Neuronal Mechanism for Neuropathic Pain

Zhuo, Min

doi:10.1186/1744-8069-3-14

Cited by 109 publications

(108 citation statements)

References 74 publications

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“…Hippocampus and hippocampus-related limbic structures are proposed to be critical for spatial learning and memory (Kandel, 2001). Unlike the hippocampus, the ACC is critical for affective cognitive functions, including decision making, trace memory, attention, and persistent pain (Zhuo, 2007). ACC LTP can be induced by different induction protocols.…”

Section: Discussionmentioning

confidence: 99%

“…First, peripheral injuries trigger plastic changes in the ACC, including an array of activity-dependent immediate early genes, and enhanced synaptic responses (Wei et al, 1999;Wu et al, 2005;Zhuo, 2007). No identification of presynaptic versus postsynaptic mechanisms have been performed in the ACC in case of nerve Figure 5.…”

Section: Discussionmentioning

confidence: 99%

“…It is believed that such changes in synaptic transmission play key roles in fear memory. Similarities between persistent pain and memory have been recently reported (Woolf and Salter, 2000;Wei et al, 2001Wei et al, , 2002Sandkühler, 2007;Zhuo, 2007). Long-term changes in synaptic transmission, occurring in sensory synapses located along the somatosensory pathway or pain-processing brain regions, contribute to chronic inflammatory and neuropathic pain (Woolf and Salter, 2000;Wei et al, 2001;Sandkühler, 2007;Zhuo, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex

Xu¹,

Wu²,

Wang³

et al. 2008

J. Neurosci.

323

324

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Neuropathic pain is caused by a primary lesion or dysfunction in the nervous system. Investigations have mainly focused on the spinal mechanisms of neuropathic pain, and less is known about cortical changes in neuropathic pain. Here, we report that peripheral nerve injury triggered long-term changes in excitatory synaptic transmission in layer II/III neurons within the anterior cingulate cortex (ACC). Both the presynaptic release probability of glutamate and postsynaptic glutamate AMPA receptor-mediated responses were enhanced after injury using the mouse peripheral nerve injury model. Western blot showed upregulated phosphorylation of GluR1 in the ACC after nerve injury. Finally, we found that both presynaptic and postsynaptic changes after nerve injury were absent in genetic mice lacking calcium-stimulated adenylyl cyclase 1 (AC1). Our studies therefore provide direct integrative evidence for both long-term presynaptic and postsynaptic changes in cortical synapses after nerve injury, and that AC1 is critical for such long-term changes. AC1 thus may serve as a potential therapeutic target for treating neuropathic pain.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex

Xu¹,

Wu²,

Wang³

et al. 2008

J. Neurosci.

323

324

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show abstract

“…2,21 Evidence for the involvement of cortical NR2B receptor in pathological pain comes first from the so-called Doogie smart mice. 69 In this transgenic mouse with selective forebrain NMDA NR2B overexpression, electrophysiological and behavioral studies found that the NR2B transgenic mice are superior performers in memory tests, with significant enhanced hippocampal CA1 LTP.…”

Section: Function In Chronic Painmentioning

confidence: 99%

“…Understanding neuropathic pain therefore requires understanding of plastic changes in somatosensory pathways, and targeting central plasticity is becoming a major direction for identifying pain-relieving medications. 1,2 Signaling molecules that are involved in injury-related plasticity may provide potential drug targets for treating neuropathic pain. Among several candidates, the NMDA receptor, one of the major glutamate receptors that is important for synaptic plasticity, has been intensively investigated by both academic and pharmaceutical companies.…”

Section: Introductionmentioning

confidence: 99%

Targeting the NMDA Receptor Subunit NR2B for the Treatment of Neuropathic Pain

2009

Self Cite

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Summary:Neuropathic pain is generally defined as a chronic pain state resulting from peripheral or central nerve injury, or both. An effective treatment for neuropathic pain is still lacking. The NMDA receptor, one type of the ionotropic glutamate receptors, is known to be important for triggering long-lasting changes in synapses. NMDA receptor-dependent synaptic plasticity plays roles not only in physiological functions such as learning and memory, but also in unwanted pathological conditions such as chronic pain. This review addresses recent progress on NMDA receptors in neuropathic pain, with particular emphasis on the NR2B-subunitcontaining receptors. The expression and function of NMDA receptors in synaptic plasticity in the pain transmission pathway from dorsal root ganglia to the anterior cingulate cortex is reviewed, and preclinical and clinical investigations of selective NMDA receptor in neuropathic pain are discussed. The NMDA receptors, in particular NR2B-containing NMDA receptors, serve as promising targets for treatment of neuropathic pain.

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Fractional amplitude of low‐frequency fluctuation changes of specific cerebral regions in patients with toothache: A functional magnetic resonance imaging study

et al. 2023

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Background Previous studies have indicated that pain‐related diseases can result in significant functional alterations in the brain. However, differences in spontaneous brain activity in toothache (TA) patients remain unclear. Objective To investigate altered spontaneous brain activity in patients with TA and its underlying mechanisms using the resting‐state functional magnetic resonance imaging–fractional amplitude of low‐frequency fluctuation (rsfMRI–fALFF) technique. Methods Twelve patients with TA and 12 non‐toothache controls (NTCs) (matched for sex, age, and level of education) were enrolled. Spontaneous cerebral activity variations were investigated using the rsfMRI–fALFF technique in all individuals. The mean fALFF values of the TA patients and NTCs were classified using receiver operating characteristic (ROC) curves. The correlations between fALFF signals of distinct brain regions and clinical manifestations of TA patients were evaluated using Pearson's correlation analysis. Results TA patients showed lower fALFF values in the left superior frontal gyrus, medial; right superior frontal gyrus, dorsolateral; and left median cingulate and paracingulate gyri (LDCG) than the NTCs. Moreover, ROC curve analysis indicated that the area under the curve of each cerebral region studied had high accuracy. Besides, in the TA group, the visual analog scale score was negatively correlated with fALFF signal values of the LDCG ( r = .962, p < .001). Conclusion Abnormal spontaneous activity was detected in numerous brain regions in patients with TA, which may be valuable for understanding the brain processing mechanism underlying TA. These regional changes in brain activity may serve as effective clinical indicators of TA.

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Neuronal Mechanism for Neuropathic Pain

Cited by 109 publications

References 74 publications

Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex

Presynaptic and Postsynaptic Amplifications of Neuropathic Pain in the Anterior Cingulate Cortex

Targeting the NMDA Receptor Subunit NR2B for the Treatment of Neuropathic Pain

Fractional amplitude of low‐frequency fluctuation changes of specific cerebral regions in patients with toothache: A functional magnetic resonance imaging study

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