Sci. STKE, 18 September 2001
Learning PI3K: Fear and Plasticity in Amygdala
Compelling evidence suggests that the amygdala is important for the memory of fear. NMDA-dependent calcium influx in the lateral amygdala leads to the activation of protein kinases and transcription factors in the process of memory formation. However, the signaling involved in fear is not well understood. Lin et al. found a critical role for phosphatidylinositol 3-kinase (PI3K) in fear conditioning in the amygdala. Phosphorylation of Akt, a kinase that is a substrate of PI3K, was observed in the amygdala, but not in the hippocampus or cerebellum, after fear training in rats. Treatment of amygdala slices with forskolin (an activator of protein kinase A) or with tetanic stimulus to induce long-term potentiation (LTP) also resulted in PI3K activation; however, LTP and mitogen-activated protein kinase activation were blocked by PI3K inhibitors, suggesting that PI3K may be important for LTP induction. Injection of wortmannin, a PI3K inhibitor, into the amygdala of rats disrupted fear conditioning, indicating that PI3K is required for the generation of fear memory.
C.-H. Lin, S.-H. Yeh, C.-H. Lin, K.-T. Lu, T.-H. Leu, W.-C. Chang, P.-W. Gean, A role for the PI-3 kinase signaling pathway in fear conditioning and synaptic plasticity in the amygdala. Neuron 31, 841-851 (2001). [Online Journal]
Citation: PI3K: Fear and Plasticity in Amygdala. Sci. STKE 2001, tw331 (2001).
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