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

2021 ◽  
pp. 100081
Author(s):  
Stephanie Shiers ◽  
Hajira Elahi ◽  
Stephanie Hennenb ◽  
Theodore J Price
Keyword(s):  
Neuropathic Pain ◽  
Mrna Expression ◽  
Adenylyl Cyclase ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate

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 Gene expression profile of sodium channel subunits in the anterior cingulate cortex during experimental paclitaxel-induced neuropathic pain in mice

2016 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Sodium Channel ◽  
Mrna Expression ◽  
Anterior Cingulate Cortex ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Beta Subunits ◽  
Channel Expression

Paclitaxel, a chemotherapeutic agent, causes neuropathic pain whose supraspinal pathophysiology is not fully understood. Dysregulation of sodium channel expression, studied mainly in the periphery and spinal cord level, contributes to the pathogenesis of neuropathic pain. We examined gene expression of sodium channel subunits by real time PCR in the anterior cingulate cortex (ACC) at day 7 post first administration of paclitaxel, when mice had developed paclitaxel-induced thermal hyperalgesia. The ACC was chosen because increased activity in the ACC has been observed during neuropathic pain. In the ACC of control animals the Ct values for Nav1.4, Nav1.5, Nav1.7, Nav1.8 and Nav1.9 were above 30 and/or not detectable in some samples. Thus, comparison in mRNA expression between control and paclitaxel treated animals was done for Nav1.1, Nav1.2, Nav1.3, Nav1.6, Nax as well as Navβ1-Navβ4. Paclitaxel treatment significantly increased the mRNA expression of Nav1.1, Nav1.2, Nav1.6 and Nax, but not Nav1.3, sodium channel alpha subunits compared to vehicle-treated controls. Amongst the sodium channel beta subunits treatment with paclitaxel significantly increased the expression of Navβ1 and Navβ3, but not Navβ2 and Navβ4, compared to vehicle-treated controls. These findings suggest that during PINP there is differential upregulation of sodium channels in the ACC, which might contribute to the increased neuronal activity observed in the area during neuropathic pain.

scholarly journals Gene expression profile of sodium channel subunits in the anterior cingulate cortex during experimental paclitaxel-induced neuropathic pain in mice

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e2702 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Sodium Channel ◽  
Mrna Expression ◽  
Anterior Cingulate Cortex ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Channel Expression ◽  
Vehicle Treatment

Paclitaxel, a chemotherapeutic agent, causes neuropathic pain whose supraspinal pathophysiology is not fully understood. Dysregulation of sodium channel expression, studied mainly in the periphery and spinal cord level, contributes to the pathogenesis of neuropathic pain. We examined gene expression of sodium channel (Nav) subunits by real time polymerase chain reaction (PCR) in the anterior cingulate cortex (ACC) at day 7 post first administration of paclitaxel, when mice had developed paclitaxel-induced thermal hyperalgesia. The ACC was chosen because increased activity in the ACC has been observed during neuropathic pain. In the ACC of vehicle-treated animals the threshold cycle (Ct) values for Nav1.4, Nav1.5, Nav1.7, Nav1.8 and Nav1.9 were above 30 and/or not detectable in some samples. Thus, comparison in mRNA expression between untreated control, vehicle-treated and paclitaxel treated animals was done for Nav1.1, Nav1.2, Nav1.3, Nav1.6, Naxas well as Navβ1–Navβ4. There were no differences in the transcript levels of Nav1.1–Nav1.3, Nav1.6, Nax, Navβ1–Navβ3 between untreated and vehicle-treated mice, however, vehicle treatment increased Navβ4 expression. Paclitaxel treatment significantly increased the mRNA expression of Nav1.1, Nav1.2, Nav1.6 and Nax, but not Nav1.3, sodium channel alpha subunits compared to vehicle-treated animals. Treatment with paclitaxel significantly increased the expression of Navβ1 and Navβ3, but not Navβ2 and Navβ4, sodium channel beta subunits compared to vehicle-treated animals. These findings suggest that during paclitaxel-induced neuropathic pain (PINP) there is differential upregulation of sodium channels in the ACC, which might contribute to the increased neuronal activity observed in the area during neuropathic pain.

scholarly journals Gene expression profile of sodium channel subunits in the anterior cingulate cortex during experimental paclitaxel-induced neuropathic pain in mice

2016 ◽  
Author(s):  
Willias Masocha
Keyword(s):  
Gene Expression ◽  
Neuropathic Pain ◽  
Sodium Channel ◽  
Mrna Expression ◽  
Anterior Cingulate Cortex ◽  
Thermal Hyperalgesia ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Beta Subunits ◽  
Channel Expression

Paclitaxel, a chemotherapeutic agent, causes neuropathic pain whose supraspinal pathophysiology is not fully understood. Dysregulation of sodium channel expression, studied mainly in the periphery and spinal cord level, contributes to the pathogenesis of neuropathic pain. We examined gene expression of sodium channel subunits by real time PCR in the anterior cingulate cortex (ACC) at day 7 post first administration of paclitaxel, when mice had developed paclitaxel-induced thermal hyperalgesia. The ACC was chosen because increased activity in the ACC has been observed during neuropathic pain. In the ACC of control animals the Ct values for Nav1.4, Nav1.5, Nav1.7, Nav1.8 and Nav1.9 were above 30 and/or not detectable in some samples. Thus, comparison in mRNA expression between control and paclitaxel treated animals was done for Nav1.1, Nav1.2, Nav1.3, Nav1.6, Nax as well as Navβ1-Navβ4. Paclitaxel treatment significantly increased the mRNA expression of Nav1.1, Nav1.2, Nav1.6 and Nax, but not Nav1.3, sodium channel alpha subunits compared to vehicle-treated controls. Amongst the sodium channel beta subunits treatment with paclitaxel significantly increased the expression of Navβ1 and Navβ3, but not Navβ2 and Navβ4, compared to vehicle-treated controls. These findings suggest that during PINP there is differential upregulation of sodium channels in the ACC, which might contribute to the increased neuronal activity observed in the area during neuropathic pain.

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

Author response: Insular and anterior cingulate cortex deep stimulation for central neuropathic pain: Disassembling the percept of pain

Neurology ◽  
2020 ◽  
Vol 94 (16) ◽  
pp. 721-722
Author(s):  
Daniel Ciampi de Andrade ◽  
Ricardo Galhardoni ◽  
Valquíria Aparecida da Silva ◽  
Luís García-Larrea ◽  
Camila Dale ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Author Response ◽  
Central Neuropathic Pain

Expression of muscarinic M1 and M2 receptors in the anterior cingulate cortex associated with neuropathic pain

2010 ◽  
Vol 14 (9) ◽  
pp. 901-910 ◽  
Author(s):  
J. Manuel Ortega-Legaspi ◽  
Martha León-Olea ◽  
Patricia de Gortari ◽  
María Isabel Amaya ◽  
Ulises Coffeen ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate

Astrocytic activation in the anterior cingulate cortex is critical for sleep disorder under neuropathic pain

Synapse ◽  
2014 ◽  
Vol 68 (6) ◽  
pp. 235-247 ◽  
Author(s):  
Akira Yamashita ◽  
Asami Hamada ◽  
Yuki Suhara ◽  
Rui Kawabe ◽  
Makoto Yanase ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Sleep Disorder ◽  
Anterior Cingulate Cortex ◽  
Cingulate Cortex ◽  
Anterior Cingulate
Sign in / Sign up

Export Citation Format

Share Document