Hypoalgesia induced by the local injection of carbachol into the nucleus raphe magnus.
The medial region of the caudal medulla which contains the nucleus raphe magnus and magnocellular reticular formation has been demonstrated to modulate pain perception. Recent reports from this laboratory have shown that neurons in this region are under tonic inhibitory control by noradrenergic neurons. The excitability of neurons in the raphe magnus and adjacent reticular formation may also be controlled by cholinergic neurons since there is evidence that cholinergic terminals are located in the medial region of the caudal medulla. The present study was designed to examine this possibility by microinjecting carbachol, a cholinergic agonist, into the region of the nucleus raphe magnus. The results indicate that the injection of carbachol into the caudal brainstem produces dose-dependent hypoalgesia, i.e. decreased pain sensitivity. This hypoalgesia appears to be mediated by cholinergic muscarinic receptors since it was reversed by the muscarinic antagonist atropine. The cholinergic innervation of the raphe magnus does not appear to be important in the maintenance of nociceptive threshold since injection of atropine alone did not alter pain responses.
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D001285:Atropine / Q000008:administration & dosage; D001931:Brain Mapping; D001933:Brain Stem / Q000503:physiopathology*; D002217:Carbachol / Q000008:administration & dosage*; D002799:Cholinergic Fibers / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D005260:Female; D008845:Microinjections; D010146:Pain / Q000503:physiopathology*; D011903:Raphe Nuclei / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains
D001285:Atropine; D002217:Carbachol; D000109:Acetylcholine