Nicotine compensates for the loss of cholinergic function to enhance long-term potentiation induction

Long-term potentiation (LTP) in the hippocampal CA1 region is widely regarded to be the cellular substrate of learning and memory, and its induction critically depends on the activation of N-methyl- d-aspartate receptors (NMDARs). Nicotine reverses memory deficits caused by a lesion of the cholinerg...

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Bibliographic Details
Published in:Brain research 2002-08, Vol.946 (1), p.148-152
Main Authors: Yamazaki, Yoshihiko, Hamaue, Naoya, Sumikawa, Katumi
Format: Article
Language:English
Subjects:
192-IgG-saporin
Animals
Biological and medical sciences
Central nervous system
Cholinergic Fibers - physiology
Cholinergic lesion
Electrophysiology
Fundamental and applied biological sciences. Psychology
Hippocampus
Long-term potentiation
Long-Term Potentiation - drug effects
Long-Term Potentiation - physiology
N-Methyl- d-aspartate receptor
Nerve Degeneration - physiopathology
Neural Inhibition - drug effects
Nicotine
Nicotine - pharmacology
Nicotinic acetylcholine receptor
Nicotinic Agonists - pharmacology
Pyramidal Cells - physiology
Rats
Receptors, N-Methyl-D-Aspartate - physiology
Synaptic plasticity
Vertebrates: nervous system and sense organs
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Summary:Long-term potentiation (LTP) in the hippocampal CA1 region is widely regarded to be the cellular substrate of learning and memory, and its induction critically depends on the activation of N-methyl- d-aspartate receptors (NMDARs). Nicotine reverses memory deficits caused by a lesion of the cholinergic system in animals. The mechanisms underlying this effect and the effect of nicotine on LTP after cholinergic degeneration are unknown. Here we show that cholinergic lesions impaired the induction of LTP, and nicotine reversed this effect and promoted the induction of LTP. The compensatory action of nicotine appears to be due to the enhancement of NMDAR responses mediated by nicotine-induced disinhibition of pyramidal cells. This may represent the cellular basis of nicotine-mediated cognitive enhancement observed in the presence of cholinergic deficits.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(02)02935-9