Galanin Antagonizes Acetylcholine on a Memory Task in Basal Forebrain-Lesioned Rats

• Published in: Proceedings of the National Academy of Sciences - PNAS 1988-12, Vol.85 (24), p.9841-9845
• Main Authors: Mastropaolo, J., Nadi, N. S., Ostrowski, N. L., Crawley, J. N.
• Format: Article
• Language: English
• Subjects: Acetylcholine - administration & dosage; Acetylcholine - metabolism; Alzheimer Disease - physiopathology; Alzheimers disease; Animals; Atropine; Atropine - pharmacology; Behavioral neuroscience; Behavioral psychophysiology; Biological and medical sciences; Brain - drug effects; Brain - pathology; Cholinergic receptors; Cholinergics; Fundamental and applied biological sciences. Psychology; Galanin; Hippocampus; Injections, Intraventricular; Lesions; Male; Mecamylamine - pharmacology; Memory; Memory - drug effects; Memory disorders; Neurons; Peptides - pharmacology; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Rats; Rats, Inbred Strains
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.85.24.9841

Galanin coexists with acetylcholine in medial septal neurons projecting to the ventral hippocampus, a projection thought to modulate memory functions. Neurochemical lesions of the nucleus basalis-medial septal area in rats impaired choice accuracy on a delayed alternation t-maze task. Acetylcholine (7.5 or 10 μ g intraventricularly or 1 μ g microinjected into the ventral hippocampus) significantly improved performance in the lesioned rats. Atropine (5 mg/kg intraperitoneally or 10 μ g intraventricularly), but not mecamylamine (3 mg/kg intraperitoneally or 20 μ g intraventricularly), blocked this action of acetylcholine, suggesting involvement of a muscarinic receptor. Galanin (100-500 ng intraventricularly or 200 ng into the ventral hippocampus) attenuated the ability of acetylcholine to reverse the deficit in working memory in the lesioned rats. The antagonistic interaction between galanin and acetylcholine suggests that endogenous galanin may inhibit cholinergic function in memory processes, particularly in pathologies such as Alzheimer disease that involve degeneration of basal forebrain neurons.