scholarly journals The Effect of Electroacupuncture on PKMzeta in the ACC in Regulating Anxiety-Like Behaviors in Rats Experiencing Chronic Inflammatory Pain

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Junying Du ◽  
Junfan Fang ◽  
Cun Wen ◽  
Xiaomei Shao ◽  
Yi Liang ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Protein Expression ◽  
Inflammatory Pain ◽  
Direct Evidence ◽  
Anterior Cingulate ◽  
Model Group ◽  
Pain Model ◽  
Chronic Inflammatory Pain ◽  
Withdrawal Threshold ◽  
Other Substances

Chronic inflammatory pain can induce emotional diseases. Electroacupuncture (EA) has effects on chronic pain and pain-related anxiety. Protein kinase Mzeta (PKMzeta) has been proposed to be essential for the maintenance of pain and may interact with GluR1 to maintain CNS plasticity in the anterior cingulate cortex (ACC). We hypothesized that the PKMzeta-GluR1 pathway in the ACC may be involved in anxiety-like behaviors of chronic inflammatory pain and that the mechanism of EA regulation of pain emotion may involve the PKMzeta pathway in the ACC. Our results showed that chronic inflammatory pain model decreased the paw withdrawal threshold (PWT) and increased anxiety-like behaviors. The protein expression of PKCzeta, p-PKCzeta (T560), PKMzeta, p-PKMzeta (T560), and GluR1 in the ACC of the model group were remarkably enhanced. EA increased PWT and alleviated anxiety-like behaviors. EA significantly inhibited the protein expression of p-PKMzeta (T560) in the ACC, and only a downward trend effect for other substances. Further, the microinjection of ZIP remarkably reversed PWT and anxiety-like behaviors. The present study provides direct evidence that the PKCzeta/PKMzeta-GluR1 pathway is related to pain and pain-induced anxiety-like behaviors. EA treatment both increases pain-related somatosensory behavior and decreases pain-induced anxiety-like behaviors by suppressing PKMzeta activity in the ACC.

scholarly journals Electroacupuncture Ameliorates Chronic Inflammatory Pain-Related Anxiety by Activating PV Interneurons in the Anterior Cingulate Cortex

2021 ◽  
Vol 15 ◽  
Author(s):  
Fangbing Shao ◽  
Junfan Fang ◽  
Mengting Qiu ◽  
Sisi Wang ◽  
Danning Xi ◽  
...  
Keyword(s):  
Anterior Cingulate Cortex ◽  
Inflammatory Pain ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Aminobutyric Acid ◽  
Anxiety And Depression ◽  
Pain Sensation ◽  
Pain Model ◽  
Chronic Inflammatory Pain ◽  
Underlying Mechanisms

Chronic inflammatory pain is a common clinical disease that tends to be associated with negative emotions such as anxiety and depression. The anterior cingulate cortex (ACC) is involved in pain and pain-related anxiety, and γ-aminobutyric acid (GABA)-ergic interneurons play an important role in chronic pain and anxiety. Electroacupuncture (EA) has good analgesic and antianxiety effect, but the underlying mechanisms have not yet been fully elucidated. In this study, we established a chronic inflammatory pain model and observed that this model induced anxiety-like behaviors and decreased the numbers of parvalbumin (PV) and somatostatin (SOM) positive cells. Activation of PV but not SOM interneurons by chemogenetic techniques alleviated anxiety-like behaviors and pain sensation. EA treatment improved pain sensation, anxiety-like behaviors and increased the number of PV- positive cells in the ACC, but did not affect on the number of SOM-positive cells in the ACC. Moreover, specific inhibition of PV interneurons by chemogenetic methods reversed the analgesic and antianxiety effects of EA. These results suggest that EA ameliorates chronic inflammatory pain and pain-related anxiety by upregulating PV but not SOM interneurons in the ACC.

scholarly journals Anxiolytic effect of GABAergic neurons in the anterior cingulate cortex in a rat model of chronic inflammatory pain

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Fang-bing Shao ◽  
Jun-fan Fang ◽  
Si-si Wang ◽  
Meng-ting Qiu ◽  
Dan-ning Xi ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Anterior Cingulate Cortex ◽  
Rat Model ◽  
Inflammatory Pain ◽  
Pyramidal Neurons ◽  
Cingulate Cortex ◽  
Gabaergic Neurons ◽  
Gabaergic System ◽  
Anterior Cingulate ◽  
Chronic Inflammatory Pain

