Amino acid-mediated regulation of spontaneous synaptic activity patterns in the rat basolateral amygdala.
Amino acid-mediated regulation of spontaneous synaptic activity patterns in the rat basolateral amygdala.
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DOI：
10.1152/jn.1996.76.3.1958
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发表时间：
1996-09
影响因子：
2.5
通讯作者：
B. Smith;F. Dudek
中科院分区：
文献类型：
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作者：
B. Smith;F. Dudek
1.自发性突触后电流（PSC）进行了检查，在基底外侧杏仁核使用全细胞膜片钳记录冠状切片（400微米）从年轻大鼠（出生后6-25天）。在大多数细胞中，Cs+被用于电极中以阻断假定的电压激活的K（+）电流。检查内向和外向自发PSC。2.α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）/红藻氨酸受体拮抗剂6，7-硝基喹喔啉-2，3-二酮（DNQX）阻断所有内向PSC，其在0 mV附近逆转。因此，它们被认为是谷氨酸介导的兴奋性突触后电流（EPSC）。平均EPSC在负电位至约-50 mV时具有快速的10-90%上升时间（1.0 +/- 0.04 ms;平均值+/- SD）和单指数衰减（tau = 3.6 +/- 0.18 ms）。高于此电位，在检查的10个细胞中的8个中，第二个较慢的时间常数（-30 mV时tau 1 = 41 +/- 4.5 ms）占总EPSC振幅的10-30%。较慢的衰减时间常数对N-甲基-D-天冬氨酸（NMDA）受体拮抗剂DL-2-氨基-5-膦酰基戊酸（AP 5）敏感，因此可能是由于NMDA受体的激活。3.γ-氨基丁酸-A（GABAA）拮抗剂荷包牡丹碱阻断了所有外向PSC，其在-70 mV附近逆转。因此，它们被认为是GABA介导的抑制性突触后电流（IPSC）。平均IPSC显示快速的10-90%上升时间（1.0 +/- 0.03 ms）和单指数衰减时间常数（tau = 5.16 +/- 0.14 ms）。4.河豚毒素（TTX）降低了突触活动的频率，消除了最大的PSC，从而轻微降低了平均EPSC和IPSC振幅。大多数细胞接受自发IPSC和/或EPSC的爆发（30-68 Hz，持续0.5-6 s），其也是TTX敏感的。TTX数据表明，负责最大PSC和PSC爆发的细胞的胞体包含在切片内。5.除了阻断EPSC外，DNQX还阻断IPSC的爆发，但不是所有单独的IPSC。DNQX对IPSC的爆发和频率的影响与TTX相似。6.荷包牡丹碱增强自发EPSC频率（231 +/- 90%）。这种增加主要是由于EPSC爆发的增加。7.因此，基底外侧杏仁核的神经元似乎接受来自局部神经元的兴奋性（谷氨酸能）和抑制性（GABA能）突触输入。负责这些输入的神经元的活动本身在很大程度上受谷氨酸能和GABA能输入的调节。这一局部电路的癫痫发作和癫痫的相关性进行了简要讨论。
1. Spontaneous postsynaptic currents (PSCs) were examined in the basolateral amygdala using whole cell patch-clamp recordings in coronal slices (400 microns) from young rats (postnatal day 6-25). In most cells, Cs+ was used in the electrode to block putative voltage-activated K(+)-currents. Both inward and outward spontaneous PSCs were examined. 2. The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor antagonist, 6,7-nitroquinoxaline-2,3-dione (DNQX) blocked all inward PSCs, which reversed near 0 mV. They therefore were considered to be glutamate-mediated excitatory postsynaptic currents (EPSCs). Averaged EPSCs had a rapid 10-90% rise time (1.0 +/- 0.04 ms; mean +/- SD) and monoexponential decay (tau = 3.6 +/- 0.18 ms) at potentials negative to about -50 mV. Above this potential, a second, slower time constant (tau 1 = 41 +/- 4.5 ms at -30 mV), accounting for 10-30% of the total EPSC amplitude was resolved in 8 of 10 cells examined. The slower decay time constant was sensitive to the N-methyl-D-aspartate (NMDA)-receptor antagonist, DL-2-amino-5-phosphonovaleric acid (AP5) and therefore probably was due to activation of NMDA receptors. 3. The gamma-aminobutyric acid-A (GABAA) antagonist, bicuculline, blocked all outward PSCs, which reversed near -70 mV. They therefore were considered to be GABA-mediated inhibitory postsynaptic currents (IPSCs). Averaged IPSCs displayed rapid 10-90% rise times (1.0 +/- 0.03 ms) and monoexponential decay time constants (tau = 5.16 +/- 0.14 ms). 4. Tetrodotoxin (TTX) reduced the frequency of synaptic activity and eliminated the largest PSCs, thus reducing slightly the mean EPSC and IPSC amplitude. Most cells received bursts of spontaneous IPSCs and/or EPSCs (30-68 Hz lasting 0.5-6 s), which were also TTX sensitive. The TTX data suggest that the somata of the cells responsible for the largest PSCs and the PSC bursts were contained within the slice. 5. In addition to blocking EPSCs, DNQX blocked the bursts of IPSCs, but not all individual IPSCs. DNQX had similar effects as TTX on the bursts and frequency of the IPSCs. 6. Bicuculline enhanced spontaneous EPSC frequency (231 +/- 90%). Much of this increase was due to an increase in the bursts of EPSCs. 7. Neurons in the basolateral amygdala therefore appear to receive both excitatory (glutamatergic) and inhibitory (GABAergic) synaptic input from local neurons. The activity of the neurons responsible for these inputs are themselves largely regulated by glutamatergic and GABAergic inputs. The relevance of this local circuitry to seizures and epilepsy is discussed briefly.