Of Mice and Memory: New Findings for Fragile X

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This past week, mice helped UC Irvine neurobiologist, Julie Lauterborn and a team of researchers discover how to reverse the learning and memory problems that take place as a result of the most common form of mental retardation, fragile X syndrome.
This condition, caused by the loss of a specific protein, is the main cause of mental retardation in the United States.
The team used genetically altered mice, which are known as Fmr1-knockout mice due to their ability to block the transcription of a gene that gives rise to a protein called Fragile X Mental Retardation Protein (FMRP). FMRP is expressed by cells in both the brain and the body.
Reaching the result, however, was no easy task. The mice used in the experiment had some of the features of Fragile X Syndrome, including learning deficits.
Previous studies on the Fmr1-KO mouse hippocampus did not find any deficits in the Long-Term Potentiation (LTP). LTP is a cellular process that occurs in the spine and is thought to underlie learning and memory in the brain. LTP, in simpler terms, is a long-lasting enhancement of synaptic strength and, thus, helps communication between neurons.
‘The fact that there was no observed deficit in hippocampus in previous studies was interesting because that is the part of the brain that is essential to the formation of memories,’ Lauterborn said.
Noticing this inconsistency, Lauterborn and her team decided to reexamine the mice to see if deficits did not in fact exist in the fragile X mouse hippocampus. The team failed in its first attempts because the team, like everyone else before, did not see a deficit in LTP.
‘It was a bit of a joke in the lab at that time that everything we were trying to do on fragile X was doomed to fail at least once, if not more,’ Lauterborn said. ‘We called it ‘the fragile X curse.’ Plus, it seemed like every time we were geared up to do the experiment something always went wrong

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