A new study has revealed that mutations in the gene huntingtin, which cause the devastating progressive neurological condition Huntington's disease, plays a critical role in long-term memory and normal brain activity.
According to a study from The Scripps Research Institute's (TSRI's) Florida campus and Columbia University, huntingtin expression levels are necessary for what is known as long-term synaptic plasticity-the ability of the synapses to grow and change-which is critical to the formation of long-term memory.
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The research the team identified an equivalent of the human huntingtin protein in the marine snail Aplysia, a widely used animal model in genetic studies, and found that, just like its human counterpart, the protein in Aplysia is widely expressed in neurons throughout the central nervous system.
TSRI Assistant Professor Sathyanarayanan V. Puthanveettil said that during the learning, production of the huntingtin mRNAs is increased both in pre- and post-synaptic neurons and if production of the protein either in pre- or post-synaptic neuron is blocked, then there is a block in the formation of memory.
The study found that the expression of messenger RNAs of huntingtin-messenger RNAs are used to produce proteins from instructions coded in genes-is increased by serotonin, a neurotransmitter released during learning in Aplysia. After knocking down production of the huntingtin protein, neurons failed to function normally.
The study was published in the journal PLOS ONE.
