Chhatwal Jasmeer P, Stanek-Rattiner Lisa, Davis Michael, Ressler Kerry J
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, 1639 Pierce Drive, Suite 4000, Atlanta, Georgia 30322, USA.
Nat Neurosci. 2006 Jul;9(7):870-2. doi: 10.1038/nn1718. Epub 2006 Jun 18.
Brain-derived neurotrophic factor (BDNF) acting through the tyrosine kinase B receptor (TrkB) is thought to be a critical mediator of learning. As there are no available selective antagonists of TrkB, we used a lentivirus encoding a dominant-negative TrkB (TrkB.t1) to antagonize BDNF signaling during extinction of conditioned fear. Whereas TrkB.t1-infected rats showed normal within-session extinction, their retention of extinction was impaired, suggesting that amygdala TrkB activation is required for the consolidation of stable extinction memories.
脑源性神经营养因子(BDNF)通过酪氨酸激酶B受体(TrkB)发挥作用,被认为是学习的关键调节因子。由于目前尚无可用的TrkB选择性拮抗剂,我们使用了一种编码显性负性TrkB(TrkB.t1)的慢病毒,在条件性恐惧消退过程中拮抗BDNF信号传导。虽然感染TrkB.t1的大鼠在训练过程中的消退表现正常,但其消退记忆的保持受损,这表明杏仁核TrkB激活是稳定消退记忆巩固所必需的。