In vivo voltage-sensitive dye imaging of the insular cortex in nerve-injured rats

Han, Jung Suk; Cha, Min‐Ji; Kwon, Minjee; Hong, Seong-Karp; Bai, Sun Joon; Lee, Bae Hwan

doi:10.1016/j.neulet.2016.10.015

Cited by 12 publications

(15 citation statements)

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“…In the present study, amplified and expanded neuronal signals, followed by hind paw stimulation in nerve-injured rats, may provide overt evidence that persistent hyperalgesia and allodynia in neuropathic rats give rise to alteration in the pain matrix of the brain [17, 18]. fMRI studies of hyperalgesia in rats have demonstrated the involvement of the somatosensory cortex in the pain pathway originating from nociceptive inputs [24, 25].…”

Section: Discussionmentioning

confidence: 95%

“…The ability to image the spatiotemporal cortical activation pattern is beneficial for understanding the mechanisms of neural plasticity such as formation, progression, and extension. Current optical imaging studies show a high spatial resolution for neural activities in the cerebral cortex, visualize temporal patterns of activated signals in the cortical tissue, and investigate the characteristic patterns in neural activation of the brain [18–20]. In a recent study regarding spatiotemporal patterns of activated signals using optical imaging, Lusting et al [19] reported a spatial shift in the center of activation in the somatosensory cortex within a 10 to 20-ms period after whisker stimulation.…”

Section: Introductionmentioning

confidence: 99%

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Spatiotemporal changes of optical signals in the somatosensory cortex of neuropathic rats after electroacupuncture stimulation

Cha

Chae

Bai

2017

BMC Complement Altern Med

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BackgroundPeripheral nerve injury causes physiological changes in primary afferent neurons. Neuropathic pain associated with peripheral nerve injuries may reflect changes in the excitability of the nervous system, including the spinothalamic tract. Current alternative medical research indicates that acupuncture stimulation has analgesic effects in various pain symptoms. However, activation changes in the somatosensory cortex of the brain by acupuncture stimulation remain poorly understood. The present study was conducted to monitor the changes in cortical excitability, using optical imaging with voltage-sensitive dye (VSD) in neuropathic rats after electroacupuncture (EA) stimulation.MethodsMale Sprague–Dawley rats were divided into three groups: control (intact), sham injury, and neuropathic pain rats. Under pentobarbital anesthesia, rats were subjected to nerve injury with tight ligation and incision of the tibial and sural nerves in the left hind paw. For optical imaging, the rats were re-anesthetized with urethane, and followed by craniotomy. The exposed primary somatosensory cortex (S1) was stained with VSD for one hour. Optical signals were recorded from the S1 cortex, before and after EA stimulation on Zusanli (ST36) and Yinlingquan (SP9).ResultsAfter peripheral stimulation, control and sham injury rats did not show significant signal changes in the S1 cortex. However, inflamed and amplified neural activities were observed in the S1 cortex of nerve-injured rats. Furthermore, the optical signals and region of activation in the S1 cortex were reduced substantially after EA stimulation, and recovered in a time-dependent manner. The peak fluorescence intensity was significantly reduced until 90 min after EA stimulation (Pre-EA: 0.25 ± 0.04 and Post-EA 0 min: 0.01 ± 0.01), and maximum activated area was also significantly attenuated until 60 min after EA stimulation (Pre-EA: 37.2 ± 1.79 and Post-EA 0 min: 0.01 ± 0.10).ConclusionOur results indicate that EA stimulation has inhibitory effects on excitatory neuronal signaling in the S1 cortex, caused by noxious stimulation in neuropathic pain. These findings suggest that EA stimulation warrants further study as a potential adjuvant modulation of neuropathic pain.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Spatiotemporal changes of optical signals in the somatosensory cortex of neuropathic rats after electroacupuncture stimulation

Cha

Chae

Bai

2017

BMC Complement Altern Med

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“…Optical imaging was conducted as described in a previous article (Han et al, 2016) with a slight modification. Before imaging, 16 Sprague-Dawley male rats (250–300 g; n = 8/group) were deeply anesthetized with urethane (1.25 g/kg, i.p.)…”

Section: Methodsmentioning

confidence: 99%

“…Changes in optical intensity in the IC were expressed as a percentage of fractional change in fluorescence (ΔF/F × 100). Activated areas were analyzed using the activated pixel number of an ROI (previously described in Han et al, 2016)/total pixel number of the ROI × 100. Data were collected and analyzed with BV Analyzer software (Brainvision, Inc.).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Mammalian Target of Rapamycin (mTOR) Signaling in the Insular Cortex Alleviates Neuropathic Pain after Peripheral Nerve Injury

Kwon

Han

Kim

et al. 2017

Front. Mol. Neurosci.

