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The Contribution Of Nmda Receptors Within The Central Nucleus Of The Amygdala To The Suppression Of Pain Affect

机译：amygdala中央核内Nmda受体对抑制疼痛的作用

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The amygdala processes stimuli that threaten an individual and organizes the execution of affective behaviors designed to cope with the threat. The prototypical threat to an individual is exposure to a noxious stimulus. The central nucleus of the amygdala (CeA) receives nociceptive afferents and exhibits neuronal activation in response to noxious peripheral stimulation. NMDA receptors within CeA mediate this noxious-evoked neural excitation, and previous studies in the laboratory have shown that blockade of CeA NMDA receptors via the antagonist APV elevates the threshold for noxious tail-shock-induced vocalization afterdischarges (VADs), a validated measure of pain affect in the rat. The present study further evaluated the contribution of NMDA receptors to the suppression of pain affect.Intra-CeA NMDA receptor activation via the agonist NMDA elevated VAD thresholds in a dose dependent manner. That the NMDA receptor agonist and antagonist produce similar behavioral effects is hypothesized as the result of targeting separate neural populations within the CeA. Whereas the antagonist likely inhibits nociception at the level of the lateral capsular division of the CeA, the agonist likely activates antinociceptive efferents at the level of the vlPAG. In support of this hypothesis, the present study revealed that Fos expression within vlPAG is greater in rats that received intra-CeA agonist NMDA treatment compared to those that received the antagonist APV or saline. Lastly, intra-CeA NMDA agonist-induced elevations in VAD thresholds were blocked via the pre-treatment of the vlPAG with the mu-opiate antagonist CTAP. These studies provide the first demonstration of the contribution of CeA NMDA receptors to the generation of pain affect in the rat.
机译：杏仁核处理威胁个人的刺激，并组织执行旨在应对威胁的情感行为。对个人的原型威胁是暴露于有害刺激。杏仁核（CeA）的中央核接收伤害性传入和响应有害的外周刺激表现出神经元激活。 CeA内的NMDA受体介导了这种有害的神经兴奋作用，实验室中的先前研究表明，通过拮抗剂APV阻断CeA NMDA受体可提高有害的尾巴引起的发声后放电（VAD）的阈值，这是一种有效的方法。疼痛影响大鼠。本研究进一步评估了NMDA受体对抑制疼痛的影响。通过激动剂NMDA激活CeA内NMDA受体的激活以剂量依赖性方式提高了VAD阈值。假设NMDA受体激动剂和拮抗剂产生类似的行为效果，是因为在CeA中靶向了单独的神经群体。拮抗剂可能在CeA的外侧荚膜分裂水平抑制伤害感受，而激动剂则可能在vPAG水平激活抗伤害感受性传出。为支持这一假设，本研究表明，与接受拮抗剂APV或生理盐水的大鼠相比，接受CeA内激动剂NMDA治疗的大鼠在vlPAG中的Fos表达更高。最后，通过用多阿片拮抗剂CTAP对vlPAG进行预处理，可以阻止CeA内NMDA激动剂诱导的VAD阈值升高。这些研究首次证明了CeA NMDA受体对大鼠疼痛产生的影响。

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    Spuz Catherine Ann;

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