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Glycine, \u03b3\u2010aminobutyric acid, and \u03b2\u2010alanine were potent depressants of BC\u2010RN synaptic transmission, amino acid\u2010evoked firing, and spontaneous activity of all RN neurons studied. Glycine was clearly more potent than the other 2 depressant amino acids. L\u2010Glutamic and DL\u2010homocysteic acid were strong excitants of all RN neurons tested. Dopamine, noradrenaline, and 5\u2010hydroxytryptamine depressed the excitability of both parvicellular and magnocellular RN neurons; no excitatory effects were observed with these biogenic amines on RN neurons. Acetylcholine increased the rate of firing of spontaneously discharging parvicellular RN neurons and facilitated the amino acid\u2010induced firing of these same neurons. Acetylcholine did not facilitate BC\u2010RN synaptic transmission nor could this transmission be blocked by cholinergic antagonists. Unlike parvicellular RN neurons, the responsiveness of magnocellular neurons was either unaltered by acetylcholine or slightly decereased. These experiments demonstrate a difference in the pharmacologic responsiveness of parvicellular and magnocellular RN neurons to acetylcholine but do not provide evidence for a cholinergic input to RN via the brachium conjunctivum.<\/jats:p>","DOI":"10.1002\/jnr.490030302","type":"journal-article","created":{"date-parts":[[2005,1,1]],"date-time":"2005-01-01T11:06:34Z","timestamp":1104577594000},"page":"175-191","source":"Crossref","is-referenced-by-count":24,"title":["Pharmacology of the brachium conjunctivum: Red nucleus synaptic system in the baboon"],"prefix":"10.1002","volume":"3","author":[{"given":"Ronald 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