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British Journal of Anaesthesia, 2000, Vol. 85, No. 6 869-873
© 2000 The Board of Management and Trustees of the British Journal of Anaesthesia

Central cholinergic depletion induced by 192 IgG-Saporin alleviates the sedative effects of propofol in rats

L. Pain*,1, H. Jeltsch2, O. Lehmann2, C. Lazarus2, F. Z. Laalou1 and J. C. Cassel2

1GRERCA, U405 INSERM et Service d’Anesthésie, CHU Hautepierre, 1 Avenue Molière, F-67000 Strasbourg, France. 2LN2C, UMR 7521 CNRS/Université Louis Pasteur, 12 rue Goethe, F-67000 Strasbourg, France*Corresponding author

We examined the effect of central cholinergic depletion on the sedative potency of propofol in rats. Depletion was produced by intracerebroventricular administration of an immunotoxin specific to cholinergic neurones (192 IgG-Saporin; 2 µg). As a result of this lesion, acetylcholine concentration was reduced by about 40% in the frontoparietal cortex and in the hippocampus but was essentially normal in the striatum and cerebellum. Sedation in rats was assessed as the decrease in locomotor activity. Sedative potency of propofol (30 mg kg–1 i.p.) was reduced by about 50% in rats who received the injection of 192 IgG-Saporin as compared to controls. These results show that a central cholinergic depletion alleviates the sedative effect of propofol, and indicates that basal forebrain cholinergic neurones might mediate part of the sedative/hypnotic effects of propofol.

Br J Anaesth 2000; 85: 869–73


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