A Central Amygdala Input to the Parafascicular Nucleus Controls Comorbid Pain in Depression

Xia Zhu; Wenjie Zhou; Yan Jin; Haodi Tang; Peng Cao; Yu Mao; Wen Xie; Xulai Zhang; Fei Zhao; Min Hua Luo; Haitao Wang; Jie Li; Wenjuan Tao; Zahra Farzinpour; Likui Wang; Xiangyao Li; Juan Li; Zheng Quan Tang; Chenghua Zhou; Zhizhong Z. Pan; Zhi Zhang

doi:10.1016/j.celrep.2019.11.003

A Central Amygdala Input to the Parafascicular Nucleus Controls Comorbid Pain in Depression

Xia Zhu, Wenjie Zhou, Yan Jin, Haodi Tang, Peng Cao, Yu Mao, Wen Xie, Xulai Zhang, Fei Zhao, Min Hua Luo, Haitao Wang, Jie Li, Wenjuan Tao, Zahra Farzinpour, Likui Wang, Xiangyao Li, Juan Li, Zheng Quan Tang, Chenghua Zhou, Zhizhong Z. PanZhi Zhang

Pain Medicine

Research output: Contribution to journal › Article › peer-review

39 Scopus citations

Abstract

While comorbid pain in depression (CP) occurs at a high rate worldwide, the neural connections underlying the core symptoms of CP have yet to be elucidated. Here, we define a pathway whereby GABAergic neurons from the central nucleus of the amygdala (GABA^CeA) project to glutamatergic neurons in the parafascicular nucleus (Glu^PF). These Glu^PF neurons relay directly to neurons in the second somatosensory cortex (S2), a well-known area involved in pain signal processing. Enhanced inhibition of the GABA^CeA→Glu^PF→S2 pathway is found in mice exhibiting CP symptoms. Reversing this pathway using chemogenetic or optogenetic approaches alleviates CP symptoms. Together, the current study demonstrates the putative importance of the GABA^CeA→Glu^PF→S2 pathway in controlling at least some aspects of CP.

Original language	English (US)
Pages (from-to)	3847-3858.e5
Journal	Cell Reports
Volume	29
Issue number	12
DOIs	https://doi.org/10.1016/j.celrep.2019.11.003
State	Published - Dec 17 2019

Keywords

GABA neurons
central nucleus of the amygdala
chemogenetics
comorbid pain
glutamate neurons
neural circuits
optogenetics
parafascicular nucleus
retrograde trans-monosynaptic tracing
second somatosensory cortex

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

Access to Document

10.1016/j.celrep.2019.11.003

Cite this

Zhu, X., Zhou, W., Jin, Y., Tang, H., Cao, P., Mao, Y., Xie, W., Zhang, X., Zhao, F., Luo, M. H., Wang, H., Li, J., Tao, W., Farzinpour, Z., Wang, L., Li, X., Li, J., Tang, Z. Q., Zhou, C., ... Zhang, Z. (2019). A Central Amygdala Input to the Parafascicular Nucleus Controls Comorbid Pain in Depression. Cell Reports, 29(12), 3847-3858.e5. https://doi.org/10.1016/j.celrep.2019.11.003

Zhu, X, Zhou, W, Jin, Y, Tang, H, Cao, P, Mao, Y, Xie, W, Zhang, X, Zhao, F, Luo, MH, Wang, H, Li, J, Tao, W, Farzinpour, Z, Wang, L, Li, X, Li, J, Tang, ZQ, Zhou, C, Pan, ZZ & Zhang, Z 2019, 'A Central Amygdala Input to the Parafascicular Nucleus Controls Comorbid Pain in Depression', Cell Reports, vol. 29, no. 12, pp. 3847-3858.e5. https://doi.org/10.1016/j.celrep.2019.11.003

@article{c71a8942eb1e4f9facc3beb9a03f44d1,

title = "A Central Amygdala Input to the Parafascicular Nucleus Controls Comorbid Pain in Depression",

abstract = "While comorbid pain in depression (CP) occurs at a high rate worldwide, the neural connections underlying the core symptoms of CP have yet to be elucidated. Here, we define a pathway whereby GABAergic neurons from the central nucleus of the amygdala (GABACeA) project to glutamatergic neurons in the parafascicular nucleus (GluPF). These GluPF neurons relay directly to neurons in the second somatosensory cortex (S2), a well-known area involved in pain signal processing. Enhanced inhibition of the GABACeA→GluPF→S2 pathway is found in mice exhibiting CP symptoms. Reversing this pathway using chemogenetic or optogenetic approaches alleviates CP symptoms. Together, the current study demonstrates the putative importance of the GABACeA→GluPF→S2 pathway in controlling at least some aspects of CP.",

