Activation of LVGCCs and CB1 Receptors Required for Destabilization of Reactivated Contextual Fear Memories

Autor/inn/en	Suzuki, Akinobu; Mukawa, Takuya; Tsukagoshi, Akinori; Frankland, Paul W.; Kida, Satoshi
Titel	Activation of LVGCCs and CB1 Receptors Required for Destabilization of Reactivated Contextual Fear Memories
Quelle	In: Learning & Memory, 15 (2008) 6, S.426-433 (8 Seiten) PDF als Volltext Verfügbarkeit
Sprache	englisch
Dokumenttyp	gedruckt; online; Zeitschriftenaufsatz
ISSN	1072-0502
DOI	10.1101/lm.888808
Schlagwörter	Animals; Genetics; Memory; Fear; Metabolism; Physiology; Molecular Structure; Conditioning; Drug Use; Brain + Suchen Sie Ihr Suchwort? Animal; Tier; Tiere; Humangenetik; Gedächtnis; Furcht; Stoffwechsel; Physiologie; Drug consumption; Substance abuse; Drogenkonsum; Gehirn
Abstract	Previous studies have shown that inhibiting protein synthesis shortly after reactivation impairs the subsequent expression of a previously consolidated fear memory. This has suggested that reactivation returns a memory to a labile state and that protein synthesis is required for the subsequent restabilization of memory. While the molecular mechanisms underlying the restabilization of reactivated memories are being uncovered, those underlying the initial destabilization are not known at all. Using a contextual fear conditioning paradigm in mice, here we show that LVGCCs or CB1 receptors in hippocampus are required for the initial destabilization of reactivated memory. Either pharmacological blockade of hippocampal protein synthesis or genetic disruption of CREB-dependent transcription disrupts memory restabilization following reactivation. However, these effects were completely blocked when mice were treated with inhibitors of either LVGCCs or CB1 receptors, indicating that LVGCCs or CB1 receptors are required for the initial destabilization of reactivated memory. In control experiments, we show that blockade of LVGCCs or CB1 receptors does not interfere with the ability of ANI to block protein synthesis, or with the ability of ANI to impair initial consolidation. These experiments begin to reveal mechanisms underlying the destabilization of previously consolidated memories following reactivation and indicate the importance of activation of LVGCCs and CB1 in this process. (Author).
Anmerkungen	Cold Spring Harbor Laboratory Press. 500 Sunnyside Blvd, Woodbury, NY 11797-2924. Tel: 800-843-4388; Tel: 516-367-8800; Fax: 516-422-4097; e-mail: cshpres@cshl.edu; Web site: http://www.learnmem.org/
Erfasst von	ERIC (Education Resources Information Center), Washington, DC
Update	2017/4/10