Ca(2+)-dependent plasticity of miniature inhibitory postsynaptic currents after amputation of dendrites in central neurons.
Ca(2+)-dependent plasticity of miniature inhibitory postsynaptic currents after amputation of dendrites in central neurons.
复制标题
中枢神经元树突截除后微型抑制性突触后电流的 Ca(2) 依赖性可塑性。
DOI：
10.1152/jn.1995.73.5.1763
复制
发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Mody,I
中科院分区：
文献类型：
--
作者：
Soltesz,I;Mody,I
1.在400微米厚的脑片上，观察了切断树突2/3对成年大鼠齿状回颗粒细胞GABA能微小抑制性突触后电流(MIPCs)的影响。2.在高温(32℃)对照的人工脑脊液(ACSF)中进行树突切断后，在颗粒细胞层仅能诱发到少量的反向群峰电位，无法获得有效的全细胞记录。然而，当在冷(8-10摄氏度)对照的ACSF中进行树突切断术时，反向群体峰的幅度增加，稳定的全细胞记录成为可能。3.冷对照组ACSF去树枝后颗粒细胞的全细胞记录显示，mIPSACs的衰变动力学发生了持续10小时的显著变化。这种变化包括从正常的单指数衰减到延长的双指数衰减的钙依赖变化，这有效地增加了突触事件转移的电荷(电流的总面积)67%。当移液管中加入30 mM的1，2-二(2-氨基苯氧基)-N，N，N‘，N’-四乙酸(BAPTA)时，仍能观察到切断树枝后mIPSCs衰变动力学的变化，表明这种可塑性的维持阶段不依赖于细胞内钙水平的升高。4.在树枝状颗粒细胞中，当树突与细胞内钙离子螯合剂BAPTA-AM(50微米)孵育2小时后在32℃下进行截断，或在含有兴奋性氨基酸受体拮抗剂2-氨基-5-磷酸戊酸(APV；25微米)+6-氰基-7-硝基喹恶啉-2，3-二酮(CNQX；10微米)或电压门控性钠通道阻滞剂(TTX；1微米)的ACSF中进行切割过程，也可以获得活的全细胞记录。5.切断BAPTA-AM、APV+CNQX、APV+CNQX+TTX和/或丹曲林后，细胞衰变动力学的改变被阻止，表明细胞内钙离子浓度的升高在这种可塑性中起关键作用。6.对mIPSC的计算机模拟表明，单通道动力学的改变原则上可以解释mIPSC衰减动力学中钙离子依赖的变化。7.这些发现与在树突物理损伤中存活的细胞的伽马-氨基丁酸-A(GABAA)受体功能持续的钙依赖增强是一致的。
1. The effects of cutting off the bulk (> 2/3) of the dendritic tree (dendrotomy) on GABAergic miniature inhibitory postsynaptic currents (mIPCSs) were studied in granule cells of the adult rat dentate gyrus in 400-microns-thick slices in vitro. 2. After dendrotomy carried out in warm (32 degrees C) control artificial cerebrospinal fluid (ACSF), only small antidromic population spikes could be evoked in the granule cell layer, and no viable whole cell recordings could be obtained. However, when dendrotomy was performed in cold (8-10 degrees C) control ACSF, the amplitude of the antidromic population spikes increased, and stable whole cell recordings became possible. 3. Whole cell recordings, with CsCl-filled pipettes, from granule cells dendrotomized in cold control ACSF, revealed significant alterations, lasting > 10 h, in the decay kinetics of mIPSACs. The change consisted of a calcium-dependent transformation of the normal, single exponential decay into a prolonged double exponential that effectively increased the charge transferred by the synaptic events (the total area of the currents) by 67%. When 30 mM 1,2 bis-(2-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA) was included in the pipette, the changes in the mIPSCs decay kinetics could still be observed after dendrotomy, indicating that the maintenance phase of this plasticity did not depend on elevated intracellular calcium levels. 4. Viable whole cell recordings could also be obtained in dendrotomized granule cells when the amputation of dendrites was carried out at 32 degrees C after incubation for 2 h with the cell-permeant Ca2+ chelator, BAPTA-AM (50 microM), or the cutting process was done in an ACSF containing either a combination of excitatory amino acid receptor antagonists 2-amino-5-phosphonovaleric acid (APV; 25 microM) + 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM), a blocker of intracellular Ca2+ release dantrolene-Na (20 microM), or the voltage-gated Na+ channel blocker tetrodotoxin (TTX; 1 microM). 5. After dendrotomy in BAPTA-AM, APV + CNQX, APV + CNQX + TTX, and/or dantrolene, the changes in decay kinetics were prevented, indicating that a rise in intracellular Ca2+ concentration plays a pivotal role in this plasticity. 6. Computer simulations of mIPSCs suggested that changes in single channel kinetics alone can, in principle, account for the Ca(2+)-dependent changes in mIPSC decay kinetics. 7. These findings are consistent with a lasting Ca(2+)-dependent increase in gamma-aminobutyric acid-A (GABAA) receptor function in cells that survive physical injury to their dendrites.