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The Journal of Neuroscience, June 29, 2005, 25(26):6084-6091; doi:10.1523/JNEUROSCI.0542-05.2005

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Cellular/Molecular
Nicotinic Acetylcholine Receptors at Glutamate Synapses Facilitate Long-Term Depression or Potentiation

Shaoyu Ge and John A. Dani

Department of Neuroscience, Menninger Department of Psychiatry and Behavioral Science, Program in Structural and Computational Biology and Molecular Biophysics, Baylor College of Medicine, Houston, Texas 77030-3498

The hippocampus is a center for learning and memory that receives abundant cholinergic innervation and richly expresses nicotinic acetylcholine receptors (nAChRs). Nicotinic mechanisms acting on the hippocampus influence attention, learning, and memory. During Alzheimer's dementia, nAChRs and cholinergic innervation decline in the hippocampus. Using mouse hippocampal slices, we examined the potential diversity of nAChR influences at the Schaffer collateral synapse onto CA1 pyramidal neurons. When nAChR currents were elicited locally at those excitatory synapses, various outcomes were possible depending on the relationship between the nAChR-mediated excitation and mild electrical stimulation. When mild presynaptic stimulation coincided with or preceded nAChR-induced action potentials by 1-5 s, then long-term potentiation was induced. However, if the nAChR-induced action potentials fell within 1 s before the electrical stimulation, then long-term depression resulted. Outside of these time frames, the mismatch of nAChR activity and stimulation led to short-term potentiation. The results indicate that nAChRs may have various influences over excitatory events in the hippocampus. Ongoing nAChR activity likely modulates the impact of glutamate transmission and alters the probabilities for various forms of synaptic plasticity. The fine network of cholinergic fibers running through the hippocampus forms synaptic contacts onto pyramidal cells, granule cells, and interneurons, ensuring continual modulatory influence by nicotinic mechanisms throughout the hippocampal complex. Disruption of events such as those described here may contribute to the deficits associated with the decline of nicotinic cholinergic functions during degenerative diseases such as Alzheimer's dementia.

Key words: cholinergic; nicotinic receptors; nicotine addiction; synaptic modulation; synaptic plasticity; hippocampus

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Received Nov 9, 2004; revised May 5, 2005; accepted May 17, 2005.

This article has been cited by other articles:

				C. Zhong, C. Du, M. Hancock, M. Mertz, D. A. Talmage, and L. W. Role Presynaptic Type III Neuregulin 1 Is Required for Sustained Enhancement of Hippocampal Transmission by Nicotine and for Axonal Targeting of {alpha}7 Nicotinic Acetylcholine Receptors J. Neurosci., September 10, 2008; 28(37): 9111 - 9116. [Abstract] [Full Text] [PDF]

				B. Lendvai and E. S. Vizi Nonsynaptic Chemical Transmission Through Nicotinic Acetylcholine Receptors Physiol Rev, April 1, 2008; 88(2): 333 - 349. [Abstract] [Full Text] [PDF]

				M. Rosato-Siri, A. Cattaneo, and E. Cherubini Nicotine-induced enhancement of synaptic plasticity at CA3-CA1 synapses requires GABAergic interneurons in adult anti-NGF mice J. Physiol., October 15, 2006; 576(2): 361 - 377. [Abstract] [Full Text] [PDF]

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