Substance P-, neurokinin A-, calcitonin gene-related peptide- and neuropeptide Y-like immunoreactivity (-LI) in rat knee joint synovial fluid during acute monoarthritis is not correlated with concentrations of neuropeptide-LI in cerebrospinal fluid and plasma

Bileviciute, Indre; Lundeberg, Thomas; Ekblom, A.; Theodorsson, Elvar

doi:10.1016/0304-3940(94)91048-0

Cited by 28 publications

(13 citation statements)

References 15 publications

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“…Taken together, the majority of findings support the notion that physiological activation of contralateral afferents through spinal mechanisms could initiate contralateral joint inflammation. Further evidence in support of the hypothesis is that contralateral peripheral release of pro-inflammatory neuropeptides such as substance P and calcitonin gene-related peptide was not correlated with plasma neuropeptide levels, which suggests the source of synovial neuropeptides was neuronal rather than systemic [42].…”

Section: Discussionmentioning

confidence: 80%

Time course and substance P effects on the vascular and morphological changes in adjuvant-induced monoarthritic rats

Lam¹,

Wong²,

Ng³

2004

International Immunopharmacology

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Section: Discussionmentioning

confidence: 80%

Time course and substance P effects on the vascular and morphological changes in adjuvant-induced monoarthritic rats

Lam¹,

Wong²,

Ng³

2004

International Immunopharmacology

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“…Mechanical nociceptive thresholds are altered bilaterally after unilateral inflammation induced by carrageenan (Kayser & Guilbaud, 1987) and FCA (Millan & Colpaert, 1991), although this is variable (Traub, Solodkin & Gebhart, 1994). Contralateral intra-articular release of substance P and CGRP has been shown in a monoarthritis of the rat knee (Bileviciute, Lundeberg, Ekblom & Theodorsson, 1993) and this is thought to be due to a neural mechanism rather than a systemic release (Bileviciute, Lundeberg, Ekblom & Theodorsson, 1994 receptive fields which become more responsive to both ipsilateral and contralateral stimuli on induction of monoarthritis in the knee. The receptive fields of these neurons also expand both ipsilateral and contralateral to the inflammatory focus .…”

Section: Discussionmentioning

confidence: 99%

Neuropeptide gene expression and capsaicin‐sensitive primary afferents: maintenance and spread of adjuvant arthritis in the rat.

Donaldson

McQueen

1995

The Journal of Physiology

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1. Many experimental and clinical arthritides are characterized by their bilateral nature.There is strong evidence to suggest that this bilateral spread may be mediated by a neuronal mechanism. We have previously shown early and sustained induction of mRNAs encoding preprotachykinin (PPT) and calcitonin gene-related peptide (CGRP) PPT and CGRP mRNA expression in L5 DRG. SS mRNA expression in right DRG was unaffected by spread of inflammation. FCA-L + Cap-L reduced left joint swelling and prevented spread of arthritis to the right joint when assessed by joint swelling. This inhibition of spread of arthritis was associated with significant reductions in all left L5 DRG neuropeptide mRNAs compared with controls, and the rise in right L5 DRG PPT mRNA expression seen in FCA-L-alone animals was blocked. FCA-L + Cap-R also reduced left joint swelling and prevented the spread of inflammation to the right ankle. This lesion prevented the rise in PPT and CGRP mRNA expression seen in right DRG with FCA-L alone. 4. These findings suggest a role for capsaicin-sensitive primary afferents and the primary afferent neuropeptides encoded by PPT and CGRP mRNA in the maintenance and spread of arthritis.

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“…Carrageenin-induced inflammation is a commonly used model for the study of oedema formation and/or nociception (Winter et al, 1962;Vinegar et al, 1969;Mayer et al, 1988;Satoh et al, 1992;Lundeberg et al, 1993;Bilevicuiute et al, 1993;1994a). In the present study injection of carrageenin into the left plantar hindpaw of the rat resulted in an ipsilateral in- Draisci, 1988;Hanesch et al, 1993) and increased release of CGRP-like immunoreactivity in the spinal cord (Nanayama et al, 1989;Bileviciute et al, 1993;1994a, b), in response to experimentally induced inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, Kur-the previously mentioned peptides in the cerebrospinal fluid during acute monoarthritis (Bileviciute et al, 1994a). Inflammation has also been shown to induce an up-regulation of the expression of preprodynorphin mRNA and the mRNA of the proto-oncogene c-fos in the dorsal horn of the spinal cord (Draisci et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Intrathecal CGRP_8–37‐induced bilateral increase in hindpaw withdrawal latency in rats with unilateral inflammation

