NMDA receptors and L-type voltage-gated calcium channels contribute to long-term potentiation and different components of fear memory formation in the lateral amygdala
NMDA receptors and L-type voltage-gated calcium channels contribute to long-term potentiation and different components of fear memory formation in the lateral amygdala
复制标题
DOI：
10.1523/jneurosci.22-12-05239.2002
复制
发表时间：
2002-06-15
影响因子：
5.3
通讯作者：
LeDoux, JE
中科院分区：
文献类型：
--
作者：
Bauer, EP;Schafe, GE;LeDoux, JE
外侧杏仁核（LA）感觉输入突触的长时程增强（LTP）是恐惧条件反射记忆储存的一种可能机制。我们评估了L-型电压门控钙通道（VGCC）和NMDA受体（NMDAR）的封锁在LA对LTP在丘脑输入突触诱导的两种不同的协议在体外和在体内的恐惧记忆的影响。当在体外通过配对弱突触前刺激与强（尖峰诱发）突触后去极化诱导时，LTP依赖于VGCC，而不是NMDAR，但是，当由产生延长的突触后去极化（但不是尖峰）的强直刺激形式诱导时，LTP依赖于NMDAR，而不是VGCC。在行为研究中，双侧注入NMDAR拮抗剂到LA损害短期和长期记忆的恐惧条件反射，而VGCC封锁选择性损害长期记忆的形成。总的来说，结果表明，两种不同形式的LTP可以在体外LA中分离，两者的组合有助于在体内细胞水平上形成恐惧记忆。
Long-term potentiation (LTP) at sensory input synapses to the lateral amygdala (LA) is a candidate mechanism for memory storage during fear conditioning. We evaluated the effect of L-type voltage-gated calcium channel (VGCC) and NMDA receptor (NMDAR) blockade in LA on LTP at thalamic input synapses induced by two different protocols in vitro and on fear memory in vivo. When induced in vitro by pairing weak presynaptic stimulation with strong (spike eliciting) postsynaptic depolarization, LTP was dependent on VGCCs and not on NMDARs, but, when induced by a form of tetanic stimulation that produced prolonged postsynaptic depolarization (but not spikes), LTP was dependent on NMDARs and not on VGCCs. In behavioral studies, bilateral infusions of NMDAR antagonists into the LA impaired both short-term and long-term memory of fear conditioning, whereas VGCC blockade selectively impaired long-term memory formation. Collectively, the results suggest that two pharmacologically distinct forms of LTP can be isolated in the LA in vitro and that a combination of both contribute to the formation of fear memories in vivo at the cellular level.