Neugebauer Volker
Professor and Chair, Department of Pharmacology and Neuroscience, Giles McCrary Endowed Chair in Addiction Medicine, Director, Center of Excellence for Translational Neuroscience and Therapeutics, Texas Tech University Health Sciences Center | School of Medicine, 3601 4th Street | Mail Stop 6592, Lubbock, Texas 79430-6592.
Handb Behav Neurosci. 2020;26:101-113. doi: 10.1016/b978-0-12-815134-1.00004-0. Epub 2020 Mar 31.
The amygdala has emerged as an important brain area for the emotional-affective dimension of pain and pain modulation. The amygdala receives nociceptive information through direct and indirect routes. These excitatory inputs converge on the amygdala output region (central nucleus) and can be modulated by inhibitory elements that are the target of (prefrontal) cortical modulation. For example, inhibitory neurons in the intercalated cell mass in the amygdala project to the central nucleus to serve gating functions, and so do inhibitory (PKCdelta) interneurons within the central nucleus. In pain conditions, synaptic plasticity develops in output neurons because of an excitation-inhibition imbalance and drives pain-like behaviors and pain persistence. Mechanisms of pain related neuroplasticity in the amygdala include classical transmitters, neuropeptides, biogenic amines, and various signaling pathways. An emerging concept is that differences in amygdala activity are associated with phenotypic differences in pain vulnerability and resilience and may be predetermining factors of the complexity and persistence of pain.
杏仁核已成为疼痛及疼痛调节情感维度的一个重要脑区。杏仁核通过直接和间接途径接收伤害性信息。这些兴奋性输入汇聚于杏仁核输出区域（中央核），并可受到作为（前额叶）皮质调节靶点的抑制性元件的调制。例如，杏仁核内插细胞群中的抑制性神经元投射至中央核以发挥门控功能，中央核内的抑制性（蛋白激酶Cδ）中间神经元亦是如此。在疼痛状态下，由于兴奋 - 抑制失衡，输出神经元会发生突触可塑性，从而引发疼痛样行为和疼痛持续。杏仁核中与疼痛相关的神经可塑性机制包括经典递质、神经肽、生物胺及各种信号通路。一个新出现的概念是，杏仁核活动的差异与疼痛易感性和恢复力的表型差异相关，并且可能是疼痛复杂性和持续性的决定性因素。
