首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Activation of D1-like dopamine receptors increases the NMDA-induced gain modulation through a PKA-dependent pathway in the premotor nucleus of adult zebra finches
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Activation of D1-like dopamine receptors increases the NMDA-induced gain modulation through a PKA-dependent pathway in the premotor nucleus of adult zebra finches

机译:D1样多巴胺受体的激活通过成年斑马雀的运动前核中的PKA依赖性途径增加NMDA诱导的增益调节。

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Interaction between dopamine (DA) and N-methyl-p-aspartate (NMDA) in the brain plays an important role in learning and memory. In the songbirds, the premotor robust nucleus of the arcopallium (RA) receives excitatory glutamatergic inputs from the high vocal center (HVC) and lateral magnocellular nucleus of the anterior nidopallium (LMAN), as well as dopaminergic inputs mostly from the periaqueductal gray (PAG) and ventral tegmental area (VTA). In zebra finch, DA potentiates the excitability of projection neurons in the RA through activation of D1-like dopamine receptors (D1 receptors). The relationship between D1 receptors and NMDA in the RA projection neurons is essentially unknown. Our previous work showed that NMDA can induce gain modulation in the RA projection neurons. Here, using the whole-cell current-clamp recording from brain slices of male zebra finches, we observed whether D1 receptors regulate the NMDA-induced gain modulation in the RA projection neurons. Our results showed that activation of D1 receptors further increased the slope (gain) of the firing frequency-injected current (f-I) relationship induced by NMDA in the RA projection neurons. Blocking D1 receptors had no effect on the NMDA-induced gain modulation in the RA projection neurons. The enhanced effects of D1 receptors agonists were blocked by protein kinase A (MA) inhibitors. Our results suggest that activation of D1 receptors can increase the NMDA-induced gain modulation through a MA-dependent pathway. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
机译:脑中多巴胺(DA)和N-甲基-p-天冬氨酸(NMDA)之间的相互作用在学习和记忆中起着重要作用。在鸣禽中,arcopallium的运动前健壮核(RA)接收来自前声带神经((LMAN)的高声带中心(HVC)和侧生核细胞核的兴奋性谷氨酸能输入,以及多半来自导水管周围灰质(PAG)的多巴胺能输入)和腹侧被盖区(VTA)。在斑马雀科中,DA通过激活D1样多巴胺受体(D1受体)来增强RA中投射神经元的兴奋性。 RA投射神经元中D1受体与NMDA之间的关系基本上是未知的。我们以前的工作表明,NMDA可以诱导RA投射神经元的增益调节。在这里,我们使用雄性斑马雀科大脑切片的全细胞电流钳记录,我们观察到D1受体是否调节了RA投射神经元中NMDA诱导的增益调节。我们的结果表明,D1受体的激活进一步增加了NMDA在RA投射神经元中引起的发射频率注入电流(f-I)关系的斜率(增益)。阻断D1受体对RA投射神经元中NMDA诱导的增益调节没有影响。 D1受体激动剂的增强作用被蛋白激酶A(MA)抑制剂阻断。我们的结果表明,D1受体的激活可以通过MA依赖性途径增加NMDA诱导的增益调节。 (C)2015 Elsevier Ireland Ltd.保留所有权利。

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