Peptide plasticity in primary sensory neurons and spinal cord during adjuvant-induced arthritis in the rat: an immunocytochemical and in situ hybridization study

Calzà, Laura; Pozza, Monica; Zanni, Massimo; Manzini, Carlo Umberto; Manzini, E; Hökfelt, Tomas

doi:10.1016/s0306-4522(97)00272-8

Cited by 126 publications

(60 citation statements)

References 64 publications

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“…Accordingly, quantification of our immunolabeling demonstrates that FCA-induced inflammation enhances the expression of CRF receptors and ENK in interneurons within the superficial laminae of the spinal cord. This finding is consistent with previous studies (Ji et al, 1994;Spetea et al, 2002;Calza et al, 1998) demonstrating an upregulation in the expression of ENK after FCA-induced inflammation. However, another explanation for the differences in ipsi-and contralateral antinociceptive effects of i.t.…”

Section: Opioid-mediated Inhibition Of Inflammatory Pain Following Isupporting

confidence: 94%

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Mousa

Bopaiah

Richter

et al. 2007

Neuropsychopharmacol

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There is conflicting evidence on the antinociceptive effects of corticotropin-releasing factor (CRF) along the neuraxis of pain transmission and the responsible anatomical sites of CRF's action at the level of the brain, spinal cord and periphery. In an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation, we systematically investigated CRF's ability to modulate inflammatory pain at those three levels of pain transmission by algesiometry following the intracerebroventricular, intrathecal, and intraplantar application of low, systemically inactive doses of CRF. At each level, CRF elicits potent antinociceptive effects, which are dose dependent and antagonized by local, but not systemic CRF receptor antagonist a-helical CRF indicating CRF receptor specificity. Consistently, we have identified by immunohistochemistry multiple brain areas, inhibitory interneurons within the dorsal horn of the spinal cord as well as immune cells within subcutaneous tissueFbut not peripheral sensory neuronsFthat coexpress both CRF receptors and opioid peptides. In line with these anatomical findings, local administration of CRF together with the opioid receptor antagonist naloxone dosedependently reversed CRF's antinociceptive effects at each of these three levels of pain transmission. Therefore, local application of low, systemically inactive doses of CRF at the level of the brain, spinal cord and periphery inhibits tonic inflammatory pain most likely through an activation of CRF receptors on cells that coexpress opioid peptides which results in opioid-mediated pain inhibition. Future studies have to delineate whether endogenous CRF at these three levels contributes to the body's response to cope with the stressful stimulus pain in an opioid-mediated manner.

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Section: Opioid-mediated Inhibition Of Inflammatory Pain Following Isupporting

confidence: 94%

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Mousa

Bopaiah

Richter

et al. 2007

Neuropsychopharmacol

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“…Relatively few studies addressed the consequences of tissue damage. One report found neither PENK nor prodynorphin mRNA in DRG of normal or polyarthritic rats (Calzà et al, 1998). Others detected mRNA for POMC, PENK, or prodynorphin in DRG of normal rats (Pohl et al, 1994;Braz et al, 2001;Obara et al, 2009).…”

Section: Opioid Peptides In Peripheral Sensorymentioning

confidence: 98%

Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

2011

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“…Similarly to peripheral nerve injury, inflammation of the peripheral tissues also induces plastic changes to cell markers in primary sensory neurons (Calzà et al, 1998;Ji et al, 2002). Thus, we also studied whether inflammation of peripheral tissues induces any changes in the FAAH expression pattern.…”

Section: Inflammation Of Peripheral Tissues Does Not Induce Changes Imentioning

confidence: 99%

Localization of the Endocannabinoid-Degrading Enzyme Fatty Acid Amide Hydrolase in Rat Dorsal Root Ganglion Cells and Its Regulation after Peripheral Nerve Injury

Lever¹,

Robinson²,

Cibelli³

et al. 2009

J. Neurosci.

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Fatty acid amide hydrolase (FAAH) is a degradative enzyme for a group of endogenous signaling lipids that includes anandamide (AEA).AEA acts as an endocannabinoid and an endovanilloid by activating cannabinoid and vanilloid type 1 transient receptor potential (TRPV1) receptors, respectively, on dorsal root ganglion (DRG) sensory neurons. Inhibition of FAAH activity increases AEA concentrations in nervous tissue and reduces sensory hypersensitivity in animal pain models. Using immunohistochemistry, Western blotting, and reverse transcription-PCR, we demonstrate the location of the FAAH in adult rat DRG, sciatic nerve, and spinal cord. In naive rats, FAAH immunoreactivity localized to the soma of 32.7 Ϯ 0.8% of neurons in L4 and L5 DRG. These were small-sized (mean soma area, 395.96 Ϯ 5.6 m 2 ) and predominantly colabeled with peripherin and isolectin B4 markers of unmyelinated C-fiber neurons; 68% colabeled with antibodies to TRPV1 (marker of nociceptive DRG neurons), and Ͻ2% colabeled with NF200 (marker of large myelinated neurons). FAAH-IR was also present in small, NF200-negative cultured rat DRG neurons. Incubation of these cultures with the FAAH inhibitor URB597 increased AEA-evoked cobalt uptake in a capsazepine-sensitive manner. After sciatic nerve axotomy, there was a rightward shift in the cell-size distribution of FAAH-immunoreactive (IR) DRG neurons ipsilateral to injury: FAAH immunoreactivity was detected in larger-sized cells that colabeled with NF200. An ipsilateral versus contralateral increase in both the size and proportion of FAAH-IR DRG occurred after spinal nerve transection injury but not after chronic inflammation of the rat hindpaw 2 d after injection of complete Freund's adjuvant. This study reveals the location of FAAH in neural tissue involved in peripheral nociceptive transmission.

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Peptide plasticity in primary sensory neurons and spinal cord during adjuvant-induced arthritis in the rat: an immunocytochemical and in situ hybridization study

Cited by 126 publications

References 64 publications

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

Localization of the Endocannabinoid-Degrading Enzyme Fatty Acid Amide Hydrolase in Rat Dorsal Root Ganglion Cells and Its Regulation after Peripheral Nerve Injury

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