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基底外侧杏仁核中的抑制性传递。

Inhibitory transmission in the basolateral amygdala.

作者信息

Rainnie D G, Asprodini E K, Shinnick-Gallagher P

机构信息

Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston 77550.

出版信息

J Neurophysiol. 1991 Sep;66(3):999-1009. doi: 10.1152/jn.1991.66.3.999.

Abstract
  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)
摘要
  1. 采用细胞内记录技术对从杏仁核基底外侧核(BLA)神经元记录到的突触抑制性突触后电位(IPSP)进行特征描述。将双极电极置于终纹床核(ST)或外侧杏仁核(LA),以0.25 Hz的频率诱发突触反应。2. 电刺激任一通路均可诱发两种具有IPSP成分的突触波形:一种双相兴奋性突触后电位(EPSP)、快速IPSP(f - IPSP)波形,以及一种多相的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部位。刺激ST诱发的双相(45%)和多相(50%)突触反应数量相似。相比之下,刺激LA通路主要诱发(80%)多相突触反应。3. ST刺激诱发的f - IPSP和s - IPSP在存在谷氨酸能N - 甲基 - D - 天冬氨酸(NMDA)拮抗剂(DL) - 2 - 氨基 - 5 - 膦酰基戊酸(APV,50 μM)时,幅度均可降低,并被谷氨酸能非NMDA拮抗剂6 - 氰基 - 7 - 硝基喹喔啉 - 2,3 - 二酮(CNQX,10 μM)消除。相反,LA刺激可诱发一种对CNQX耐药的f - IPSP,并在随后加入γ - 氨基丁酸(GABAA)受体拮抗剂甲磺酸荷包牡丹碱(BMI)后被消除,提示GABA能LA中间神经元对BLA神经元有直接抑制作用。s - IPSP和f - IPSP对谷氨酸能拮抗剂的敏感性提示存在对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,即反转电位为 - 70 mV,在 - 60 mV记录到膜电阻降低(13.5 MΩ),被BMI阻断,并被戊巴比妥钠(NaPB)增强。5. s - IPSP与4.5 MΩ的电阻降低、 - 95 mV的反转电位相关,并被2 - 羟基 - 舒氯芬(100 μM)可逆性抑制(约66%),提示GABAB受体被激活。6. 与f - IPSP相关的大电阻变化、其与诱发EPSP的时间重叠,以及在存在BMI时自发和诱发爆发性放电的出现表明,f - IPSP决定了BLA神经元的主要兴奋性状态。(摘要截选至400字)

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