Dopamine D1 and NMDA receptors mediate potentiation of basolateral amygdala-evoked firing of nucleus accumbens neurons
Dopamine D1 and NMDA receptors mediate potentiation of basolateral amygdala-evoked firing of nucleus accumbens neurons
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DOI：
10.1523/jneurosci.21-16-06370.2001
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发表时间：
2001-08-15
影响因子：
5.3
通讯作者：
Phillips, AG
中科院分区：
文献类型：
--
作者：
Floresco, SB;Blaha, CD;Phillips, AG
基底外侧杏仁核（BLA）和中脑核（NAc）之间的相互作用介导了由中脑多巴胺（DA）传递调节的奖赏相关过程。目前在体内的电生理研究评估：（1）在放电概率的变化，次最大的BLA诱发的单一神经元放电活动后，在NAc强直刺激的BLA，和（2）DA和NMDA受体在这些过程中的功能作用。强直刺激的BLA增强BLA-evoked放电活动NAc神经元的持续时间短（类似于25分钟）。这种短时程增强与DA氧化电流的增加有关，用计时电流法监测。全身或离子导入应用BLA破伤风的D-1受体拮抗剂SCH 23390，但不是D-2受体拮抗剂舒必利，取消增强的BLA诱发的NAc活性，而SCH 23390 3分钟后破伤风没有效果。然而，系统管理的NMDA拮抗剂3-（2-羧基哌嗪-4-基）-丙基-1-膦酸（CPP），无论是之前或之后BLA破伤风，取消增强BLA-evoked发射NAc神经元。这些数据表明，BLA传出神经的高频活动可以通过促进DA的释放和激活DA D-1和NMDA受体来自动调节它们对NAc神经元神经活动的兴奋性影响。这可能代表了一种细胞机制，该机制促进了由BLA-NAc电路介导的针对奖励相关刺激的接近行为。
Interactions between the basolateral amygdala (BLA) and the nucleus accumbens (NAc) mediate reward-related processes that are modulated by mesoaccumbens dopamine (DA) transmission. The present in vivo electrophysiological study assessed: (1) changes in the firing probability of submaximal BLA-evoked single neuronal firing activity in the NAc after tetanic stimulation of the BLA, and (2) the functional roles of DA and NMDA receptors in these processes. Tetanic stimulation of the BLA potentiated BLA-evoked firing activity of NAc neurons for a short duration (similar to 25 min). This short-term potentiation was associated with an increase in DA oxidation currents that was monitored with chronoamperometry. Systemic or iontophoretic application before BLA tetanus of the D-1 receptor antagonist SCH23390, but not the D-2 receptor antagonist sulpiride, abolished the potentiation of BLA-evoked NAc activity, whereas administration of SCH23390 3 min after tetanus had no effect. However, systemic administration of the NMDA antagonist 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), either before or after BLA tetanus, abolished the potentiation of BLA-evoked firing of NAc neurons. These data suggest that higher-frequency activity in BLA efferents can autoregulate their excitatory influence over neural activity of NAc neurons by facilitating the release of DA and activating both DA D-1 and NMDA receptors. This may represent a cellular mechanism that facilitates approach behaviors directed toward reward-related stimuli that are mediated by BLA-NAc circuitries.