CLASSICAL-CONDITIONING REDUCES AMPLITUDE AND DURATION OF CALCIUM-DEPENDENT AFTERHYPERPOLARIZATION IN RABBIT HIPPOCAMPAL PYRAMIDAL CELLS
CLASSICAL-CONDITIONING REDUCES AMPLITUDE AND DURATION OF CALCIUM-DEPENDENT AFTERHYPERPOLARIZATION IN RABBIT HIPPOCAMPAL PYRAMIDAL CELLS
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DOI：
10.1152/jn.1989.61.5.971
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发表时间：
1989-05-01
影响因子：
2.5
通讯作者：
ALKON, DL
中科院分区：
文献类型：
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作者：
COULTER, DA;LOTURCO, JJ;ALKON, DL
1.对经典状态下和正常对照兔CA1区锥体细胞动作电位后超极化(AHP)进行研究。AHP的测量是通过海马片内CA1细胞的细胞内记录获得的。2.兔CA1区锥体细胞的AHP反应伴随着电导的增加。通过钙通道阻滞剂镉和钴的浸泡、胆碱能激动剂氯化氨甲酰胆碱的浸浴和细胞内注射钙离子螯合剂乙二醇双(B-氨基乙醚)-N，N，N‘，N’-四乙酸(EGTA)来降低AHP。3.与假条件动物和幼稚对照动物相比，接受过瞬膜训练的兔细胞的AHP显著降低。随着刺激脉冲诱发的尖峰数目从一个增加到四个，条件组和对照组之间的AHP幅度差异增大。在条件化动物的细胞中，AHP的持续时间(以AHP衰变的时间常数衡量)和幅度都减少了。4.在含有0.5微米河豚毒素(TTX)和5.0 mM四乙基氯化铵(TEA)的培养液中，条件化动物细胞内还原的AHP仍然是还原的；在此条件下，测量钙离子峰后的AHP。由于该介质消除了Schaeffer侧支刺激引起的突触传递，因此条件动物锥体细胞中AHP的减少并不是由于突触特性的改变。三组动物细胞的平均电压阈值、幅度或钙尖峰持续时间没有显著差异。因此，AHP的降低似乎是由于钙依赖的K+电导的改变，而不是由于尖峰下的钙电导降低的次要影响。5.在含TTX和TEA的培养液中，条件动物细胞产生钙尖峰所需的注入电流量(电流阈值)明显大于对照动物细胞。这种电流阈值的增加在含有4-氨基吡啶(4-AP)的介质中持续存在，因此不能完全归因于A电流的条件性增加。6.条件性AHP的降低导致条件性动物细胞的兴奋性高于假条件性对照动物。来自条件化动物的细胞比来自对照的细胞向100ms的去极化电流脉冲序列发射更多的尖峰。
1. The afterhyperpolarization (AHP) that follows action potentials was studied in CA1 hippocampal pyramidal cells from classically conditioned and control rabbits. Measurements of the AHP were obtained with intracellular recordings from CA1 cells within hippocampal slices. 2. The AHP of rabbit CA1 pyramidal cells was found to be accompanied by a conductance increase. The AHP was reduced by bath applications of the calcium channel blockers, cadmium and cobalt, by bath application of the cholinergic agonist, carbamylcholine chloride, and intracellular injection of the calcium chelator, ethylene glycol-bis(B-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). 3. The AHP was markedly reduced in cells from rabbits that were well-trained with the nictitating membrane conditioning procedure, as compared with cells from pseudoconditioned or naive control animals. The difference in AHP amplitudes between conditioned and control groups increased as the number of spikes elicited by the stimulation pulse increased from one to four. Both the duration (measured as the time constant of AHP decay) and amplitude of the AHP were reduced in cells from conditioned animals. 4. The reduced AHP in cells from conditioned animals remained reduced in a medium that contained 0.5 microM tetrodotoxin (TTX) and 5.0 mM tetraethylammonium chloride (TEA); the AHP following calcium spikes was measured under these conditions. Since this medium eliminated synaptic transmission elicited by Schaeffer collateral stimulation, the AHP reduction in pyramidal cells from conditioned animals was not due to a modification in synaptic properties. There were no significant differences in the mean voltage thresholds, amplitudes, or durations of calcium spikes between cells from animals in the three groups. Thus the AHP reduction appears to be due to a modification of a Ca2+ -dependent K+ conductance and was not due to a secondary effect of reductions in calcium conductances underlying the spike. 5. In medium containing TTX and TEA, the amount of injected current required to elicit a calcium spike (current threshold) was significantly greater in cells from conditioned animals than in cells from control animals. This increase in current threshold persisted in 4-aminopyridine (4-AP)-containing medium and so cannot be attributed entirely to conditioning-specific increases in the A-current. 6. The conditioning-specific AHP reduction resulted in increased excitability in cells from conditioned animals versus pseudoconditioned control animals. Cells from conditioned animals fired more spikes to trains of 100-ms depolarizing current pulses than did cells from controls.