keywords = "GABA neurons, central nucleus of the amygdala, chemogenetics, comorbid pain, glutamate neurons, neural circuits, optogenetics, parafascicular nucleus, retrograde trans-monosynaptic tracing, second somatosensory cortex",

author = "Xia Zhu and Wenjie Zhou and Yan Jin and Haodi Tang and Peng Cao and Yu Mao and Wen Xie and Xulai Zhang and Fei Zhao and Luo, {Min Hua} and Haitao Wang and Jie Li and Wenjuan Tao and Zahra Farzinpour and Likui Wang and Xiangyao Li and Juan Li and Tang, {Zheng Quan} and Chenghua Zhou and Pan, {Zhizhong Z.} and Zhi Zhang",

note = "Publisher Copyright: {\textcopyright} 2019 The Author(s)",

year = "2019",

month = dec,

day = "17",

doi = "10.1016/j.celrep.2019.11.003",

language = "English (US)",

volume = "29",

pages = "3847--3858.e5",

journal = "Cell Reports",

issn = "2211-1247",

publisher = "Cell Press",

number = "12",

}

TY - JOUR

T1 - A Central Amygdala Input to the Parafascicular Nucleus Controls Comorbid Pain in Depression

AU - Zhu, Xia

AU - Zhou, Wenjie

AU - Jin, Yan

AU - Tang, Haodi

AU - Cao, Peng

AU - Mao, Yu

AU - Xie, Wen

AU - Zhang, Xulai

AU - Zhao, Fei

AU - Luo, Min Hua

AU - Wang, Haitao

AU - Li, Jie

AU - Tao, Wenjuan

AU - Farzinpour, Zahra

AU - Wang, Likui

AU - Li, Xiangyao

AU - Li, Juan

AU - Tang, Zheng Quan

AU - Zhou, Chenghua

AU - Pan, Zhizhong Z.

AU - Zhang, Zhi

PY - 2019/12/17

Y1 - 2019/12/17

N2 - While comorbid pain in depression (CP) occurs at a high rate worldwide, the neural connections underlying the core symptoms of CP have yet to be elucidated. Here, we define a pathway whereby GABAergic neurons from the central nucleus of the amygdala (GABACeA) project to glutamatergic neurons in the parafascicular nucleus (GluPF). These GluPF neurons relay directly to neurons in the second somatosensory cortex (S2), a well-known area involved in pain signal processing. Enhanced inhibition of the GABACeA→GluPF→S2 pathway is found in mice exhibiting CP symptoms. Reversing this pathway using chemogenetic or optogenetic approaches alleviates CP symptoms. Together, the current study demonstrates the putative importance of the GABACeA→GluPF→S2 pathway in controlling at least some aspects of CP.

AB - While comorbid pain in depression (CP) occurs at a high rate worldwide, the neural connections underlying the core symptoms of CP have yet to be elucidated. Here, we define a pathway whereby GABAergic neurons from the central nucleus of the amygdala (GABACeA) project to glutamatergic neurons in the parafascicular nucleus (GluPF). These GluPF neurons relay directly to neurons in the second somatosensory cortex (S2), a well-known area involved in pain signal processing. Enhanced inhibition of the GABACeA→GluPF→S2 pathway is found in mice exhibiting CP symptoms. Reversing this pathway using chemogenetic or optogenetic approaches alleviates CP symptoms. Together, the current study demonstrates the putative importance of the GABACeA→GluPF→S2 pathway in controlling at least some aspects of CP.

KW - GABA neurons

KW - central nucleus of the amygdala

KW - chemogenetics

KW - comorbid pain

KW - glutamate neurons

KW - neural circuits

KW - optogenetics

KW - parafascicular nucleus

KW - retrograde trans-monosynaptic tracing

KW - second somatosensory cortex

UR - http://www.scopus.com/inward/record.url?scp=85076373682&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85076373682&partnerID=8YFLogxK

U2 - 10.1016/j.celrep.2019.11.003

DO - 10.1016/j.celrep.2019.11.003

M3 - Article

C2 - 31851918

AN - SCOPUS:85076373682

SN - 2211-1247

VL - 29

SP - 3847-3858.e5

JO - Cell Reports

JF - Cell Reports

IS - 12

ER -

A Central Amygdala Input to the Parafascicular Nucleus Controls Comorbid Pain in Depression

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this