Role of NMDA receptors in the lateralized potentiation of amygdala afferent and efferent neural transmission produced by predator stress
Role of NMDA receptors in the lateralized potentiation of amygdala afferent and efferent neural transmission produced by predator stress
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DOI：
10.1016/j.physbeh.2005.06.026
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发表时间：
2005-09-15
影响因子：
2.9
通讯作者：
Burton, P
中科院分区：
文献类型：
--
作者：
Adamec, R;Blundell, J;Burton, P
本研究探讨了NMDA受体在杏仁核传出（中央杏仁核到中脑导水管周围灰质-ACE-PAG）和杏仁核传入（腹角束到基底外侧杏仁核-VAB-BLA）通路响应捕食者应激的行为和神经可塑性变化中的作用。以3-（2-羧基哌嗪-4-基）丙基-1-膦酸（3-（2-carboxypiperazin 4-yl）propyl-1-phosphonicacid，CPP）为受体，研究了竞争性阻断NMDA受体对捕食应激的脑和行为反应的影响。采用洞板、高架十字迷宫、明暗箱、社会互动和声惊吓试验检测应激行为反应。CPP在捕食者应激前30分钟腹腔注射，并在8 - 9天后阻断捕食者对部分但非全部行为的影响。在捕食者应激后10 - 11天，评估捕食者应激和CPP对由ACE的单脉冲刺激在PAG中诱发的电位和由VAB的单脉冲刺激在BLA中诱发的电位的影响。捕食者压力增强ACE-PAG诱发电位在右半球，但不是左半球，复制以前的工作。捕食者压力增强VAB-BLA传输在两个半球10 - 11天后捕食者压力。右半球VAB-BLA增强复制和扩展了过去的研究表明，右半球增强1和9天后的压力。左侧VAB-BLA增强效应不同于先前研究中在应激后1天和9天时在VAB-BLA中观察到的长期抑制。CPP阻断捕食者应激诱导的右半球ACE-PAG和VAB-BLA诱发电位增强。CPP不阻断左侧VAB-BLA增强，而CPP放大了左侧VAB-BLA增强，CPP的左半球效应被解释为阻断了NMDA依赖的长时程抑制，揭示了非NMDA依赖的增强。总之，这些发现增加了一系列证据，表明捕食者压力后会出现行为变化综合征。这种综合征的成分可能取决于可分离神经基质的变化。右半球ACE-PAG和VAB-BLA诱发电位的增强可能介导行为变化的子集。此外，中间ACE-PAG通路涉及介导应激诱导的惊吓幅度变化。相反，一个横向ACE-PAG通路涉及介导的惊吓习惯化的变化。最后，与猫和人类的研究一致，右半球在对压力的长期反应中显得特别重要。(c)2005年爱思唯尔公司All rights reserved.
The present study investigated the role of NMDA receptors in behavioral and neuroplastic changes in amygdala efferent (central amygdala to periaqueductal gray-ACE-PAG) and amygdala afferent (ventral angular bundle to basolateral amygdala-VAB-BLA) pathways in response to predator stress. Effects on brain and behavioral response to predator stress of competitive block of NMDA receptors with a dose of 10 mg/kg of CPP (3-(2-carboxypiperazin4-yl)propyl-1-phosphonic acid) were studied. Behavioral response to stress was tested with hole board, elevated plus maze, light/dark box, social interaction and acoustic startle tests. CPP was administered i.p. 30 min prior to predator stress and blocked the effects of predator on some but not all behaviors measured 8 - 9 days later. Effects of predator stress and CPP on potentials evoked in the PAG by single pulse stimulation of the ACE and in the BLA by single pulse stimulation of VAB were assessed 10 - 11 days after predator stress. Predator stress potentiated ACE-PAG evoked potentials in the right but not the left hemisphere, replicating previous work. Predator stress potentiated VAB-BLA transmission in both hemispheres 10 - 11 days after predator stress. Right hemisphere VAB-BLA potentiation replicated and extended past studies showing right hemisphere potentiation at 1 and 9 days after stress. Left VAB-BLA potentiation effects differed from the long term depression seen in VAB-BLA at 1 and 9 days after stress in previous studies. CPP blocked predator stress-induced potentiation of ACE-PAG and VAB-BLA evoked potentials in the right hemisphere. CPP did not block left VAB-BLA potentiation, rather CPP amplified it. Left hemisphere effects of CPP were interpreted as reflecting block of NMDA dependent long term depression, which unmasked a non-NMDA dependent potentiation. Taken together, the findings add to a body of evidence suggesting that a syndrome of behavioral changes follows predator stress. Components of this syndrome likely depend on changes in separable neural substrates. Potentiation of ACE-PAG and VAB-BLA evoked potentials in the right hemisphere likely mediates a subset of changes in behavior. Moreover, a medial ACE-PAG pathway is implicated in mediating stress-induced changes in startle amplitude. In contrast, a lateral ACE-PAG pathway is implicated in mediating changes in startle habituation. Finally, consistent with cat and human studies, the right hemisphere appears particularly important in long term response to stress. (c) 2005 Elsevier Inc. All rights reserved.