scholarly journals The Role of miR-539 in the Anterior Cingulate Cortex in Chronic Neuropathic Pain

Pain Medicine ◽  
2017 ◽  
Vol 18 (12) ◽  
pp. 2433-2442 ◽  
Author(s):  
Mingxia Ding ◽  
Weihong Shen ◽  
Yifeng Hu
Keyword(s):  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Chronic Neuropathic Pain

Attenuation of Neuropathic Pain by Inhibiting Electrical Synapses in the Anterior Cingulate Cortex

2016 ◽  
Vol 124 (1) ◽  
pp. 169-183 ◽  
Author(s):  
Zhi-Yu Chen ◽  
Feng-Yan Shen ◽  
Lai Jiang ◽  
Xuan Zhao ◽  
Xiao-Lu Shen ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Synaptic Plasticity ◽  
Anterior Cingulate Cortex ◽  
Nerve Injury ◽  
Cingulate Cortex ◽  
Gamma Oscillations ◽  
Anterior Cingulate ◽  
Neuronal Oscillations ◽  
Electrical Synapses

Abstract Background Synaptic mechanisms and neuronal oscillations have been proposed to be responsible for neuropathic pain formation. Many studies have also highlighted the important role of electrical synapses in synaptic plasticity and in neuronal oscillations. Thus, electrical synapses may contribute to neuropathic pain generation. However, previous studies have primarily focused on the role of chemical synapses, while ignoring the role of electrical synapses, in neuropathic pain generation. Methods The authors adopted microinjection, RNA interference techniques, and behavioral tests to verify the link between connexin 36 (Cx36) and neuropathic pain. They also studied the selective Cx36 blocker mefloquine in rat chronic constriction injury and spared nerve injury model of neuropathic pain. Electrophysiologic recordings were used to further confirm the behavioral data. Results The authors found that Cx36, which constitutes the neuron–neuron electrical synapses, was up-regulated in the anterior cingulate cortex after nerve injury (n = 5). Meanwhile, Cx36-mediated neuronal oscillations in the gamma frequency range (30 to 80 Hz) (n = 7 to 8) and the neuronal synaptic transmission (n = 13 to 19) were also enhanced. Neuropathic pain was relieved by disrupting Cx36 function or expression in the anterior cingulate cortex. They also found that mefloquine, which are clinically used for treating malaria, affected gamma oscillations and synaptic plasticity, leading to a sustained pain relief in chronic constriction injury and spared nerve injury models (n = 7 to 12). Conclusion The electrical synapses blocker mefloquine could affect gamma oscillations and synaptic plasticity in the anterior cingulate cortex and relieve neuropathic pain. Cx36 may be a new therapeutic target for treating chronic pain.

scholarly journals Deep brain stimulation of the dorsal anterior cingulate cortex for the treatment of chronic neuropathic pain

2015 ◽  
Vol 38 (6) ◽  
pp. E11 ◽  
Author(s):  
Jennifer F. Russo ◽  
Sameer A. Sheth
Keyword(s):  
Neuropathic Pain ◽  
Deep Brain Stimulation ◽  
Anterior Cingulate Cortex ◽  
Brain Stimulation ◽  
Cingulate Cortex ◽  
The United States ◽  
Anterior Cingulate ◽  
Dorsal Anterior Cingulate Cortex ◽  
Chronic Neuropathic Pain ◽  
Deep Brain

Chronic neuropathic pain is estimated to affect 3%-4.5% of the worldwide population. It is associated with significant loss of productive time, withdrawal from the workforce, development of mood disorders such as depression and anxiety, and disruption of family and social life. Current medical therapeutics often fail to adequately treat chronic neuropathic pain. Deep brain stimulation (DBS) targeting subcortical structures such as the periaqueductal gray, the ventral posterior lateral and medial thalamic nuclei, and the internal capsule has been investigated for the relief of refractory neuropathic pain over the past 3 decades. Recent work has identified the dorsal anterior cingulate cortex (dACC) as a new potential neuromodulation target given its central role in cognitive and affective processing. In this review, the authors briefly discuss the history of DBS for chronic neuropathic pain in the United States and present evidence supporting dACC DBS for this indication. They review existent literature on dACC DBS and summarize important findings from imaging and neurophysiological studies supporting a central role for the dACC in the processing of chronic neuropathic pain. The available neurophysiological and empirical clinical evidence suggests that dACC DBS is a viable therapeutic option for the treatment of chronic neuropathic pain and warrants further investigation.

