scholarly journals The PKCγ neurons in anterior cingulate cortex contribute to the development of neuropathic allodynia and pain-related emotion

2021 ◽  
Vol 17 ◽  
pp. 174480692110619
Author(s):  
Xiao Zhang ◽  
Peng Liu ◽  
Xiaolan He ◽  
Zhenhua Jiang ◽  
Qun Wang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Patch Clamp ◽  
Anterior Cingulate Cortex ◽  
Mechanical Allodynia ◽  
Pain Perception ◽  
Cingulate Cortex ◽  
Brain Regions ◽  
Anterior Cingulate ◽  
Fos Expression ◽  
Aversive Behavior

Background While the PKCγ neurons in spinal dorsal horn play an indispensable part in neuropathic allodynia, the exact effect of PKCγ neurons of brain regions in neuropathic pain remains elusive. Mounting research studies have depicted that the anterior cingulate cortex (ACC) is closely linked with pain perception and behavior, the present study was designed to investigate the contribution of PKCγ neurons in ACC to neuropathic allodynia and pain-related emotion in newly developed Prkcg-P2A-Tdtomato mice. Methods The c-fos expression in response to innocuous stimulation was used to monitor the activity of PKCγ in CCI (chronic constriction injury of the sciatic nerve) induced neuropathic pain condition. Activating or silencing ACC PKCγ neurons by chemogenetics was applied to observe the changes of pain behavior. The excitability of ACC PKCγ neurons in normal and CCI mice was compared by patch-clamp whole-cell recordings. Results The PKCγ-Tdtomato neurons were mainly distributed in layer III-Vof ACC. The Tdtomato was mainly expressed in ACC pyramidal neurons demonstrated by intracellular staining. The c-fos expression in ACC PKCγ neurons in response to innocuous stimulation was obviously elevated in CCI mice. The patch clamp recordings showed that ACC PKCγ-Tdtomato neurons were largely activated in CCI mice. Chemogenetic activation of ACC PKCγ neurons in Prkcg-icre mice induced mechanical allodynia and pain-related aversive behavior, conversely, silencing them in CCI condition significantly reversed the mechanical allodynia and pain-related place aversive behavior. Conclusion We conclude that the PKCγ neurons in ACC are closely linked with neuropathic allodynia and pain-related emotional behaviors.

scholarly journals Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice

PeerJ ◽  
2015 ◽  
Vol 3 ◽  
pp. e1350 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Glutamate Receptor ◽  
Pain Perception ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Glutamate Transporters ◽  
Anterior Cingulate ◽  
Astrocyte Activation

Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity and gene expression of GFAP, glutamate transporters and receptor subunits by real time PCR in the anterior cingulate cortex (ACC) at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. The ACC, an area in the brain involved in pain perception and modulation, was chosen because changes in this area might contribute to the pathophysiology of PINP. GFAP transcripts levels were elevated by more than fivefold and GFAP immunoreactivity increased in the ACC of paclitaxel-treated mice. The 6 glutamate transporters (GLAST, GLT-1 EAAC1, EAAT4, VGLUT-1 and VGLUT-2) quantified were not significantly altered by paclitaxel treatment. Of the 12 ionotropic glutamate receptor subunits transcripts analysed 6 (GLuA1, GLuA3, GLuK2, GLuK3, GLuK5 and GLuN1) were significantly up-regulated, whereas GLuA2, GLuK1, GLuK4, GLuN2A and GLuN2B were not significantly altered and GLuA4 was lowly expressed. Amongst the 8 metabotropic receptor subunits analysed only mGLuR8 was significantly elevated. In conclusion, during PINP there is astrocyte activation, with no change in glutamate transporter expression and differential up-regulation of glutamate receptor subunits in the ACC. Thus, targeting astrocyte activation and the glutamatergic system might be another therapeutic avenue for management of PINP.

scholarly journals Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice

2015 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Glutamate Receptor ◽  
Pain Perception ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Glutamate Transporters ◽  
Anterior Cingulate ◽  
Astrocyte Activation

Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined gene expression of glial fibrillary acidic protein (GFAP; an astrocyte marker), glutamate transporters and receptor subunits in the anterior cingulate cortex (ACC) by real time PCR at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. Changes in the ACC, an area in the brain involved in pain perception and modulation, might contribute to the pathophysiology of PINP. GFAP transcripts levels were elevated by more than fivefold in the ACC of paclitaxel-treated mice. The 6 glutamate transporters (GLAST, GLT-1 EAAC1, EAAT4, VGLUT-1 and VGLUT-2) quantified were not significantly altered by paclitaxel treatment. Of the 12 ionotropic glutamate receptor subunits transcripts analysed 6 (GLuA1, GLuA3, GLuK2, GLuK3, GLuK5 and GLuN1) were significantly up-regulated, whereas GLuA2, GLuK1, GLuK4, GLuN2A and GLuN2B were not significantly altered and GLuA4 was lowly expressed. Amongst the 8 metabotropic receptor subunits analysed only mGLuR 8 was significantly elevated. In conclusion, during PINP there is astrocyte activation, no change in glutamate transporter expression and differential up-regulation of glutamate receptor subunits in the ACC. Thus, targeting astrocyte activation and the glutamatergic system might be another therapeutic avenue for management of PINP.

scholarly journals Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice

2015 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Glutamate Receptor ◽  
Pain Perception ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Glutamate Transporters ◽  
Anterior Cingulate ◽  
Astrocyte Activation

Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity and gene expression of GFAP, glutamate transporters and receptor subunits by real time PCR in the anterior cingulate cortex (ACC) at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. The ACC, an area in the brain involved in pain perception and modulation, was chosen because changes in this area might contribute to the pathophysiology of PINP. GFAP transcripts levels were elevated by more than fivefold and GFAP immunoreactivity increased in the ACC of paclitaxel-treated mice. The 6 glutamate transporters (GLAST, GLT-1 EAAC1, EAAT4, VGLUT-1 and VGLUT-2) quantified were not significantly altered by paclitaxel treatment. Of the 12 ionotropic glutamate receptor subunits transcripts analysed 6 (GLuA1, GLuA3, GLuK2, GLuK3, GLuK5 and GLuN1) were significantly up-regulated, whereas GLuA2, GLuK1, GLuK4, GLuN2A and GLuN2B were not significantly altered and GLuA4 was lowly expressed. Amongst the 8 metabotropic receptor subunits analysed only mGLuR8 was significantly elevated. In conclusion, during PINP there is astrocyte activation, no change in glutamate transporter expression and differential up-regulation of glutamate receptor subunits in the ACC. Thus, targeting astrocyte activation and the glutamatergic system might be another therapeutic avenue for management of PINP.

scholarly journals Alleviating Neuropathic Pain Mechanical Allodynia by Increasing Cdh1 in the Anterior Cingulate Cortex

2015 ◽  
Vol 11 ◽  
pp. s12990-015-0058 ◽  
Author(s):  
Wei Tan ◽  
Wen-Long Yao ◽  
Rong Hu ◽  
You-You Lv ◽  
Li Wan ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Mechanical Allodynia ◽  
Cingulate Cortex ◽  
Anterior Cingulate

scholarly journals Astrocyte activation in the anterior cingulate cortex and altered glutamatergic gene expression during paclitaxel-induced neuropathic pain in mice

2015 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Glutamate Receptor ◽  
Pain Perception ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Glutamate Transporters ◽  
Anterior Cingulate ◽  
Astrocyte Activation

