Neuroscience 2005 Abstract
| Presentation Number: | 415.8 |
|---|---|
| Abstract Title: | NMDA receptor-independent hippocampal activity is required for short-interval trace fear conditioning measured using fear-potentiated startle. |
| Authors: |
Burman, M. A.*1,3
; Jepsen, S. E.1
; Gewirtz, J. C.1,2,3
1Dept Psych, Univ. of Minnesota, Minneapolis, MN 2Dept Neurosci, Univ. of Minnesota, Minneapolis, MN 3Center for Cognit. Sci., Univ. of Minnesota, Minneapolis, MN |
| Primary Theme and Topics |
Cognition and Behavior - Animal Cognition and Behavior -- Emotional learning, memory systems, and modulation of memory |
| Secondary Theme and Topics | Cognition and Behavior<br />- Animal Cognition and Behavior<br />-- Cognitive learning and memory systems |
| Session: |
415. Emotional Learning IV Poster |
| Presentation Time: | Monday, November 14, 2005 11:00 AM-12:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # HH24 |
| Keywords: | HIPPOCAMPUS, CLASSICAL CONDITIONING, LEARNING AND MEMORY, CONSOLIDATION |
The dorsal hippocampus is required for trace fear conditioning, where the CS and US are separated in time, but not for delay fear conditioning, where the stimuli overlap. Despite evidence for the key role of glutamatergic NMDA receptors in a variety of forms of hippocampus-dependent memory, recent findings suggest that trace fear conditioning is only dependent on hippocampal NMDA receptor activity when the interval between CS offset and US onset is relatively long (i.e., >= 5 s Wanish et al. 2005, Misane et al. 2005, Chowdhury et al. SFN 2004). This suggests either that short-interval trace conditioning is not dependent on the dorsal hippocampus, or that it is dependent on NMDA receptor-independent mechanisms within the dorsal hippocampus. To investigate this issue further, the current experiments compared the effects of intrahippocampal infusion of the NMDA receptor antagonist AP5 and the AMPA receptor antagonist NBQX on fear conditioning with a 3-s trace interval. Fear-potentiated startle was used to measure conditioned fear. As in the earlier studies that had measured freezing behavior, NMDA receptor blockade did not disrupt acquisition of trace conditioning. In contrast, trace conditioning was disrupted by blockade of hippocampal AMPA receptors. This indicates that short-interval trace conditioning is dependent on the hippocampus, consistent with recent lesion data from our laboratory, but not on NMDA receptor activity in that structure. Interestingly, AMPA receptor blockade disrupted conditioning both when the antagonist was infused immediately before training and when it was infused immediately after training. Similar posttraining disruption was also found using the GABA-A agonist muscimol. Collectively, these findings suggest that acquisition and consolidation of short-interval trace fear conditioning require NMDA receptor-independent cellular activity in the hippocampus.
Supported by NIH training grant T32 HD007151 to the Center for Cognitive Sciences
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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