Bauer Elizabeth P, LeDoux Joseph E
W. M. Keck Foundation Laboratory of Neurobiology, Center for Neural Science, New York University, New York, New York 10003, USA.
J Neurosci. 2004 Oct 27;24(43):9507-12. doi: 10.1523/JNEUROSCI.3567-04.2004.
Long-term potentiation (LTP) of synaptic transmission in the lateral amygdala (LA) is believed to underlie the formation and retention of fear memories. To explore the role of inhibitory transmission in amygdala plasticity, we recorded from LA inhibitory interneurons in vitro before and after tetanization of the thalamo-LA pathway, one of the major inputs to LA involved in fear learning. Tetanization resulted in LTP of the EPSPs elicited in both the tetanized thalamic pathway and the untetanized cortical pathway to LA. This LTP was NMDA-dependent and associated with a decrease in paired-pulse facilitation in both pathways. In LA excitatory cells, LTP of interneurons resulted in an increase in the amplitude of GABAergic IPSPs in both input pathways. Finally, isolated GABAergic IPSPs between inhibitory and excitatory neurons could be potentiated as well. Plasticity of inhibitory transmission within the LA may therefore contribute significantly to LA-mediated functions, such as fear conditioning.
外侧杏仁核(LA)突触传递的长时程增强(LTP)被认为是恐惧记忆形成和保留的基础。为了探究抑制性传递在杏仁核可塑性中的作用,我们在体外记录了丘脑 - LA通路(参与恐惧学习的LA主要输入之一)强直刺激前后LA抑制性中间神经元的活动。强直刺激导致在强直刺激的丘脑通路和未强直刺激的通向LA的皮质通路中诱发的兴奋性突触后电位(EPSP)出现LTP。这种LTP依赖于N - 甲基 - D - 天冬氨酸(NMDA),并且与两条通路中配对脉冲易化的降低相关。在LA兴奋性细胞中,中间神经元的LTP导致两条输入通路中γ - 氨基丁酸能抑制性突触后电位(IPSP)的幅度增加。最后,抑制性神经元与兴奋性神经元之间分离的γ - 氨基丁酸能IPSP也可以被增强。因此,LA内抑制性传递的可塑性可能对LA介导的功能(如恐惧条件反射)有显著贡献。