NotesFAQContact Us
Collection
Advanced
Search Tips
Peer reviewed Peer reviewed
Direct linkDirect link
ERIC Number: EJ920354
Record Type: Journal
Publication Date: 2010-Nov
Pages: 11
Abstractor: As Provided
Reference Count: 0
ISBN: N/A
ISSN: ISSN-0898-929X
A Single Brief Burst Induces GluR1-Dependent Associative Short-Term Potentiation: A Potential Mechanism for Short-Term Memory
Erickson, Martha A.; Maramara, Lauren A.; Lisman, John
Journal of Cognitive Neuroscience, v22 n11 p2530-2540 Nov 2010
Recent work showed that short-term memory (STM) is selectively reduced in GluR1 knockout mice. This raises the possibility that a form of synaptic modification dependent on GluR1 might underlie STM. Studies of synaptic plasticity have shown that stimuli too weak to induce long-term potentiation induce short-term potentiation (STP), a phenomenon that has received little attention. Here we examined several properties of STP and tested the dependence of STP on GluR1. The minimal requirement for inducing STP was examined using a test pathway and a conditioning pathway. Several closely spaced stimuli in the test pathway, forming a single brief burst, were sufficient to induce STP. Thus, STP is likely to be induced by the similar bursts that occur in vivo. STP induction is associative in nature and dependent on the NMDAR. STP decays with two components, a fast component (1.6 plus or minus 0.26 min) and a slower one (19 plus or minus 6.6 min). To test the role of GluR1 in STP, experiments were conducted on GluR1 knockout mice. We found that STP was greatly reduced. These results, taken together with the behavioral work of D. Sanderson et al. [Sanderson, D., Good, M. A., Skelton, K., Sprengel, R., Seeburg, P. H., Nicholas, J., et al. "Enhanced long-term and impaired short-term spatial memory in GluA1 AMPA receptor subunit knockout mice: Evidence for a dual-process memory model." "Learning and Memory," 2009], provide genetic evidence that STP is a likely mechanism of STM.
MIT Press. 55 Hayward Street, Cambridge, MA 02142. Tel: 617-253-2889; Fax: 617-253-1709; e-mail: journals-orders@mit.edu; Web site: http://www.mitpressjournals.org/loi/jocn
Publication Type: Journal Articles; Reports - Research
Education Level: N/A
Audience: N/A
Language: English
Sponsor: N/A
Authoring Institution: N/A