scholarly journals Decreased dopaminergic inhibition of pyramidal neurons in anterior cingulate cortex maintains chronic neuropathic pain

Cell Reports ◽  
2021 ◽  
Vol 37 (9) ◽  
pp. 109933
Author(s):  
Kevin Lançon ◽  
Chaoling Qu ◽  
Edita Navratilova ◽  
Frank Porreca ◽  
Philippe Séguéla
Keyword(s):  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Pyramidal Neurons ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Chronic Neuropathic Pain

scholarly journals Evaluation of calcium-sensitive adenylyl cyclase AC1 and AC8 mRNA expression in the anterior cingulate cortex of mice with neuropathic pain

2021 ◽  
Author(s):  
Stephanie Shiers ◽  
Hajira Elahi ◽  
Stephanie Hennen ◽  
Theodore J Price
Keyword(s):  
Neuropathic Pain ◽  
Animal Models ◽  
Mrna Expression ◽  
Anterior Cingulate Cortex ◽  
Nerve Injury ◽  
Visceral Pain ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Mechanical Hypersensitivity

AbstractThe anterior cingulate cortex (ACC) is a critical region of the brain for the emotional and affective components of pain in rodents and humans. Hyperactivity in this region has been observed in neuropathic pain states in both patients and animal models and ablation of this region from cingulotomy, or inhibition with genetics or pharmacology can diminish pain and anxiety. Two adenylyl cyclases (AC), AC1 and AC8 play an important role in regulating nociception and anxiety-like behaviors through an action in the ACC, as genetic and pharmacological targeting of these enzymes reduces mechanical hypersensitivity and anxietylike behavior, respectively. However, the distribution of these ACs in the ACC has not been studied in the context of neuropathic pain. To address this gap in knowledge, we conducted RNAscope in situ hybridization to assess AC1 and AC8 mRNA distribution in mice with spared nerve injury (SNI). Given the key role of AC1 in nociception in neuropathic, inflammatory and visceral pain animal models, we hypothesized that AC1 would be upregulated in the ACC of mice following nerve injury. This hypothesis was also founded on data showing increased AC1 expression in the ACC of mice with zymosan-induced visceral inflammation. We found that AC1 and AC8 are widely expressed in many regions of the mouse brain including the hippocampus, ACC, medial prefrontal cortex and midbrain regions, but AC1 is more highly expressed. Contrary to our hypothesis, SNI causes an increase in AC8 mRNA expression in NMDAR-2B (Nr2b) positive neurons in the contralateral ACC but does not affect AC1 mRNA expression. Our findings show that changes in Adcy1 mRNA expression in the ACC are insufficient to explain the important role of this AC in mechanical hypersensitivity in mice following nerve injury and suggest a potential unappreciated role of AC8 in regulation of ACC synaptic changes after nerve injury.

scholarly journals Role of mu-opioid receptor in nociceptive modulation in anterior cingulate cortex of rats

2020 ◽  
Vol 16 ◽  
pp. 174480692096614
Author(s):  
Linlin Wang ◽  
Kesai Hou ◽  
Hongbo Wang ◽  
Fenghua Fu ◽  
Longchuan Yu
Keyword(s):  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Opioid Receptor ◽  
Cingulate Cortex ◽  
Mu Opioid Receptor ◽  
Receptor Expression ◽  
Anterior Cingulate ◽  
Down Regulation ◽  
Mu Opioid

