Injecting NMDA and Ro 25‐6981 in insular cortex induce neuroplastic changes and neuropathic pain‐like behaviour

Koh, Chin Su; Lee, J.; Shin, Jaewoo; Kong, Chanho; Jung, Hyun Ho; Chang, Jin Woo

doi:10.1002/ejp.1254

Cited by 2 publications

(1 citation statement)

References 48 publications

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“…Excitatory synapses are highly plastic, and LTP of glutamatergic transmission within IC is a key cellular mechanism for pathological pain [13]. Inducing LTP-like neuroplastic changes via injecting NMDA into IC in naïve rats produces mechanical allodynia [53], while inhibiting insular LTP via PKM휁 inhibitor elicited analgesic effects under the condition of neuropathic pain [20]. In the present study, insular post-LTP could be induced via TBS stimulation in sham rats instead of TNBS-treated rats.…”

Section: Discussionmentioning

confidence: 99%

Anterior insular cortex mediates hyperalgesia induced by chronic pancreatitis in rats

Bai

Chen

et al. 2019

Mol Brain

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Central sensitization plays a pivotal role in the maintenance of chronic pain induced by chronic pancreatitis (CP), but cortical modulation of painful CP remains elusive. This study was designed to examine the role of anterior insular cortex (aIC) in the pathogenesis of hyperalgesia in a rat model of CP. CP was induced by intraductal administration of trinitrobenzene sulfonic acid (TNBS). Abdomen hyperalgesia and anxiety were assessed by von Frey filament and open field tests, respectively. Two weeks after surgery, the activation of aIC was indicated by FOS immunohistochemical staining and electrophysiological recordings. Expressions of VGluT1, NMDAR subunit NR2B and AMPAR subunit GluR1 were analyzed by immunoblottings. The regulatory roles of aIC in hyperalgesia and pain-related anxiety were detected via pharmacological approach and chemogenetics in CP rats. Our results showed that TNBS treatment resulted in long-term hyperalgesia and anxiety-like behavior in rats. CP rats exhibited increased FOS expression and potentiated excitatory synaptic transmission within aIC. CP rats also showed up-regulated expression of VGluT1, and increased membrane trafficking and phosphorylation of NR2B and GluR1 within aIC. Blocking excitatory synaptic transmission significantly attenuated abdomen mechanical hyperalgesia. Specifically inhibiting the excitability of insular pyramidal cells reduced both abdomen hyperalgesia and pain-related anxiety. In conclusion, our findings emphasize a key role for aIC in hyperalgesia and anxiety of painful CP, providing a novel insight into cortical modulation of painful CP and shedding light on aIC as a potential target for neuromodulation interventions in the treatment of CP.

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Section: Discussionmentioning

confidence: 99%

Anterior insular cortex mediates hyperalgesia induced by chronic pancreatitis in rats

Bai

Chen

et al. 2019

Mol Brain

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Arc-Mediated Synaptic Plasticity Regulates Cognitive Function in a Migraine Mouse Model

Gong

Zhou

et al. 2023

Brain Sciences

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Previous clinical and basic studies have shown that migraine is associated with cognitive impairment, anxiety, and depression. It severely affects the quality of life. In this study, C57BL/6 mice were randomly divided into four groups: IS group, IS+M group, and IS+S group with repeated application of dural inflammatory soup (IS) stimulation to establish a migraine model, followed by PBS, memantine, and sumatriptan interventions, respectively; the blank control group underwent the same treatment procedure but with PBS instead of IS and intervention drugs. The cognitive function of the mice was used as the main outcome indicator. After application of the IS, mice showed reduced pain threshold for mechanical stimulation, decreased learning memory capacity, attention deficit, a reduced number of dendritic spines in hippocampal neurons, and altered synaptic ultrastructure. The cognitive function indexes of mice in the IS+M group recovered with changes in Arc protein expression to a level not statistically different from that of the Control group, while the IS and IS+S groups remained at lower levels. The present results suggest that Arc-mediated synaptic plasticity may be an essential mechanism of cognitive dysfunction in migraine.

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Injecting NMDA and Ro 25‐6981 in insular cortex induce neuroplastic changes and neuropathic pain‐like behaviour

Cited by 2 publications

References 48 publications

Anterior insular cortex mediates hyperalgesia induced by chronic pancreatitis in rats

Anterior insular cortex mediates hyperalgesia induced by chronic pancreatitis in rats

Arc-Mediated Synaptic Plasticity Regulates Cognitive Function in a Migraine Mouse Model

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