RT Journal Article
SR Electronic
T1 Deficits in Trace Fear Memory and Long-Term Potentiation in a Mouse Model for Fragile X Syndrome
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 7385
OP 7392
DO 10.1523/JNEUROSCI.1520-05.2005
VO 25
IS 32
A1 Ming-Gao Zhao
A1 Hiroki Toyoda
A1 Shanelle W. Ko
A1 Hoi-Ki Ding
A1 Long-Jun Wu
A1 Min Zhuo
YR 2005
UL http://www.jneurosci.org/content/25/32/7385.abstract
AB 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.