Role of the basolateral amygdala in the storage of fear memories across the adult lifetime of rats
Role of the basolateral amygdala in the storage of fear memories across the adult lifetime of rats
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DOI：
10.1523/jneurosci.4100-03.2004
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发表时间：
2004-04-14
影响因子：
5.3
通讯作者：
Fanselow, MS
中科院分区：
文献类型：
--
作者：
Gale, GD;Anagnostaras, SG;Fanselow, MS
基底外侧杏仁核（BLA）与条件性恐惧的发展密切相关。证据支持这一区域在存储恐惧记忆中的作用，但不排除在记忆巩固中的时间限制作用。为了研究这个问题，我们评估了BLA对大鼠成年期获得的恐惧记忆的贡献的稳定性。恐惧条件反射包括在一个背景下（远程记忆）的10个音调-电击配对，16个月后，在一个新的背景下（最近的记忆）的10个额外的音调-电击配对。在最近的训练后24小时，大鼠给予NMDA或BLA的假损伤。语境和语气冻结独立评估在个别测试会话。假损伤大鼠在所有的上下文和音调测试中表现出较高的和相当的冻结水平。相比之下，在最近和远程测试中，BLA损伤的大鼠显示出强大的冷冻缺陷。随后的旷场测试显示，在黑暗的旷场或强光照射期间，BLA病变对活动模式没有影响。在过度训练程序（76次无信号电击）后，受损大鼠能够重新获得正常水平的上下文特异性冻结。总之，这些发现表明，BLA病变不会通过产生多动、无法抑制行为或无法冻结来破坏冻结行为。相反，在两个训练到损伤间隔的冻结赤字的一致模式支持BLA在恐惧记忆的永久存储中的作用。
The basolateral amygdala (BLA) is intimately involved in the development of conditional fear. Converging lines of evidence support a role for this region in the storage of fear memory but do not rule out a time-limited role in the memory consolidation. To examine this issue, we assessed the stability of BLA contribution to fear memories acquired across the adult lifetime of rats. Fear conditioning consisted of 10 tone-shock pairings in one context (remote memory), followed 16 months later by 10 additional tone-shock pairings with a novel tone in a novel context (recent memory). Twenty-four hours after recent training, rats were given NMDA or sham lesions of the BLA. Contextual and tone freezing were independently assessed in individual test sessions. Sham-lesioned rats showed high and comparable levels of freezing across all context and tone tests. In contrast, BLA-lesioned rats displayed robust freezing deficits across both recent and remote tests. Subsequent open-field testing revealed no effects of BLA lesions on activity patterns in a dark open field or during bright light exposure. Lesioned rats were able to reacquire normal levels of context-specific freezing after an overtraining procedure (76 unsignaled shocks). Together, these findings indicate that BLA lesions do not disrupt freezing behavior by producing hyperactivity, an inability to suppress behavior, or an inability to freeze. Rather, the consistent pattern of freezing deficits at both training-to-lesion intervals supports a role for the BLA in the permanent storage of fear memory.