The role of signaling molecules in reward-related incentive learning
The role of signaling molecules in reward-related incentive learning
复制标题
DOI：
10.1007/bf03033301
复制
发表时间：
2004-01-01
影响因子：
3.7
通讯作者：
Gerdjikov, TV
中科院分区：
文献类型：
--
作者：
Beninger, RJ;Gerdjikov, TV
奖励相关的激励学习涉及通过中性刺激获得增强的能力，以引起接近和其他反应。以前的研究表明，多巴胺（DA）和谷氨酸（Glu）在这种类型的学习中起着关键作用。信号分子是细胞内的信使，其参与递质-受体事件对细胞内功能的影响，包括细胞核中的转录。近年来的研究已经开始暗示信号分子在激励学习。因此，抑制环磷酸腺苷依赖性蛋白激酶（PKA）在延髓核（NAc），这是激活DA作用于D-1样受体，阻止收购条件的方法反应，杠杆挤压食物，条件位置偏好（CPP）的基础上NAc注射安非他明或可卡因，和条件活动的基础上NAc注射安非他明。在基底外侧杏仁核或内侧前额叶皮层中也观察到了PKA抑制的类似效果。如果在NAc中测试PKA抑制剂之前训练动物，则没有观察到效果，表明PKA对于获得比激励学习的表达更重要。抑制NAc中的钙依赖性蛋白激酶或丝裂原活化蛋白激酶也同样可以阻断激励性学习的获得。结果支持DA-Glu突触相互作用的模型，形成激励学习的基础。
Reward-related incentive learning involves the acquisition by neutral stimuli of an enhanced ability to elicit approach and other responses. Previous studies have shown that both dopamine (DA) and glutamate (Glu) play critical roles in this type of learning. Signaling molecules are intracellular messengers that participate in the influence of transmitter-receptor events on intracellular function including transcription in the nucleus. In recent years studies have begun to implicate signaling molecules in incentive learning. Thus, inhibition of cyclic adenosine monophosphate-dependent protein kinase (PKA) in the nucleus accumbens (NAc), that is activated by DA acting at D-1-like receptors, blocks the acquisition of conditioned approach responses, lever pressing for food, conditioned place preference (CPP) based on NAc injections of amphetamine or cocaine, and conditioned activity based on NAc injections of amphetamine. Similar effects have been observed with PKA inhibition in the basolateral amygdala or medial prefrontal cortex. If animals were trained prior to testing with PKA inhibitors in NAc, no effect was seen suggesting that PKA is more important for acquisition than expression of incentive learning. Inhibition of calcium-dependent protein kinase or mitogen-activated protein kinases in NAc similarly has been shown to block the acquisition of incentive learning. Results support a model of DA-Glu synaptic interactions that form the basis of incentive learning.