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Spinal cholinergic involvement after treatment with aspirin and paracetamol in rats
Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för neurovetenskap.
2004 Ingår i: Neurosci. Lett., ISSN 0304-3940, Vol. 368, nr 1, s. 116-120Artikel i tidskrift (Refereegranskat) Published
Ort, förlag, år, upplaga, sidor
2004. Vol. 368, nr 1, s. 116-120
Identifikatorer
URN: urn:nbn:se:uu:diva-92740OAI: oai:DiVA.org:uu-92740DiVA, id: diva2:165925
Tillgänglig från: 2005-03-30 Skapad: 2005-03-30Bibliografiskt granskad
Ingår i avhandling
1. Acetylcholine in Spinal Pain Modulation: An in vivo Study in the Rat
Öppna denna publikation i ny flik eller fönster >>Acetylcholine in Spinal Pain Modulation: An in vivo Study in the Rat
2005 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

The spinal cord is an important component in the processing and modulation of painful stimuli. Nerve signals from the periphery are relayed and further conducted to the brain (nociception) in the spinal cord, and the most essential modulation of painful information (antinociception) occurs here. Several neurotransmitters are involved in spinal pain modulation, among them acetylcholine. However, the role of acetylcholine has previously been little investigated.

In the present thesis, the acetylcholine release in the spinal cord was studied in vivo. By using spinal microdialysis on anaesthetised rats, the effects on the intraspinal acetylcholine release of various receptor ligands and analgesic agents were examined. This, together with pain behavioural tests and in vitro pharmacological assays, was used to evaluate the role of acetylcholine in spinal pain modulation. The four studies in this thesis resulted in the following conclusions:

An increased release of spinal acetylcholine is associated with an elevated pain threshold, while a decreased acetylcholine release is associated with hyperalgesia, as seen after systemic treatment with a muscarinic agonist and an antagonist.

Lidocaine is a potent analgesic when given systemically. It was found to produce an increase of intraspinal acetylcholine after intravenous injection of analgesic doses. This effect was attenuated after muscarinic, and abolished after nicotinic, receptor blockade.

Various a2-adrenergic ligands, associated with nociceptive or antinociceptive effects, were found to affect intraspinal acetylcholine release via action on nicotinic receptors.

Finally, the involvement of spinal acetylcholine in the analgesic effects of aspirin and paracetamol was examined. It was found that spinal acetylcholine could participate in the analgesic effects of aspirin, but not of paracetamol.

The present thesis provides data that clearly demonstrate a relationship between intraspinal acetylcholine and antinociception, and elucidate interactions between acetylcholine and other mechanisms that mediate antinociception in the spinal cord.

Ort, förlag, år, upplaga, sidor
Uppsala: Acta Universitatis Upsaliensis, 2005. s. 55
Serie
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 19
Nyckelord
Laboratory animals, Pain, Nociception, Antinociception, Acetylcholine, Muscarinic, Nicotinic, Spinal cord, Microdialysis, Försöksdjursvetenskap
Nationell ämneskategori
Biomedicinsk laboratorievetenskap/teknologi
Identifikatorer
urn:nbn:se:uu:diva-4834 (URN)91-554-6178-6 (ISBN)
Disputation
2005-04-22, B41, BMC, Husargatan 3, Uppsala, 09:15 (Engelska)
Opponent
Handledare
Tillgänglig från: 2005-03-30 Skapad: 2005-03-30 Senast uppdaterad: 2009-10-14Bibliografiskt granskad

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