Section of Anatomy and Histology, Department of Bio-Medical Sciences, University of Catania, Via S. Sofia, 87, 95123, Catania, Italy.
Neurochem Res. 2013 Dec;38(12):2516-23. doi: 10.1007/s11064-013-1164-3. Epub 2013 Oct 8.
Dopamine D3 receptors (D3Rs) are implicated in synaptic plasticity and memory processes. Previously we have shown that D3Rs mediate inhibitory effects on learning, since D3R knockout (D 3 (-/-) ) mice display enhanced performance in the passive avoidance task (PA). Formation of new memories is known to require de novo synthesis of proteins related to synaptic function through the activation of signaling pathways including the mitogen-activated protein kinases (MAPKs) and activation of the nuclear transcription factor cAMP response element binding protein (CREB). However, there are no clear indications regarding the specific involvement of D3Rs in the activation of these signaling cascades after acquisition of PA. Therefore, in this study we assessed whether phosphorylation levels of several MAPKs, Akt and CREB were differentially affected by PA in both wild-type (WT) and D 3 (-/-) mice hippocampi. Animals were divided in Naïve, unconditioned stimulus trained, conditioned stimulus trained and conditioned animals. Phosphorylation of extracellular signal-regulated kinase 1/2 (ERK 1/2), c-Jun-N-terminal kinase (JNK) and p38, as well as of Akt and CREB were determined. Acquisition of PA significantly increased pCREB levels both in WT and D 3 (-/-) mice. The extent of PA-driven increase in pCREB levels was significantly higher in mice lacking D3Rs. Similarly, pERK 1/2 was further augmented in trained D 3 (-/-) mice as compared to trained WTs, whereas JNK and p38 phosphorylation was not affected neither by PA nor by genetic background. Finally, Akt activation was observed in D 3 (-/-) mice, but not in response to PA. In conclusion, these data supports the notion that D3Rs might modulate CREB phosphorylation after acquisition of PA, probably via activation of ERK signaling.
多巴胺 D3 受体 (D3Rs) 参与突触可塑性和记忆过程。先前我们已经表明,D3R 介导对学习的抑制作用,因为 D3R 敲除 (D3(-/-)) 小鼠在被动回避任务 (PA) 中表现出增强的性能。新记忆的形成需要与突触功能相关的蛋白质的从头合成,这是通过包括丝裂原活化蛋白激酶 (MAPKs) 在内的信号通路的激活以及核转录因子 cAMP 反应元件结合蛋白 (CREB) 的激活来实现的。然而,对于 D3R 在 PA 获得后这些信号级联的激活中的具体参与,目前尚无明确迹象。因此,在这项研究中,我们评估了几种 MAPKs、Akt 和 CREB 的磷酸化水平是否因 PA 而在 WT 和 D3(-/-) 小鼠海马中受到不同影响。动物分为未处理、未条件刺激训练、条件刺激训练和条件动物。测定了细胞外信号调节激酶 1/2 (ERK 1/2)、c-Jun-N 末端激酶 (JNK) 和 p38 的磷酸化以及 Akt 和 CREB 的磷酸化。PA 的获得显著增加了 WT 和 D3(-/-) 小鼠中 pCREB 的水平。缺乏 D3R 的小鼠中 pCREB 水平的 PA 驱动增加幅度明显更高。同样,与训练 WT 相比,训练 D3(-/-) 小鼠中 pERK 1/2 进一步增加,而 JNK 和 p38 的磷酸化既不受 PA 也不受遗传背景的影响。最后,在 D3(-/-) 小鼠中观察到 Akt 的激活,但对 PA 没有反应。总之,这些数据支持了 D3R 可能通过激活 ERK 信号来调节 PA 获得后 CREB 磷酸化的观点。