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Research article summary (published 12 Apr 1998):
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All-or-none potentiation at CA3-CA1 synapses.

Full Abstract

The molecular mechanisms underlying long-term potentiation in the hippocampus have received much attention because of the likely functional importance of synaptic plasticity for information storage and the development of neuronal connectivity. Surprisingly, it remains unclear whether activity modifies the strength of individual synapses in a digital (all-or-none) or analog (graded) manner. Here we characterize step-like all-or-none transitions from baseline synaptic transmission to potentiated states following protocols for inducing potentiation at putative single CA3-CA1 synaptic connections. Individual synapses appear to have all-or-none potentiation indicative of highly cooperative processes but different thresholds for undergoing potentiation. These results raise the possibility that some forms of synaptic memory may be stored in a digital manner in the brain.

 

Author information

Author/s: Petersen, C C (CC); Malenka, R C (RC); Nicoll, R A (RA); Hopfield, J J (JJ);

Affiliation: Department of Cellular and Molecular Pharmacology, The University of California, San Francisco, San Francisco, CA, 94143, USA.

Journal and publication information

Publication Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.

Journal: Proceedings of the National Academy of Sciences of the United States of America (Proc Natl Acad Sci U S A), published in UNITED STATES. (Language: eng)

Reference: 1998-Apr; vol 95 (issue 8) : pp 4732-7

Dates: Created 1998/05/13; Completed 1998/05/13; Revised 2008/11/20;

PMID: 9539807, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

Comments and Corrections

CommentIn: Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4086-8. (PMID: 9539692)

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Associated Chemicals: Receptors, N-Methyl-D-Aspartate (0)

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