This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Folco, E. J. Articles by Koren, G. Search for Related Content PubMed PubMed Citation Articles by Folco, E. J. Articles by Koren, G. Related Collections Arrythmias-basic studies Electrocardiology

(Circulation Research. 2003;93:384.)
© 2003 American Heart Association, Inc.

Editorials

"Cardiac Memory"

A Struggle Against Forgetting

Eduardo J. Folco, Karim Roder, Gary F. Mitchell, Gideon Koren

From the Bioelectricity Laboratory (E.J.F., K.R., G.K.), Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass; Cardiovascular Engineering Inc (G.F.M.), Holliston, Mass.

Correspondence to Gideon Koren, MD, Bioelectricity Laboratory, Brigham and Women’s Hospital, Cardiovascular Division, 75 Francis St, Boston, MA 02115. E-mail koren@calvin.bwh.harvard.edu

Key Words: cAMP response element binding protein • inducible cAMP early repressor • calcium channels • potassium channels • cardiac memory

An extract of the first 250 words of the full text is provided, because this article has no abstract.

One of the most remarkable characteristics of living organisms is their ability to alter their behavior by learning. Human beings excel at processing new information, retaining it in their memory, and using it to develop new ideas. Studies in the mollusk Aplysia showed that learning involves the strengthening and increased effectiveness of preexisting synapses. Over time, it has become clear that synaptic plasticity is the fundamental mechanism for learning and memory. Short-term memory, lasting minutes to hours, involves to a large extent a serotonin-mediated release of cAMP, which activates protein kinase A (PKA), leading to the covalent modifications of S-type K⁺ channels and delayed-rectifier K⁺ channels. These modifications, which cause spike broadening, an increase in Ca²⁺ influx, and enhanced transmitter release, do not require protein synthesis. Long-term memory, lasting days to weeks, differs from short-term memory and requires the synthesis of new proteins. Studies in Aplysia, the fruit fly Drosophila, and later in rodents have revealed that this process involves activation of the cAMP response element binding protein (CREB)-mediated transcriptional cascade. Inactivation of CREB or inhibition of its phosphorylation interferes with learning and memory (see reviews^1,2).

The CREB family of transcription factors includes CREB, CREM (cAMP response element modulator), and ATF-1 (activating transcription factor 1). Each member of the family contains a basic DNA-binding domain at the C-terminus and a leucine zipper domain that mediates homodimerization or heterodimerization of these factors (bZIP). All three factors bind to a cAMP response cis-regulatory element (CRE) that consists of . . . [Full Text of this Article]

This article has been cited by other articles:

				K. W. Patberg and M. R. Rosen On the Role of the cAMP Response Element Binding Protein in Long-Term Cardiac Memory Circ. Res., October 31, 2003; 93 (9): e87 - e87. [Full Text] [PDF]