Hansson

Brodda-Jansen

et al. 1996

British J Pharmacology

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1 Recent work in our laboratory has demonstrated that intrathecal administration of a selective antagonist of calcitonin gene-related peptide (CGRP), CGRP8-37, increased the hindpaw withdrawal latency (HWL) to thermal stimulation and hindpaw withdrawal threshold (HWT) to pressure in normal rats, and that these effects were more pronounced than in rats with mononeuropathy. 2 The present study was performed to investigate the effects of intrathecal administration of CGRP8-37 on the HWL and HWT in rats with unilateral hindpaw inflammation induced by subcutaneous injection of carrageenin. The effect of naloxone was also studied. 3 Subcutaneous injection of 0.1 ml of carrageenin into the plantar region of the left hindpaw induced a significant increase in the volume of the ipsilateral hindpaw (P <0.001), and significant bilateral decreases of the HWL to thermal stimulation (ipsilateral: P<0.001; contralateral: P<0.01) and HWT to pressure (ipsilateral: P<0.001; contralateral: P<0.01). 4 Intrathecal administration of 10 nmol of CGRP8 37, but not of 1 or 5 nmol, induced a significant bilateral increase in the HWL and HWT in rats with experimentally induced inflammation (thermal test: P<0.001; mechanical test: P<0.001). 5 The effect of intrathecal administration of 10 nmol CGRP8-37 on HWL and HWT was significantly more pronounced in intact rats than in rats with experimentally induced inflammation (ipsilateral: P<0.001; contralateral: P<0.001). 6 The effect of CGRP8 37 on withdrawal responses in the inflamed paw was partly reversed by intrathecal injection of naloxone at a dose of 88 nmol in the thermal (ipsilateral: P<0.01; contralateral: P=0.14) and mechanical tests (ipsilateral: P<0.05; contralateral: P=0.60). 7 A significant bilateral increase in the concentration of CGRP-like immunoreactivity in the perfusate of both hindpaws was demonstrated 24 h after unilateral injection of carrageenin (ipsilateral: P<0.001; contralateral: P<0.05). There was also an increase in the amount of CGRP-like immunoreactivity in the cerebrospinal fluid (P<0.001), but not in plasma (P=0.75). 8 The present study demonstrates that acute experimentally-induced unilateral hindpaw inflammation, induces bilateral increases in the amount of CGRP-like immunoreactivity in hindpaw perfusates. Intrathecal administration of CGRP8_37 increased the HWL to thermal stimulation and HWT to pressure bilaterally. 9 The results indicate that CGRP plays a role in the transmission of presumed nociceptive information in the spinal cord of rats with experimentally induced inflammation. Furthermore, our findings suggest that opioids can modulate CGRP-related effects in the spinal cord.

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Substance P-, neurokinin A-, calcitonin gene-related peptide- and neuropeptide Y-like immunoreactivity (-LI) in rat knee joint synovial fluid during acute monoarthritis is not correlated with concentrations of neuropeptide-LI in cerebrospinal fluid and plasma

Cited by 28 publications

References 15 publications

Time course and substance P effects on the vascular and morphological changes in adjuvant-induced monoarthritic rats

Time course and substance P effects on the vascular and morphological changes in adjuvant-induced monoarthritic rats

Neuropeptide gene expression and capsaicin‐sensitive primary afferents: maintenance and spread of adjuvant arthritis in the rat.

Intrathecal CGRP_8–37‐induced bilateral increase in hindpaw withdrawal latency in rats with unilateral inflammation

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Substance P-, neurokinin A-, calcitonin gene-related peptide- and neuropeptide Y-like immunoreactivity (-LI) in rat knee joint synovial fluid during acute monoarthritis is not correlated with concentrations of neuropeptide-LI in cerebrospinal fluid and plasma

Cited by 28 publications

References 15 publications

Time course and substance P effects on the vascular and morphological changes in adjuvant-induced monoarthritic rats

Time course and substance P effects on the vascular and morphological changes in adjuvant-induced monoarthritic rats

Neuropeptide gene expression and capsaicin‐sensitive primary afferents: maintenance and spread of adjuvant arthritis in the rat.

Intrathecal CGRP8–37‐induced bilateral increase in hindpaw withdrawal latency in rats with unilateral inflammation

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Intrathecal CGRP_8–37‐induced bilateral increase in hindpaw withdrawal latency in rats with unilateral inflammation