Joint inflammation is reduced by dorsal rhizotomy and not by sympathectomy or spinal cord transection
- PMID: 8017984
- PMCID: PMC1005329
- DOI: 10.1136/ard.53.5.309
Joint inflammation is reduced by dorsal rhizotomy and not by sympathectomy or spinal cord transection
Abstract
Objectives: To investigate the role of primary afferents, sympathetic postganglionic efferents and descending systems on the central control of peripheral inflammation.
Methods: Acute inflammation was induced by intra-articular injection of kaolin and carrageenan into the knee joint cavity of the rat. Before the induction of the arthritis, a unilateral dorsal rhizotomy, a chemical (phentolamine) and/or surgical sympathectomy, or a spinal transection was performed. Joint inflammation (joint circumference and thermographic readings) and behavioural signs were assessed.
Results: Only arthritic animals with a dorsal rhizotomy showed a significant reduction of the inflammatory response compared with control arthritic animals. No significant differences in the inflammatory response occurred following sympathectomy or spinal transection. The animals who received sympathectomy showed similar behavioural manifestations to the arthritic animals.
Conclusions: The central terminals of primary afferents are important in the development of acute joint inflammation since dorsal rhizotomy attenuated the inflammatory response in the knee joint. The sympathetic nervous system is not involved in the acute inflammatory phase of this arthritis model. The central processes controlling acute inflammation involve a local spinal circuit since spinal cord transection at T9 has no effect on the inflammation.
Similar articles
-
Do dorsal root reflexes augment peripheral inflammation?Neuroreport. 1994 Mar 21;5(7):821-4. doi: 10.1097/00001756-199403000-00021. Neuroreport. 1994. PMID: 8018857
-
Contribution of sensory afferents and sympathetic efferents to joint injury in experimental arthritis.J Neurosci. 1986 Dec;6(12):3423-9. doi: 10.1523/JNEUROSCI.06-12-03423.1986. J Neurosci. 1986. PMID: 3794780 Free PMC article.
-
Enhancement of the responses of ascending tract cells in the cat spinal cord by acute inflammation of the knee joint.Exp Brain Res. 1987;66(3):489-99. doi: 10.1007/BF00270681. Exp Brain Res. 1987. PMID: 3475211
-
Changes in the effect of spinal prostaglandin E2 during inflammation: prostaglandin E (EP1-EP4) receptors in spinal nociceptive processing of input from the normal or inflamed knee joint.J Neurosci. 2004 Jan 21;24(3):642-51. doi: 10.1523/JNEUROSCI.0882-03.2004. J Neurosci. 2004. PMID: 14736850 Free PMC article.
-
Mechanisms of pain in arthritis.Ann N Y Acad Sci. 2002 Jun;966:343-54. doi: 10.1111/j.1749-6632.2002.tb04234.x. Ann N Y Acad Sci. 2002. PMID: 12114291 Review.
Cited by
-
Monoarticular antigen-induced arthritis leads to pronounced bilateral upregulation of the expression of neurokinin 1 and bradykinin 2 receptors in dorsal root ganglion neurons of rats.Arthritis Res. 2000;2(5):424-7. doi: 10.1186/ar121. Epub 2000 Aug 3. Arthritis Res. 2000. PMID: 11056677 Free PMC article.
-
Activation of CNS circuits producing a neurogenic cystitis: evidence for centrally induced peripheral inflammation.J Neurosci. 1998 Dec 1;18(23):10016-29. doi: 10.1523/JNEUROSCI.18-23-10016.1998. J Neurosci. 1998. PMID: 9822756 Free PMC article.
-
The Role of Type 1 Metabotropic Glutamate Receptors in the Generation of Dorsal Root Reflexes Induced by Acute Arthritis or the Spinal Infusion of 4-Aminopyridine in the Anesthetized Rat.J Pain. 2000 Summer;1(2):151-161. doi: 10.1016/S1526-5900(00)90100-7. J Pain. 2000. PMID: 20882110 Free PMC article.
-
Role of neurogenic inflammation in pancreatitis and pancreatic pain.Neurosignals. 2005;14(4):158-65. doi: 10.1159/000087654. Neurosignals. 2005. PMID: 16215298 Free PMC article. Review.
-
Differential contribution of electrically evoked dorsal root reflexes to peripheral vasodilatation and plasma extravasation.J Neuroinflammation. 2011 Feb 28;8:20. doi: 10.1186/1742-2094-8-20. J Neuroinflammation. 2011. PMID: 21356101 Free PMC article.
References
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Medical