Bilateral changes of substance P-, neurokinin A-, calcitonin gene-related peptide- and neuropeptide Y-like immunoreactivity in rat knee joint synovial fluid during acute monoarthritis

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

doi:10.1016/0304-3940(93)90071-r

Cited by 86 publications

(49 citation statements)

References 16 publications

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“…Although there is no previous disease model in which the CNS is the primary initiator of peripheral inflammation, there is ample evidence of spinally mediated neurogenic inflammation induced by a stimulus to a distant body area (Denko and Petricevic, 1978;Levine et al, 1985a,b;Kolston et al, 1991;Bileviciute et al, 1993;Wesselmann and Lai, 1997). Accordingly, modulation of spinal non-NMDA, GABA-A, A 1 adenosine, or nicotinic receptors reduces peripheral inflammation (Miao et al, 1992;Rees et al, 1994Rees et al, , 1995Rees et al, , 1996Bong et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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We present a model of neurogenic cystitis induced by viral infection of specific neuronal circuits of the rat CNS. Retrograde infection by pseudorabies virus (PRV) of neuronal populations neighboring those that innervate the bladder consistently led to a localized immune response in the CNS and bladder inflammation. Infection of bladder circuits themselves or of circuits distant from these rarely produced cystitis. Absence of virus in bladder and urine ruled out an infectious cystitis. Total denervation of the bladder, selective C-fiber deafferentation, or bladder sympathectomy prevented cystitis without affecting the CNS disease, indicating a neurogenic component to the inflammation. The integrity of central bladder-related circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting bladder circuits, i.e., bilateral dorsolateral or ventrolateral funiculectomy, as well as bilateral lesions of Barrington's nucleus/locus coeruleus area, prevented bladder inflammation. The close proximity in the CNS of noninfected visceral circuits to infected somatic neurons would thus permit a bystander effect, leading to activation of the sensory and autonomic circuits innervating the bladder and resulting in a neurogenic inflammation localized to the bladder. The present study indicates that CNS dysfunction can bring about a peripheral inflammation.

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Section: Discussionmentioning

confidence: 99%

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

et al. 1999

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“…In addiction, such neuropeptides (substance P, acetylcholine, catecholamines and glutamate) seems to be related to the bilateral nature of changes seen in Achilles tendinopathy; many patients present with bilateral Achilles tendinosis [107] and many of those initially presenting unilateral symptoms develop contralateral ones over time [108] . It has been demonstrated in the rat that unilateral training leads to bilateral changes in levels of neuropeptides in the synovial fluids [109,110] ; on the basis of these and other observation has recently been formulated the hypothesis of the "central neuronal Bondi M et al Achilles tendinopathy mechanism" as a possible explanation for the frequent bilateral involvement in Achilles tendinopathy [30,111] .…”

Section: Extrinsic Risk Factorsmentioning

confidence: 99%

The Achilles Tendinopathy: Pathogenesis Review

Bondi¹,

Rossi²,

Magnan³

et al. 2015

International Journal of Orthopaedics

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Achilles tendinopathy is a degenerative disease with high prevalence in runners. For the comprehension of achilles tendinopathy we have to consider intrinsic conditions such as age, sex, BMI, tendon temperature, systemic diseases, flexibility, previous injuries and anatomical variations, genetic predisposition and blood supply and extrinsic factors such as drugs and overuse. Both categories can be responsible for development of achilles' degenerative tendinopathy. Different hypothesis were studied, those concerning the pathogenesis of tendinopathy and those concerning the etiology of complaints in patients. This review of the literature demonstrates the heterogeneity of Achilles tendinopathy pathogenesis.

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“…The first phase seems to be caused predominantly by C-fiber activation due to the peripheral stimulus, while the second phase appears to be dependent on the combination of an inflammatory reaction in the peripheral tissue and functional changes in the dorsal horn of the spinal cord (41). In response to experimentally induced inflammation, the biosynthesis of CGRP increased in the DRG (13), and release of CGRPlike immunoreactive substance increased in the spinal cord (4,5,35). Thus, there is accumulating evidence which suggests that CGRP is related to the pathophysiology of inflammatory pain.…”

Section: Effects Of Cgrp Antagonist On Histamine-induced Hyperalgesiamentioning

confidence: 99%

Interaction of histamine and calcitonin gene-related peptide in the formalininduced pain perception in rats

et al. 2011

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Histamine and calcitonin gene-related peptide (CGRP) contribute to the pain perception. The aim of the present study is to clarify the interaction of histamine and CGRP in the perception of inflammatory pain. The effects of a histamine H1 receptor antagonist (pyrilamine, i.p.), an H2 receptor antagonist (ranitidine, i.p.) and a CGRP antagonist (CGRP 8-37, i.t.) on the formalininduced pain was studied in rats. Pyrilamine and ranitidine produced a dose-dependent antinociceptive response in the first and the second phases of the formalin test. A single administration of pyrilamine (1 mg/kg, i.p.), ranitidine (10 mg/kg, i.p.) or CGRP 8-37 (10 μg/μL, i.t.) had no significant effects on the pain perception in the second phase. A combination of CGRP 8-37 and pyrilamine or ranitidine at these sub-effective doses, however, showed nociceptive response in the second phase. Moreover, a histamine (i.t.)-induced hyperalgesia was completely prevented by treatment with GGRP 8-37 at this dose. Our findings have raised the possibility that the CGRP system has interaction with histamine in the perception of inflammatory pain.Pain perception is modulated in the spinal cord by many bioactive substances, such as histamine (38, 39), substance P and calcitonin gene-related peptide (CGRP) (12, 28). Histamine is mostly derived from two cell types, neurons and mast cells. The cell bodies of histaminergic neurons are localized in the tuberomammillary nucleus of the posterior hypothalamus (15). The descending histaminergic neurons terminate at the periaqueductal gray and the dorsal horn of the spinal cord (30,31,43), which is an important site for nociceptive transmission (2). All three histamine H1, H2 and H3 receptors (16) are found in the dorsal horn (26,33,42) and play important roles in the pain perception (22)(23)(24)(25). CGRP is a 37-amino-acid neuropeptide widely distributed in the peripheral and central nervous systems including the dorsal root ganglion (DRG) and its primary afferent terminals in the spinal cord (1, 37). The actions mediated by CGRP type 1 receptor, which is considered to consist of calcitonin receptor-like receptor and receptor activity modifying protein-1 (21), is antagonized by CGRP 8-37 (8). CGRP and its receptors are involved in many stages of pain neurotransmission, especially in the spinal cord (12, 28). As a neurotransmitter, CGRP itself had no obvious effect in pain modulation, but potentiated the excitatory effect induced by substance P or other nociceptive stimuli in the dorsal horn of the spinal cord (3). CGRP stimulated histamine release from mast cells and potentiated histamine ac-

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Bilateral changes of substance P-, neurokinin A-, calcitonin gene-related peptide- and neuropeptide Y-like immunoreactivity in rat knee joint synovial fluid during acute monoarthritis

Cited by 86 publications

References 16 publications

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

Activation for CNS Circuits Producing a Neurogenic Cystitis: Evidence for Centrally Induced Peripheral Inflammation

The Achilles Tendinopathy: Pathogenesis Review

Interaction of histamine and calcitonin gene-related peptide in the formalininduced pain perception in rats

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