Chronic inflammatory pain induced GABAergic synaptic plasticity in the adult mouse anterior cingulate cortex

Koga, Katsumi; Shimoyama, Shuji; Yamada, Akira; Furukawa, Tatsuo; Nikaido, Yoshikazu; Furue, Hidemasa; Nakamura, Kazuhiko; Ueno, Shinji

doi:10.1177/1744806918783478

Cited by 34 publications

(33 citation statements)

References 46 publications

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“…GABA is the cardinal inhibitory neurotransmitter in the mammalian CNS which involves different functions, such as pain modulation. In fact, GABA exerts its action via ionotropic GABA A and metabotropic BABA B receptors [8–10,25,34–36]. GABA A receptors seem to be the most important and abundant inhibitory receptors in the CNS [11,19].…”

Section: Discussionmentioning

confidence: 99%

The antinociceptive effect of artemisinin on the inflammatory pain and role of GABAergic and opioidergic systems

et al. 2019

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Background Pain is a complex mechanism which involves different systems, including the opioidergic and GABAergic systems. Due to the side effects of chemical analgesic agents, attention toward natural agents have been increased. Artemisinin is an herbal compound with widespread modern and traditional therapeutic indications, which its interaction with the GABAergic system and antinoniceptive effects on neuropathic pain have shown. Therefore, this study was designed to evaluate the antinociceptive effects of artemisinin during inflammatory pain and interaction with the GABAergic and opioidergic systems by using a writhing response test. Methods On the whole, 198 adult male albino mice were used in 4 experiments, including 9 groups (n = 6) each with three replicates, by intraperitoneal (i.p.) administration of artemisinin (2.5, 5, and 10 mg/kg), naloxone (2 mg/kg), bicuculline (2 mg/kg), saclofen (2 mg/kg), indomethacin (5 mg/kg), and ethanol (10 mL/kg). Writhing test responses were induced by i.p. injection of 10 mL/kg of 0.6% acetic acid, and the percentage of writhing inhibition was recorded. Results Results showed significant dose dependent anti-nociceptive effects from artemisinin which, at a 10 mg/kg dose, was statistically similar to indomethacin. Neither saclofen nor naloxone had antinociceptive effects and did not antagonize antinociceptive effects of artemisinin, whereas bicuculline significantly inhibited the antinocicptive effect of artemisinin. Conclusions It seems that antinocicptive effects of artemisinin are mediated by GABA A receptors.

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Section: Discussionmentioning

confidence: 99%

The antinociceptive effect of artemisinin on the inflammatory pain and role of GABAergic and opioidergic systems

et al. 2019

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“…In complete Freund adjuvant-induced chronic inflammatory pain mice, there are no changes in the protein levels of GABA A subunits, but reduced GAT expression is observed in the ACC. 111 Cancer-induced bone pain (CIBP) is a challenge in patients with advanced cancer. Zhou et al.…”

Section: Effects Of the Gabaergic System In Other Type Of Chronic Painmentioning

confidence: 99%

The etiological contribution of GABAergic plasticity to the pathogenesis of neuropathic pain

Lei

Tian

et al. 2019

Mol Pain

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Neuropathic pain developing after peripheral or central nerve injury is the result of pathological changes generated through complex mechanisms. Disruption in the homeostasis of excitatory and inhibitory neurons within the central nervous system is a crucial factor in the formation of hyperalgesia or allodynia occurring with neuropathic pain. The central GABAergic pathway has received attention for its extensive distribution and function in neural circuits, including the generation and development of neuropathic pain. GABAergic inhibitory changes that occur in the interneurons along descending modulatory and nociceptive pathways in the central nervous system are believed to generate neuronal plasticity, such as synaptic plasticity or functional plasticity of the related genes or proteins, that is the foundation of persistent neuropathic pain. The primary GABAergic plasticity observed in neuropathic pain includes GABAergic synapse homo- and heterosynaptic plasticity, decreased synthesis of GABA, down-expression of glutamic acid decarboxylase and GABA transporter, abnormal expression of NKCC1 or KCC2, and disturbed function of GABA receptors. In this review, we describe possible mechanisms associated with GABAergic plasticity, such as central sensitization and GABAergic interneuron apoptosis, and the epigenetic etiologies of GABAergic plasticity in neuropathic pain. Moreover, we summarize potential therapeutic targets of GABAergic plasticity that may allow for successful relief of hyperalgesia from nerve injury. Finally, we compare the effects of the GABAergic system in neuropathic pain to other types of chronic pain to understand the contribution of GABAergic plasticity to neuropathic pain.

