Mapping Cortical Integration of Sensory and Affective Pain Pathways

Singh, Amrita; Patel, Divya; Li, Anna; Hu, Lu; Zhang, Qiaosheng; Liu, Yaling; Guo, Xinling; Robinson, Eric; Martinez, Erik; Doan, Lisa; Rudy, Bernardo; Chen, Zhe; Wang, Jing

doi:10.1016/j.cub.2020.02.091

Cited by 88 publications

(107 citation statements)

References 63 publications

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“…The rACC-injected NMDA receptor antagonist significantly inhibited F-CPA in rats; however, it did not reduce acute formalin-induced nociceptive behaviors ( Ren et al, 2006 ). The engagement of the rACC circuitry has been shown to be associated with the modulation of the affective component without altering pain intensity ( Singh et al, 2020 ). Interestingly, our present study also demonstrated that chemogenetic inhibition of glutamatergic neurons in the rACC-thalamus circuitry only reduced anxiety disorders without changing the rats’ pain thresholds induced by CFA.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Alleviates Chronic Pain-Induced Anxiety Disorders by Regulating the rACC-Thalamus Circuitry

Shen

Zhang

et al. 2021

Front. Neurosci.

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Anxiety is a common comorbidity associated with chronic pain, which results in chronic pain complexification and difficulty in treatment. Electroacupuncture (EA) is commonly used to treat chronic pain and anxiety. However, the underlying mechanisms of the EA effect are largely unknown. Here, we showed that a circuitry underlying chronic pain induces anxiety disorders, and EA can treat them by regulating such circuitry. Using chemogenetic methods, we found that chemogenetic activation of the rostral anterior cingulate cortex (rACC) glutamatergic output to the thalamus induced anxiety disorders in control rats. Then, chemogenetic inhibition of the rACC-thalamus circuitry reduced anxiety-like behavior produced by intraplantar injection of the complete Freund’s adjuvant (CFA). In this study, we examined the effects of EA on a rat model of CFA-mediated anxiety-like behaviors and the related mechanisms. We found that chemogenetic activation of the rACC-thalamus circuitry effectively blocked the effects of EA on chronic pain-induced anxiety-like behaviors in CFA rats. These results demonstrate an underlying rACC-thalamus glutamatergic circuitry that regulates CFA-mediated anxiety-like behaviors. This study also provides a potential mechanistic explanation for EA treatment of anxiety caused by chronic pain.

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Section: Discussionmentioning

confidence: 99%

Electroacupuncture Alleviates Chronic Pain-Induced Anxiety Disorders by Regulating the rACC-Thalamus Circuitry

Shen

Zhang

et al. 2021

Front. Neurosci.

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“…[ 4 , 26 – 28 ] These findings have been replicated in other model systems, including rabbits and monkeys, where increases in extracellular activity in the ACC have been observed to occur in response to stimulations in freely moving animals and humans [ 29 – 32 ]. Furthermore, studies have shown that ACC neurons undergo synaptic plasticity in chronic pain conditions [ 7 , 25 , 33 ]. Thus, there is a possibility that neuronal responses to noxious stimuli in the ACC may show distinct patterns in the chronic pain state.…”

Section: Introductionmentioning

confidence: 99%

Ketamine normalizes high-gamma power in the anterior cingulate cortex in a rat chronic pain model

et al. 2020

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Chronic pain alters cortical and subcortical plasticity, causing enhanced sensory and affective responses to peripheral nociceptive inputs. Previous studies have shown that ketamine had the potential to inhibit abnormally amplified affective responses of single neurons by suppressing hyperactivity in the anterior cingulate cortex (ACC). However, the mechanism of this enduring effect has yet to be understood at the network level. In this study, we recorded local field potentials from the ACC of freely moving rats. Animals were injected with complete Freund’s adjuvant (CFA) to induce persistent inflammatory pain. Mechanical stimulations were administered to the hind paw before and after CFA administration. We found a significant increase in the high-gamma band (60–100 Hz) power in response to evoked pain after CFA treatment. Ketamine, however, reduced the high-gamma band power in response to evoked pain in CFA-treated rats. In addition, ketamine had a sustained effect on the high-gamma band power lasting up to five days after a single dose administration. These results demonstrate that ketamine has the potential to alter maladaptive neural responses in the ACC induced by chronic pain.

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“…In ACC the increased activity is most likely because, the activation is limited when using a stimulus less than ten times the motor threshold (Chang & Shyu, 2001; Shyu et al., 2008; Yang et al., 2006). In addition, several studies confirm this finding as ACC has increased activation when using noxious stimuli compared to non‐noxious stimuli (Singh et al., 2020; Zhang et al., 2018). Based on previous research, it was expected that the peak activity in ACC would be smaller (Chang & Shyu, 2001) and slower (Kuo & Yen, 2005; Wang et al., 2008; Xiao et al., 2019) than that in SI when using noxious stimuli.…”

Section: Discussionmentioning

confidence: 75%

“…Several studies using complete Freund's adjuvant (CFA) showed modulated activity in SI to non‐noxious stimuli (Tan et al., 2019) and noxious stimuli (Singh et al., 2020) and in ACC to noxious stimuli (Singh et al., 2020; Zhang et al., 2018). The processing in ACC of electrical stimuli in Onishi et al.…”

Section: Introductionmentioning

confidence: 99%

Modulation of SI and ACC response to noxious and non‐noxious electrical stimuli after the spared nerve injury model of neuropathic pain

Tøttrup

Diaz-Valencia

Kamavuako

et al. 2020

European Journal of Pain

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Background The current knowledge on the role of SI and ACC in acute pain processing and how these contribute to the development of chronic pain is limited. Our objective was to investigate differences in and modulation of intracortical responses from SI and ACC in response to different intensities of peripheral presumed noxious and non‐noxious stimuli in the acute time frame of a peripheral nerve injury in rats. Methods We applied non‐noxious and noxious electrical stimulation pulses through a cuff electrode placed around the sciatic nerve and measured the cortical responses (six electrodes in each cortical area) before and after the spared nerve injury model. Results We found that the peak response correlated with the stimulation intensity and that SI and ACC differed in both amplitude and latency of cortical response. The cortical response to both noxious and non‐noxious stimulation showed a trend towards faster processing of non‐noxious stimuli in ACC and increased cortical processing of non‐noxious stimuli in SI after SNI. Conclusions We found different responses in SI and ACC to different intensity electrical stimulations based on two features and changes in these features following peripheral nerve injury. We believe that these features may be able to assist to track cortical changes during the chronification of pain in future animal studies. Significance This study showed distinct cortical processing of noxious and non‐noxious peripheral stimuli in SI and ACC. The processing latency in ACC and accumulated spiking activity in SI appeared to be modulated by peripheral nerve injury, which elaborated on the function of these two areas in the processing of nociception.

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Mapping Cortical Integration of Sensory and Affective Pain Pathways

Cited by 88 publications

References 63 publications

Electroacupuncture Alleviates Chronic Pain-Induced Anxiety Disorders by Regulating the rACC-Thalamus Circuitry

Electroacupuncture Alleviates Chronic Pain-Induced Anxiety Disorders by Regulating the rACC-Thalamus Circuitry

Ketamine normalizes high-gamma power in the anterior cingulate cortex in a rat chronic pain model

Modulation of SI and ACC response to noxious and non‐noxious electrical stimuli after the spared nerve injury model of neuropathic pain

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