Restoring Acid-sensing ion channel-1a in the amygdala of knock-out mice rescues fear memory but not unconditioned fear responses.
Restoring Acid-sensing ion channel-1a in the amygdala of knock-out mice rescues fear memory but not unconditioned fear responses.
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DOI：
10.1523/jneurosci.3907-08.2008
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发表时间：
2008-12-17
期刊：
影响因子：
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通讯作者：
Wemmie JA
中科院分区：
文献类型：
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作者：
Coryell MW;Wunsch AM;Haenfler JM;Allen JE;McBride JL;Davidson BL;Wemmie JA
ASIC 1a参与多种恐惧行为，但ASIC 1a在行为中的作用部位尚不清楚。为了探索ASIC 1a作用的特定位置，我们使用病毒载体介导的基因转移在ASIC 1a-/-小鼠的基底外侧杏仁核中表达ASIC 1a。这拯救了依赖于背景的恐惧记忆，但没有拯救训练期间的冻结缺陷或对捕食者气味的无条件恐惧反应。这些数据指出，基底外侧杏仁核是ASIC 1a促进恐惧记忆的部位。他们还区分恐惧记忆与训练过程中表达的恐惧和无条件恐惧。此外，这项工作说明了一种识别离散大脑区域的策略，在这些区域中特定的基因有助于复杂的行为。
ASIC1a contributes to multiple fear behaviors, however the site of ASIC1a action in behavior is not known. To explore a specific location of ASIC1a action, we expressed ASIC1a in the basolateral amygdala of ASIC1a–/– mice using viral vector-mediated gene transfer. This rescued context-dependent fear memory, but not the freezing deficit during training or the unconditioned fear response to predator odor. These data pinpoint the basolateral amygdala as the site where ASIC1a contributes to fear memory. They also discriminate fear memory from fear expressed during training and from unconditioned fear. Furthermore, this work illustrates a strategy for identifying discrete brain regions where specific genes contribute to complex behaviors.