Deficits in trace fear memory and long-term potentiation in a mouse model for fragile X syndrome
Abstract
Trace fear memory requires the activity of the anterior cingulate cortex (ACC) and is sensitive to attention-distracting stimuli. Fragile X syndrome is the most common form of mental retardation with many patients exhibiting attention deficits. Previous studies in fragile X mental retardation 1 ( FMR1 ) knock-out (KO) mice, a mouse model for fragile X, focused mainly on hippocampal-dependent plasticity and spatial memory. We demonstrate that FMR1 knock-out mice show a defect in trace fear memory without changes in locomotion, anxiety, and pain sensitivity. Whole-cell path-clamp recordings in the ACC show that long-term potentiation (LTP) was completely abolished. A similar decrease in LTP was found in the lateral amygdala, another structure implicated in fear memory. No significant changes were found in basal synaptic transmission. This suggests that synaptic plasticity in the ACC and amygdala of FMR1 KO mice plays an important role in the expression of behavioral phenotypes similar to the symptoms of fragile X syndrome.
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Loss of FMRP enhances NMDAR function in young mice but not in adult mice.
“Loss of FMRP enhances NMDAR function in young (Pfeiffer and Huber, 2007; Pilpel et al., 2008), but not in adult mice (Pilpel et al., 2008; Zhao et al., 2005).”
From Regulation of Synaptic Structure and Function by FMRP-Associated MicroRNAs miR-125b and miR-132 (2010) · cites this paper as Zhao et al., 2005
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- Authors
- Zhao, M.-G., Toyoda, H., Ko, S. W., Ding, H.-K., Wu, L.-J., & Zhuo, M.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2005-08-10
- Volume
- 25
- Issue
- 32
- Pages
- 7385-7392
- ISSN
- 0270-6474
- 1529-2401
- Cited by
- 258
- References
- 9
- Language
- en
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