Hippocampal and Extrahippocampal Systems Compete for Control of Contextual Fear: Role of Ventral Subiculum and Amygdala

Autor/inn/en	Biedenkapp, Joseph C.; Rudy, Jerry W.
Titel	Hippocampal and Extrahippocampal Systems Compete for Control of Contextual Fear: Role of Ventral Subiculum and Amygdala
Quelle	In: Learning & Memory, 16 (2009) 1, S.38-45 (8 Seiten) PDF als Volltext Verfügbarkeit
Sprache	englisch
Dokumenttyp	gedruckt; online; Zeitschriftenaufsatz
ISSN	1072-0502
DOI	10.1101/lm.1099109
Schlagwörter	Conditioning; Cognitive Processes; Fear; Brain Hemisphere Functions; Role; Drug Use; Neurological Impairments; Hypothesis Testing + Suchen Sie Ihr Suchwort? Cognitive process; Kognitiver Prozess; Furcht; Rollen; Drug consumption; Substance abuse; Drogenkonsum; Neurodegenerative Erkrankung; Hypothesenprüfung; Hypothesentest
Abstract	Two neural systems, a hippocampal system and an extrahippocampal system compete for control over contextual fear, and the hippocampal system normally dominates. Our experiments reveal that output provided by the ventral subiculum is critical for the hippocampal system to win this competition. Bilateral electrolytic lesions of the ventral subiculum after conditioning, but not before conditioning, impaired contextual fear conditioning. Reversibly inactivating this region by bilateral injections of muscimol produced the same results--no impairment when the injection occurred prior to conditioning but a significant impairment when this region was inactivated after conditioning. Thus, the extrahippocampal system can support contextual fear conditioning if the ventral subiculum is disabled before conditioning but not if it is disabled after conditioning. Our experiments also reveal that the basolateral region of the amygdala (BLA) is where the two systems compete for associative control of the fear system. To test this hypothesis we reasoned that the extrahippocampal system would also acquire associative control over the fear system, even if the hippocampal system were functional, if the basal level of plasticity potential in the BLA could be increased. We did this by injecting the D1 dopamine agonist, SKF82958, into the BLA just prior to conditioning. This treatment resulted in a significant increase in freezing when the ventral subiculum was disabled prior to the test. These results are discussed in relationship to the idea that D1 agonists increase plasticity potential by increasing the pool of available extrasynaptic GluR1 receptors in the population of neurons supporting acquired fear. (As Provided).
Anmerkungen	Cold Spring Harbor Laboratory Press. 500 Sunnyside Boulevard, 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