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“…Thibault and his colleagues reported that brain-derived neurotrophic factor expression is increased in the ACC during inflammation and is sufficient to induce a series of plastic changes such as LTP and extracellular regulated protein kinases phosphorylation leading to cold hypersensitivity, and this could be one such mechanism behind the induction and maintenance of the affective-emotional aspect of pain [20]. Koga and his colleagues demonstrated that presynaptic but not postsynaptic changes occur in the β-aminobutyric acid system during early phases in this chronic inflammatory pain model [19].…”

Section: Discussionmentioning

confidence: 91%

“…Recent studies have found that there is a close relationship between ACC and inflammatory pain [19]. Thibault and his colleagues reported that brain-derived neurotrophic factor expression is increased in the ACC during inflammation and is sufficient to induce a series of plastic changes such as LTP and extracellular regulated protein kinases phosphorylation leading to cold hypersensitivity, and this could be one such mechanism behind the induction and maintenance of the affective-emotional aspect of pain [20].…”

Section: Discussionmentioning

confidence: 99%

Role of Mu-Opioid Receptor in Nociceptive Modulation in the Anterior Cingulate Cortex of Rats with Inflammatory Pain

LL¹,

KS²,

Hb³

et al. 2019

J Clin Exp Pharmacol

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Objective: The present study was performed to explore the role of mu opioid receptor (MOR) in nociceptive modulation in anterior cingulate cortex (ACC) of rats with inflammatory pain. Methods: To set up an inflammatory pain model, rats received a subcutaneous injection of 0.1 ml of 2% carrageenan into the left hind paw. The hind paw withdrawal latency (HWL) to thermal and mechanical stimulation, by hot plate and Randall Selitto Test respectively, was used to evaluate the rat's responses to noxious stimulation. The influence of inflammatory pain on MOR mRNA level and MOR expression in ACC were assayed by Reverse Transcription Polymerase Chain Reaction (RT-PCR) and western blot. Results: We found that intra-ACC administration of morphine-induced significant antinociceptive effects in a dosedependent manner in rats with inflammatory pain. Furthermore, the antinociceptive effects induced by morphine were attenuated by intra-ACC injection of the opioid receptor antagonist naloxone, indicating involvement of opioid receptor in nociceptive modulation in ACC in rats with inflammatory pain. Moreover, intra-ACC administration of the MOR antagonist β-funaltrexamine (β-FNA) attenuated the morphine-induced antinociception significantly in rats with inflammatory pain. Interestingly, we found that there were significant decreases in MOR mRNA level and MOR expression in ACC in rats with inflammatory pain compared with intact rats tested by RT-PCR and western blot, indicating that there is a down-regulation in MOR expression in rats with inflammatory pain, which support our above results that morphine-induced antinociception was lower in rats with inflammatory pain than that in normal rats. Conclusion: These findings suggest that MOR plays an important role in nociceptive modulation in ACC in rats with inflammatory pain and there is a down-regulation in MOR expression in rats with inflammatory pain.

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Chronic inflammatory pain induced GABAergic synaptic plasticity in the adult mouse anterior cingulate cortex

Cited by 34 publications

References 46 publications

The antinociceptive effect of artemisinin on the inflammatory pain and role of GABAergic and opioidergic systems

The antinociceptive effect of artemisinin on the inflammatory pain and role of GABAergic and opioidergic systems

The etiological contribution of GABAergic plasticity to the pathogenesis of neuropathic pain

Role of Mu-Opioid Receptor in Nociceptive Modulation in the Anterior Cingulate Cortex of Rats with Inflammatory Pain

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