，其与诱发EPSP的时间重叠，以及在BMI存在下自发和诱发爆发放电的发展表明，f-IPSP决定了BLA神经元兴奋性的主要状态。（400字处截断摘要）
1. Intracellular recording techniques were used to characterize synaptic inhibitory postsynaptic potentials (IPSPs) recorded from neurons of the basolateral nucleus of the amygdala (BLA). Bipolar electrodes positioned in the stria terminalis (ST) or lateral amygdala (LA) were used to evoke synaptic responses at a frequency of 0.25 Hz. 2. Two synaptic waveforms having IPSP components could be evoked by electrical stimulation of either pathway: a biphasic, excitatory postsynaptic potential (EPSP), fast-IPSP (f-IPSP) waveform, and a multiphasic, EPSP, f-IPSP, and subsequent slow-IPSP (s-IPSP) waveform. Expression of either waveform was dependent on the site of stimulation. ST stimulation evoked a similar number of biphasic (45%) and multiphasic (50%) synaptic responses. In contrast, stimulation of the LA pathway evoked mainly (80%) multiphasic synaptic responses. 3. Both the f- and s-IPSP elicited by ST stimulation could be reduced in amplitude in the presence of the glutamatergic, N-methyl-D-aspartate (NMDA) antagonist, (DL)-2-amino-5-phosphonovaleric acid (APV, 50 microM), and were abolished by the glutamatergic, non-NMDA antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM). In contrast, a CNQX-resistant f-IPSP was evoked with LA stimulation and abolished by subsequent addition of bicuculline methiodide (BMI), a gamma-aminobutyric acid (GABAA) receptor antagonist, suggesting direct inhibition of BLA neurons by GABAergic LA interneurons. The sensitivity of the s-IPSPs and the f-IPSPs to glutamatergic antagonists suggests the presence of feed-forward inhibition onto BLA neurons. 4. The f-IPSP possessed characteristics of potentials mediated by GABAA receptors linked to Cl- channels, namely, a reversal potential of -70 mV, a decrease in membrane resistance (13.5 M omega) recorded at -60 mV, a block by BMI, and potentiation by sodium pentobarbital (NaPB). 5. The s-IPSP was associated with a resistance decrease of 4.5 M omega, a reversal potential of -95 mV, and was reversibly depressed (approximately 66%) by 2-hydroxy-saclofen (100 microM), suggesting activation of GABAB receptors. 6. The large resistance change associated with the f-IPSP, its temporal overlap with evoked EPSPs, and the development of both spontaneous and evoked burst firing in the presence of BMI suggests that the f-IPSP determines the primary state of excitability in BLA neurons.(ABSTRACT TRUNCATED AT 400 WORDS)