Auditory fear conditioning increases CS-elicited spike firing in lateral amygdala neurons even after extensive overtraining
Auditory fear conditioning increases CS-elicited spike firing in lateral amygdala neurons even after extensive overtraining
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DOI：
10.1046/j.1460-9568.2000.00281.x
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发表时间：
2000-11-01
影响因子：
3.4
通讯作者：
Maren, S
中科院分区：
文献类型：
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作者：
Maren, S
我们研究了听觉恐惧条件反射的过度训练（75次试验）对条件刺激（CS）引起的外侧杏仁核（LA）神经元放电的影响。从植入清醒和自由活动大鼠左心房的慢性多通道电极记录单个单位。在连续的训练中，大鼠接受了5次或70次恐惧条件反射试验，其中包括白噪声CS和共同终止的足电击无条件刺激（US）。未配对（致敏）对照组接受了相同数量的试验，但CS和US明显未配对。配对CS-US演示文稿产生了强大的增加CS引起的尖峰放电在LA神经元后，5和70个条件试验，和尖峰放电增加的幅度与条件冻结CS的表达。经过75次训练试验，最大的条件反射相关的增加，在LA放电表现出20毫秒内的CS发病，表明这种增加是由直接丘脑-杏仁核的预测介导的。在未配对组中，CS引起的尖峰放电或冻结行为没有显著增加。这些结果补充了杏仁核损伤研究[例如Maren，S.（1999 a）神经科学杂志，19，8696-8703]并支持这样的观点，即杏仁核的基底外侧复合体参与了恐惧记忆的编码和储存，即使在广泛的过度训练之后。
We examined the influence of extensive overtraining (75 trials) of auditory fear conditioning on the expression of conditional stimulus (CS)-elicited spike firing in lateral amygdala (LA) neurons. Single units were recorded from chronic multichannel electrodes implanted in the LA of conscious and freely moving rats. In sequential training sessions, the rats received either five or 70 fear conditioning trials, which consisted of a white-noise CS and a coterminating footshock unconditional stimulus (US). Unpaired (sensitization) controls received the same number of trials, but the CS and US were explicitly unpaired. Paired CS-US presentations yielded robust increases in CS-elicited spike firing in LA neurons after both five and 70 conditioning trials, and the magnitude of the spike firing increases was correlated with the expression of conditional freezing to the CS. After 75 training trials, maximal conditioning-related increases in LA firing were exhibited within 20 ms of CS onset, indicating that this increase is mediated by direct thalamo-amygdala projections. There was no significant increase in CS-elicited spike firing or freezing behaviour in the unpaired group. These results complement amygdala lesion studies [e.g. Maren, S. (1999a) J. Neurosci., 19, 8696-8703] and support the view that the basolateral complex of the amygdala is involved in the encoding and storage of fear memories even after extensive overtraining.