Removing TRPV1-expressing primary afferent neurons potentiates the spinal analgesic effect of δ-opioid agonists on mechano-nociception

Chen, Shao Rui; Pan, Hui Lin

doi:10.1016/j.neuropharm.2008.05.011

Cited by 16 publications

(11 citation statements)

References 31 publications

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“…As described previously [7, 10, 36], TRPV1-ir was concentrated in lamina I and the inner part of lamina II (Fig 6). Two-way ANOVA revealed that nerve injury decreased TRPV1-ir [F(3,57)=9.8, P<0.0001].…”

Section: Resultssupporting

confidence: 79%

A Novel Method to Quantify Histochemical Changes Throughout the Mediolateral Axis of the Substantia Gelatinosa After Spared Nerve Injury: Characterization with TRPV1 and Substance P

Corder

Siegel

Intondi

et al. 2010

The Journal of Pain

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Nerve injury dramatically increases or decreases protein expression in the spinal cord dorsal horn. Whether the spatial distribution of these changes is restricted to the central innervation territories of injured nerves or could spread to adjacent territories in the dorsal horn is not understood. To address this question, we developed a simple computer software-assisted method to precisely distinguish and efficiently quantify immunohistochemical staining patterns across the mediolateral axis of the dorsal horn 2 wk after transection of either the tibial and common peroneal nerves (thus sparing the sural branch, spared nerve injury, SNI), the tibial nerve, or the common peroneal and sural nerves. Using thiamine monophosphatase (TMP) histochemistry, we determined that central terminals of the tibial, common peroneal, sural, and posterior cutaneous nerves occupy the medial 35%, medial-central 20%, central-lateral 20%, and lateral 25% of the substantia gelatinosa, respectively. We then used these calculations to show that SNI reduced the expression of SP and TRPV1 immunoreactivity within the tibial and peroneal innervation territories in the L4 dorsal horn, without changing expression in the uninjured, sural sector. We conclude that SNI-induced loss of SP and TRPV1 in central terminals of dorsal horn is restricted to injured fibers. Our new method enables direct comparison of injured and uninjured terminals in the dorsal horn so as to better understand their relative contributions to mechanisms of chronic pain.

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Section: Resultssupporting

confidence: 79%

A Novel Method to Quantify Histochemical Changes Throughout the Mediolateral Axis of the Substantia Gelatinosa After Spared Nerve Injury: Characterization with TRPV1 and Substance P

Corder

Siegel

Intondi

et al. 2010

The Journal of Pain

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“…Thus, TRPV1‐expressing dorsal horn neurons may be involved in the amplification of nociceptive input from primary afferents. We have shown that this subpopulation of dorsal horn neurons is endowed with μ‐opioid, but not δ‐opioid, receptors (Chen and Pan 2006, 2008). Our finding is consistent with the previous study showing that μ‐opioid receptors are expressed only on non‐GABAergic and non‐glycinergic neurons in the spinal cord (Kemp et al.…”

Section: Discussionmentioning

confidence: 99%

The glutamatergic nature of TRPV1‐expressing neurons in the spinal dorsal horn

Zhou

Chen²,

Chen

et al. 2008

Journal of Neurochemistry

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The transient receptor potential vanilloid receptor 1 (TRPV1) is expressed on primary afferent terminals and spinal dorsal horn neurons. However, the neurochemical phenotypes and functions of TRPV1-expressing postsynaptic neurons in the spinal cord are not clear. In this study, we tested the hypothesis that TRPV1-expressing dorsal horn neurons are glutamatergic. Immunocytochemical labeling revealed that TRPV1 and vesicular glutamate transporter-2 were colocalized in dorsal horn neurons and their terminals in the rat spinal cord. Resiniferatoxin (RTX) treatment or dorsal rhizotomy ablated TRPV1-expressing primary afferents but did not affect TRPV1- and vesicular glutamate transporter-2-expressing dorsal horn neurons. Capsaicin significantly increased the frequency of glutamatergic sEPSCs and mEPSCs in almost all the lamina II neurons tested in control rats. In RTX-treated or dorsal rhizotomized rats, capsaicin still increased the frequency of sEPSCs and mEPSCs in the majority of neurons examined, and this effect was abolished by a TRPV1 blocker or by non-NMDA receptor antagonist. In RTX-treated or in dorsal rhizotomized rats, capsaicin also produced an inward current in a subpopulation of lamina II neurons. However, capsaicin had no effect on GABAergic and glycinergic sIPSCs of lamina II neurons in RTX-treated or dorsal rhizotomized rats. Collectively, our study provides new histological and functional evidence that TRPV1-expressing dorsal horn neurons in the spinal cord are glutamatergic and that they mediate excitatory synaptic transmission. This finding is important to our understanding of the circuitry and phenotypes of intrinsic dorsal horn neurons in the spinal cord.

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“…Initial studies had suggested that the different types of opioid receptors, particularly MOPR and DOPR, were coexpressed by the same class of DRG neurons, namely unmyelinated peptidergic nociceptors. These neurons detect noxious stimuli in skin and internal organs and express the neuropeptides substance P and calcitonin gene-related protein (CGRP) and the heat-and capsaicin-sensitive transient receptor potential cation channel subfamily V member 1 (TRPV1) (Chen & Pan 2008, Ueda 2006, Vetter et al 2006). MOPR expression in these cells is thought to contribute to the remarkable utility of mu agonists for perioperative pain management (Figure 2c).…”

Section: Neuroanatomical Substrates For Opioid Analgesiamentioning

confidence: 99%

Endogenous and Exogenous Opioids in Pain

Corder

Castro

Bruchas

et al. 2018

Annu. Rev. Neurosci.

319

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Opioids are the most commonly used and effective analgesic treatments for severe pain, but they have recently come under scrutiny owing to epidemic levels of abuse and overdose. These compounds act on the endogenous opioid system, which comprises four G protein-coupled receptors (mu, delta, kappa, and nociceptin) and four major peptide families (β-endorphin, enkephalins, dynorphins, and nociceptin/orphanin FQ). In this review, we first describe the functional organization and pharmacology of the endogenous opioid system. We then summarize current knowledge on the signaling mechanisms by which opioids regulate neuronal function and neurotransmission. Finally, we discuss the loci of opioid analgesic action along peripheral and central pain pathways, emphasizing the pain-relieving properties of opioids against the affective dimension of the pain experience.

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Removing TRPV1-expressing primary afferent neurons potentiates the spinal analgesic effect of δ-opioid agonists on mechano-nociception

Cited by 16 publications

References 31 publications

A Novel Method to Quantify Histochemical Changes Throughout the Mediolateral Axis of the Substantia Gelatinosa After Spared Nerve Injury: Characterization with TRPV1 and Substance P

A Novel Method to Quantify Histochemical Changes Throughout the Mediolateral Axis of the Substantia Gelatinosa After Spared Nerve Injury: Characterization with TRPV1 and Substance P

The glutamatergic nature of TRPV1‐expressing neurons in the spinal dorsal horn

Endogenous and Exogenous Opioids in Pain

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