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The Journal of Neuroscience, December 31, 2008, 28(53):14537-14545; doi:10.1523/JNEUROSCI.2692-08.2008

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Development/Plasticity/Repair
Picomolar Amyloid-β Positively Modulates Synaptic Plasticity and Memory in Hippocampus

Daniela Puzzo,^1,2 Lucia Privitera,^1,2 Elena Leznik,¹ Mauro Fà,¹ Agnieszka Staniszewski,¹ Agostino Palmeri,² and Ottavio Arancio¹

¹Department of Pathology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York, New York 10032, and ²Department of Physiological Sciences, University of Catania, Catania 95125, Italy

Correspondence should be addressed to Dr. Ottavio Arancio, Columbia University Medical Center, Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Irving Cancer Research Center 1130 St. Nicholas Avenue, Room 603, New York, NY 10032. Email: oa1{at}columbia.edu

Amyloid-β (Aβ) peptides are produced in high amounts during Alzheimer's disease, causing synaptic and memory dysfunction. However, they are also released in lower amounts in normal brains throughout life during synaptic activity. Here we show that low picomolar concentrations of a preparation containing both Aβ₄₂ monomers and oligomers cause a marked increase of hippocampal long-term potentiation, whereas high nanomolar concentrations lead to the well established reduction of potentiation. Picomolar levels of Aβ₄₂ also produce a pronounced enhancement of both reference and contextual fear memory. The mechanism of action of picomolar Aβ₄₂ on both synaptic plasticity and memory involves 7-containing nicotinic acetylcholine receptors. These findings strongly support a model for Aβ effects in which low concentrations play a novel positive, modulatory role on neurotransmission and memory, whereas high concentrations play the well known detrimental effect culminating in dementia.

Key words: amyloid-β; synaptic plasticity; memory; hippocampus; -7 nicotinic receptors; Alzheimer's disease

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Received June 12, 2008; revised Oct. 23, 2008; accepted Nov. 18, 2008.

Correspondence should be addressed to Dr. Ottavio Arancio, Columbia University Medical Center, Department of Pathology and Cell Biology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Irving Cancer Research Center 1130 St. Nicholas Avenue, Room 603, New York, NY 10032. Email: oa1{at}columbia.edu

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