[Effects of cholinergic drugs and noradrenaline on the activity of neurons in the rat nucleus raphe magnus in vitro].
The nucleus raphe magnus (NRM) is considered to be an important descending inhibitory system in the pain transmission. Both noradrenergic and cholinergic inputs to NRM have an important role in the modulation of pain. Microinjection of cholinergic agonists or noradrenergic antagonist into the NRM produces antinociception. In order to investigate effects of carbachol (a cholinergic agonist) and epibatidine (a nicotinic cholinergic agonist) on the activity of NRM neurons, we recorded the activity of NRM neurons using extracellular recording technique in the rat brainstem slice preparation and analyzed the changes of the activity by application of carbachol and epibatidine. Further, we studied whether these cholinergic agonists and noradrenaline modulate the activity of the identical NRM neurons. Carbachol increased firing frequencies (FF) in 34 (33%) spontaneously active neurons and decreased FF in 56 (54%). In 19 (50%) silent neurons, carbachol induced firing activity. Epibatidine increased FF in 30 (62.5%) spontaneously active neurons. In 3 (25%) silent neurons, epibatidine induced firing activity. Noradrenaline increased FF in 44 (67.5%), decreased FF in 14 (21.5%) spontaneously active neurons. In 9 (64%) silent neurons, noradrenaline induced firing activity. Carbachol, epibatidine and noradrenaline had effects on a substantial number of the identical NRM neurons. All spontaneously active neurons inhibited by noradrenaline were also inhibited by carbachol. The correlative effects between carbachol and epibatidine, and between epibatidine and noradrenaline were both unremarkable. Carbachol increased or decreased the firing activity of a substantial number of NRM neurons. Carbachol may facilitate or reduce the outflow of the descending inhibitory pathway. Epibatidine increased the firing activity of a substantial number of NRM neurons. Epibatidine may facilitate the outflow of the descending inhibitory pathway. Combinations of carbachol and epibatidine, carbachol and noradrenaline, or epibatidine and noradrenaline may modulate the pain transmission through a part of the same pathway from NRM neurons.
Kanda
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Department of Anesthesiology and Critical Care Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D019086:Bridged Bicyclo Compounds, Heterocyclic / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology*; D003864:Depression, Chemical; D066298:In Vitro Techniques; D009475:Neurons, Afferent / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology*; D010146:Pain / Q000503:physiopathology; D011725:Pyridines / Q000494:pharmacology; D011903:Raphe Nuclei / Q000166:cytology* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D009435:Synaptic Transmission / Q000187:drug effects
D019086:Bridged Bicyclo Compounds, Heterocyclic; D018679:Cholinergic Agonists; D011725:Pyridines; D002217:Carbachol; C082748:epibatidine; D009638:Norepinephrine