AbstractChronic pain easily leads to concomitant mood disorders, and the excitability of anterior cingulate cortex (ACC) pyramidal neurons (PNs) is involved in chronic pain-related anxiety. However, the mechanism by which PNs regulate pain-related anxiety is still unknown. The GABAergic system plays an important role in modulating neuronal activity. In this paper, we aimed to study how the GABAergic system participates in regulating the excitability of ACC PNs, consequently affecting chronic inflammatory pain-related anxiety. A rat model of CFA-induced chronic inflammatory pain displayed anxiety-like behaviors, increased the excitability of ACC PNs, and reduced inhibitory presynaptic transmission; however, the number of GAD65/67 was not altered. Interestingly, intra-ACC injection of the GABAAR agonist muscimol relieved anxiety-like behaviors but had no effect on chronic inflammatory pain. Intra-ACC injection of the GABAAR antagonist picrotoxin induced anxiety-like behaviors but had no effect on pain in normal rats. Notably, chemogenetic activation of GABAergic neurons in the ACC alleviated chronic inflammatory pain and pain-induced anxiety-like behaviors, enhanced inhibitory presynaptic transmission, and reduced the excitability of ACC PNs. Chemogenetic inhibition of GABAergic neurons in the ACC led to pain-induced anxiety-like behaviors, reduced inhibitory presynaptic transmission, and enhanced the excitability of ACC PNs but had no effect on pain in normal rats. We demonstrate that the GABAergic system mediates a reduction in inhibitory presynaptic transmission in the ACC, which leads to enhanced excitability of pyramidal neurons in the ACC and is associated with chronic inflammatory pain-related anxiety.

scholarly journals Effect of 5-trifluoromethyl-4,5-dihydro-1H-pyrazoles on chronic inflammatory pain model in rats

2009 ◽  
Vol 616 (1-3) ◽  
pp. 91-100 ◽  
Author(s):  
Patricia D. Sauzem ◽  
Gabriela da S. Sant'Anna ◽  
Pablo Machado ◽  
Marta M.M.F. Duarte ◽  
Juliano Ferreira ◽  
...  
Keyword(s):  
Inflammatory Pain ◽  
Pain Model ◽  
Chronic Inflammatory Pain

scholarly journals The analgesic effect of refeeding on acute and chronic inflammatory pain

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jeong-Yun Lee ◽  
Grace J. Lee ◽  
Pa Reum Lee ◽  
Chan Hee Won ◽  
Doyun Kim ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Inflammatory Pain ◽  
Analgesic Effect ◽  
Cannabinoid Receptor ◽  
Pain Behavior ◽  
Spontaneous Pain ◽  
Second Phase ◽  
Pain Model ◽  
Chronic Inflammatory Pain ◽  
Effect Of Food

AbstractPain is susceptible to various cognitive factors. Suppression of pain by hunger is well known, but the effect of food intake after fasting (i.e. refeeding) on pain remains unknown. In the present study, we examined whether inflammatory pain behavior is affected by 24 h fasting and 2 h refeeding. In formalin-induced acute inflammatory pain model, fasting suppressed pain behavior only in the second phase and the analgesic effect was also observed after refeeding. Furthermore, in Complete Freund’s adjuvant-induced chronic inflammatory pain model, both fasting and refeeding reduced spontaneous pain response. Refeeding with non-calorie agar produced an analgesic effect. Besides, intraperitoneal (i.p.) administration of glucose after fasting, which mimics calorie recovery following refeeding, induced analgesic effect. Administration of opioid receptor antagonist (naloxone, i.p.) and cannabinoid receptor antagonist (SR 141716, i.p.) reversed fasting-induced analgesia, but did not affect refeeding-induced analgesia in acute inflammatory pain model. Taken together, our results show that refeeding produce analgesia in inflammatory pain condition, which is associated with eating behavior and calorie recovery effect.

scholarly journals Inhibition of calcium-stimulated adenylyl cyclase subtype 1 (AC1) for the treatment of neuropathic and inflammatory pain in adult female mice

2021 ◽  
Vol 17 ◽  
pp. 174480692110216
Author(s):  
Zhaoxiang Zhou ◽  
Wantong Shi ◽  
Kexin Fan ◽  
Man Xue ◽  
Sibo Zhou ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Animal Models ◽  
Adenylyl Cyclase ◽  
Adult Female ◽  
Inflammatory Pain ◽  
Long Term Potentiation ◽  
Anterior Cingulate ◽  
Therapeutic Drug ◽  
Female Mice ◽  
Genetic Deletion

Cortical long-term potentiation (LTP) serves as a cellular model for chronic pain. As an important subtype of adenylyl cyclases (ACs), adenylyl cyclase subtype 1 (AC1) is critical for the induction of cortical LTP in the anterior cingulate cortex (ACC). Genetic deletion of AC1 or pharmacological inhibition of AC1 blocked behavioral allodynia in animal models of neuropathic and inflammatory pain. Our previous experiments have identified a lead candidate AC1 inhibitor, NB001, which is highly selective for AC1 over other AC isoforms, and found that NB001 is effective in inhibiting behavioral allodynia in animal models of chronic neuropathic and inflammatory pain. However, previous experiments were carried out in adult male animals. Considering the potential gender difference as an important issue in researches of pain and analgesia, we investigated the effect of NB001 in female chronic pain animal models. We found that NB001, when administered orally, has an analgesic effect in female animal models of neuropathic and inflammatory pain without any observable side effect. Genetic deletion of AC1 also reduced allodynia responses in models of neuropathic pain and chronic inflammation pain in adult female mice. In brain slices of adult female mice, bath application of NB001(20 μM) blocked the induction of LTP in ACC. Our results indicate that calcium-stimulated AC1 is required for injury-related cortical LTP and behavioral allodynia in both sexes of adult animals, and NB001 can be used as a potential therapeutic drug for treating neuropathic and inflammatory pain in man and woman.

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