Spinal astrocyte activation contributes to the pathogenesis of paclitaxel-induced neuropathic pain (PINP) in animal models. We examined glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity and gene expression of GFAP, glutamate transporters and receptor subunits by real time PCR in the anterior cingulate cortex (ACC) at 7 days post first administration of paclitaxel, a time point when mice had developed thermal hyperalgesia. The ACC, an area in the brain involved in pain perception and modulation, was chosen because changes in this area might contribute to the pathophysiology of PINP. GFAP transcripts levels were elevated by more than fivefold and GFAP immunoreactivity increased in the ACC of paclitaxel-treated mice. The 6 glutamate transporters (GLAST, GLT-1 EAAC1, EAAT4, VGLUT-1 and VGLUT-2) quantified were not significantly altered by paclitaxel treatment. Of the 12 ionotropic glutamate receptor subunits transcripts analysed 6 (GLuA1, GLuA3, GLuK2, GLuK3, GLuK5 and GLuN1) were significantly up-regulated, whereas GLuA2, GLuK1, GLuK4, GLuN2A and GLuN2B were not significantly altered and GLuA4 was lowly expressed. Amongst the 8 metabotropic receptor subunits analysed only mGLuR8 was significantly elevated. In conclusion, during PINP there is astrocyte activation, no change in glutamate transporter expression and differential up-regulation of glutamate receptor subunits in the ACC. Thus, targeting astrocyte activation and the glutamatergic system might be another therapeutic avenue for management of PINP.

P.185 Nx4 influences stress-induced activity of the anterior cingulate cortex and associated brain regions

2019 ◽  
Vol 29 ◽  
pp. S141-S142
Author(s):  
L. Herrmann ◽  
V. Kasties ◽  
Y. Fan ◽  
L. Danyeli ◽  
T. Tar ◽  
...  
Keyword(s):  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Brain Regions ◽  
Anterior Cingulate

scholarly journals A transcriptomic analysis of neuropathic pain in the anterior cingulate cortex after nerve injury

Bioengineered ◽  
2022 ◽  
Vol 13 (2) ◽  
pp. 2058-2075
Author(s):  
Yu Zhang ◽  
Shiwei Jiang ◽  
Fei Liao ◽  
Zhifeng Huang ◽  
Xin Yang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Nerve Injury ◽  
Cingulate Cortex ◽  
Transcriptomic Analysis ◽  
Anterior Cingulate

scholarly journals Framing and Self-Responsibility Modulate Brain Activities in Decision Escalation

2021 ◽  
Author(s):  
Ting-Peng Liang ◽  
Yuwen Li ◽  
Nai-Shing Yen ◽  
Ofir Turel ◽  
Sen-Mou Hsu
Keyword(s):  
Anterior Cingulate Cortex ◽  
Contextual Factors ◽  
Inferior Frontal Gyrus ◽  
Cingulate Cortex ◽  
Brain Regions ◽  
Anterior Cingulate ◽  
Imaging Data ◽  
Two Factors ◽  
Human Decision

Abstract Background: Escalation of commitment is a common bias in human decision making. The present study examined (1) differences in neural recruitment for escalation and de-escalation decisions of prior investments, and (2) how the activations of these brain networks are modulated by two factors that are often argued to modulate the behavior: (i) self-responsibility, and (ii) framing of the success probabilities. Results: Imaging data were obtained from functional magnetic resonance imaging (fMRI) applied to 29 participants. A whole-brain analysis was conducted to compare brain activations between conditions. ROI analysis, then, was used to examine if these significant activations were modulated by two contextual factors. Finally, mediation analysis was applied to explore how the contextual factors affect escalation decisions through brain activations. The findings showed that (1) escalation decisions are faster than de-escalation decisions, (2) the corresponding network of brain regions recruited for escalation (anterior cingulate cortex, insula and precuneus) decisions differs from this recruited for de-escalation decisions (inferior and superior frontal gyri), (3) the switch from escalation to de-escalation is primarily frontal gyri dependent, and (4) activation in the anterior cingulate cortex, insula and precuneus were further increased in escalation decisions, when the outcome probabilities of the follow-up investment were positively framed; and activation in the inferior and superior frontal gyri in de-escalation decisions were increased when the outcome probabilities were negatively framed. Conclusions: Escalation and de-escalation decisions recruit different brain regions. Framing of possible outcomes as negative leads to escalation decisions through recruitment of the inferior frontal gyrus. Responsibility for decisions affects escalation decisions through recruitment of the superior (inferior) gyrus, when the decision is framed positively (negatively).

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