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Injury of peripheral nerves can trigger neuropathic pain, producing allodynia and hyperalgesia via peripheral and central sensitization. Recent studies have focused on the role of the insular cortex (IC) in neuropathic pain. Because the IC is thought to store pain-related memories, translational regulation in this structure may reveal novel targets for controlling chronic pain. Signaling via mammalian target of rapamycin (mTOR), which is known to control mRNA translation and influence synaptic plasticity, has been studied at the spinal level in neuropathic pain, but its role in the IC under these conditions remains elusive. Therefore, this study was conducted to determine the role of mTOR signaling in neuropathic pain and to assess the potential therapeutic effects of rapamycin, an inhibitor of mTORC1, in the IC of rats with neuropathic pain. Mechanical allodynia was assessed in adult male Sprague-Dawley rats after neuropathic surgery and following microinjections of rapamycin into the IC on postoperative days (PODs) 3 and 7. Optical recording was conducted to observe the neural responses of the IC to peripheral stimulation. Rapamycin reduced mechanical allodynia and downregulated the expression of postsynaptic density protein 95 (PSD95), decreased neural excitability in the IC, thereby inhibiting neuropathic pain-induced synaptic plasticity. These findings suggest that mTOR signaling in the IC may be a critical molecular mechanism modulating neuropathic pain.

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“…After injection of AAV-CaMKII-hM4Di-2A-GHS-R1a-GFP into a specific brain region, infected neurons co-express GHS-R1a, hM4Di, and GFP. Subsequent intraperitoneal injection of clozapine-N-oxide (CNO) [8][9][10][11] specifically activates hM4Di after 45 min and results in neuronal inactivation due to hyperpolarization. Conditioned taste aversion (CTA) is an experimental model commonly used in studies of memory and learning.…”

Section: Introductionmentioning

confidence: 99%

The Ghrelin/GHS-R1a Pathway is Involved in the Mechanism of the CTA-regulated Neuronal Loop

Wang¹

2017

ijSciences

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Abstract:Objective: We aimed to investigate the effects of ghrelin and its receptor GHS-R1a on the regulation of taste aversion-associated emotional memory. Methods: We studied the effect of selective and reversible inactivation of emotion-associated neurons on emotions processed by the local neuronal loop of the lateral amygdala and insular cortex. We used intraperitoneal clozapine-N oxide (CNO) injection, local brain microinjection, and taste aversion test. Results: Microinjection of ghrelin into the lateral amygdala blocked the acquisition of taste aversion memory in mice. However, microinjection of ghrelin did not affect memory consolidation. Adeno-associated virus (AAV) microinjection into the lateral amygdaloid nucleus blocked the acquisition of taste aversion memory in mice.Moreover, intraperitoneal injection of CNO inhibited taste aversion memory formation, altering the aversion index.Conclusion: Microinjection of ghrelin and AAV-CaMKII-hM4Di-2A-GHS-R1a-GFP into the lateral amygdala inhibited the acquisition of conditioned taste aversion in mice. The inhibition of the memory formation was achieved through the activation of growth hormone secretagogue receptor 1a (GHS-R1a).

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In vivo voltage-sensitive dye imaging of the insular cortex in nerve-injured rats

Cited by 12 publications

References 47 publications

Spatiotemporal changes of optical signals in the somatosensory cortex of neuropathic rats after electroacupuncture stimulation

Spatiotemporal changes of optical signals in the somatosensory cortex of neuropathic rats after electroacupuncture stimulation

Inhibition of Mammalian Target of Rapamycin (mTOR) Signaling in the Insular Cortex Alleviates Neuropathic Pain after Peripheral Nerve Injury

The Ghrelin/GHS-R1a Pathway is Involved in the Mechanism of the CTA-regulated Neuronal Loop

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