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The Journal of Neuroscience, July 1, 1998, 18(13):5078-5085

Coadministration of Galanin Antagonist M40 with a Muscarinic M₁ Agonist Improves Delayed Nonmatching to Position Choice Accuracy in Rats with Cholinergic Lesions

Michael P. McDonald¹, Lauren B. Willard², Gary L. Wenk², and Jacqueline N. Crawley¹

¹ Section on Behavioral Neuropharmacology, Experimental Therapeutics Branch, National Institute of Mental Health, Bethesda, Maryland 20982, and ² Division of Neural Systems, Memory, and Aging, University of Arizona, Tucson, Arizona 85724

The neuropeptide galanin is overexpressed in the basal forebrain in Alzheimer's disease (AD). In rats, galanin inhibits evoked hippocampal acetylcholine release and impairs performance on several memory tasks, including delayed nonmatching to position (DNMTP). Galanin(1-13)-Pro₂-(Ala-Leu)₂-Ala-NH₂ (M40), a peptidergic galanin receptor ligand, has been shown to block galanin-induced impairment on DNMTP in rats. M40 injected alone, however, does not improve DNMTP choice accuracy deficits in rats with selective cholinergic immunotoxic lesions of the basal forebrain. The present experiments used a strategy of combining M40 with an M₁ cholinergic agonist in rats lesioned with the cholinergic immunotoxin ¹⁹²IgG-saporin. Coadministration of intraventricular M40 with intraperitoneal 3-(3-S-n-pentyl-1,2,5-thiadiazol-4-yl)-1,2,5,6-tetrahydro-1-methylpyridine (TZTP), an M₁ agonist, improved choice accuracy significantly more than a threshold dose of TZTP alone. These results suggest that a galanin antagonist may enhance the efficacy of cholinergic treatments for the cognitive deficits of AD.

Key words: Alzheimer's disease; acetylcholine; muscarinic receptors; galanin; neuropeptide; lesion model; memory

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Copyright © 1998 Society for Neuroscience  0270-6474/98/18135078-08$05.00/0

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