Lots of studies have demonstrated that anterior cingulate cortex plays important roles in the pain perception and pain modulation. The present study explored the role of mu-opioid receptor in nociceptive modulation in anterior cingulate cortex of rats with neuropathic pain. Neuropathic pain model was set up by chronic constriction injury of the left sciatic nerve of rats. The hindpaw withdrawal latency to thermal and mechanical stimulation, by hot plate and Randall Selitto Test respectively, was used to evaluate the rat’s responses to noxious stimulation. Results showed that intra-anterior cingulate cortex injection of morphine could induce the antinociception dose-dependently. By intra-anterior cingulate cortex injection of opioid receptor antagonist, the morphine-induced antinociception could be attenuated by naloxone, as well as much significantly by the selective mu-opioid receptor antagonist β-funaltrexamine, indicating that mu-opioid receptor is involved in the morphine-induced antinociception in anterior cingulate cortex of rats with neuropathic pain. The morphine-induced antinociception was much more decreased in rats with neuropathic pain than that in normal rats, and there was a significant decrease in mu-opioid receptor messenger RNA levels in anterior cingulate cortex of rats with neuropathic pain, indicating that there may be a down-regulation in mu-opioid receptor expression in anterior cingulate cortex of rats with neuropathic pain. To further confirm the role of mu-opioid receptor in morphine-induced antinociception in anterior cingulate cortex, normal rats were received intra-anterior cingulate cortex administration of small interfering RNA targeting mu-opioid receptor and it was found that there was a down-regulation in mu-opioid receptor messenger RNA levels, as well as a down-regulation in mu-opioid receptor expression in anterior cingulate cortex tested by real-time polymerase chain reaction and western blotting. Furthermore, the morphine-induced antinociceptive effect decreased significantly in rats with small interfering RNA targeting mu-opioid receptor, which indicated that knockdown mu-opioid receptor in anterior cingulate cortex could also attenuate morphine-induced antinociceptive effect. These results strongly suggest that mu-opioid receptor plays a significant role in nociceptive modulation in anterior cingulate cortex of rats.

scholarly journals Cannabis analgesia in chronic neuropathic pain is associated with altered brain connectivity

Neurology ◽  
2018 ◽  
Vol 91 (14) ◽  
pp. e1285-e1294 ◽  
Author(s):  
Libat Weizman ◽  
Lior Dayan ◽  
Silviu Brill ◽  
Hadas Nahman-Averbuch ◽  
Talma Hendler ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Graph Theory ◽  
Functional Connectivity ◽  
Anterior Cingulate Cortex ◽  
Sensorimotor Cortex ◽  
Controlled Trial ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Emotional Modulation ◽  
Chronic Neuropathic Pain

ObjectiveTo characterize the functional brain changes involved in δ-9-tetrahydrocannabinol (THC) modulation of chronic neuropathic pain.MethodsFifteen patients with chronic radicular neuropathic pain participated in a randomized, double-blind, placebo-controlled trial employing a counterbalanced, within-subjects design. Pain assessments and functional resting state brain scans were performed at baseline and after sublingual THC administration. We examined functional connectivity of the anterior cingulate cortex (ACC) and pain-related network dynamics using graph theory measures.ResultsTHC significantly reduced patients' pain compared to placebo. THC-induced analgesia was correlated with a reduction in functional connectivity between the anterior cingulate cortex (ACC) and the sensorimotor cortex. Moreover, the degree of reduction was predictive of the response to THC. Graph theory analyses of local measures demonstrated reduction in network connectivity in areas involved in pain processing, and specifically in the dorsolateral prefrontal cortex (DLPFC), which were correlated with individual pain reduction.ConclusionThese results suggest that the ACC and DLPFC, 2 major cognitive-emotional modulation areas, and their connections to somatosensory areas, are functionally involved in the analgesic effect of THC in chronic pain. This effect may therefore be mediated through induction of functional disconnection between regulatory high-order affective regions and the sensorimotor cortex. Moreover, baseline functional connectivity between these brain areas may serve as a predictor for the extent of pain relief induced by THC.

scholarly journals Role of the Anterior Cingulate Cortex in Translational Pain Research

2021 ◽  
Vol 37 (3) ◽  
pp. 405-422
Author(s):  
Xiao Xiao ◽  
Ming Ding ◽  
Yu-Qiu Zhang
Keyword(s):  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Pain Research
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