A Central Amygdala–Ventrolateral Periaqueductal Gray Matter Pathway for Pain in a Mouse Model of Depression-like Behavior

导水管周围灰质 伤害 加巴能 扁桃形结构 谷氨酸的 神经科学 医学 去抑制 内科学 中枢神经系统 谷氨酸受体 抑制性突触后电位 中脑 心理学 受体
作者
Weiwei Yin,Lisheng Mei,Tingting Sun,Yuping Wang,Jie Li,Changmao Chen,Zahra Farzinpour,Yu Mao,Wenjuan Tao,Juan Li,Wen Xie,Zhi Zhang
出处
期刊:Anesthesiology [Lippincott Williams & Wilkins]
卷期号:132 (5): 1175-1196 被引量:40
标识
DOI:10.1097/aln.0000000000003133
摘要

Abstract Background The mechanisms underlying depression-associated pain remain poorly understood. Using a mouse model of depression, the authors hypothesized that the central amygdala–periaqueductal gray circuitry is involved in pathologic nociception associated with depressive states. Methods The authors used chronic restraint stress to create a mouse model of nociception with depressive-like behaviors. They then used retrograde tracing strategies to dissect the pathway from the central nucleus of the amygdala to the ventrolateral periaqueductal gray. The authors performed optogenetic and chemogenetic experiments to manipulate the activity of this pathway to explore its roles for nociception. Results The authors found that γ-aminobutyric acid–mediated (GABAergic) neurons from the central amygdala project onto GABAergic neurons of the ventrolateral periaqueductal gray, which, in turn, locally innervate their adjacent glutamatergic neurons. After chronic restraint stress, male mice displayed reliable nociception (control, mean ± SD: 0.34 ± 0.11 g, n = 7 mice; chronic restraint stress, 0.18 ± 0.11 g, n = 9 mice, P = 0.011). Comparable nociception phenotypes were observed in female mice. After chronic restraint stress, increased circuit activity was generated by disinhibition of glutamatergic neurons of the ventrolateral periaqueductal gray by local GABAergic interneurons via receiving enhanced central amygdala GABAergic inputs. Inhibition of this circuit increased nociception in chronic restraint stress mice (median [25th, 75th percentiles]: 0.16 [0.16, 0.16] g to 0.07 [0.04, 0.16] g, n = 7 mice per group, P < 0.001). In contrast, activation of this pathway reduced nociception (mean ± SD: 0.16 ± 0.08 g to 0.34 ± 0.13 g, n = 7 mice per group, P < 0.001). Conclusions These findings indicate that the central amygdala–ventrolateral periaqueductal gray pathway may mediate some aspects of pain symptoms under depression conditions. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New
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