JUPITER, FL, January 22, 2013 How aging affects communication between neurons is not well understood, a gap that makes it more difficult to treat a range of disorders, including Alzheimer's and Parkinson's disease.
A new study from the Florida campus of The Scripps Research Institute (TSRI) offers insights into how aging affects the brain's neural circuitry, in some cases significantly altering gene expression in single neurons. These discoveries could point the way toward a better understanding of how aging affects our cognitive ability and new therapeutic targets for the treatment of neurodegenerative disease.
"Although we don't know exactly why, we do know there is a signaling imbalance as we age, and we've captured these changes at the single neuron level," said Sathyanarayanan V. Puthanveettil, a TSRI assistant professor who led the work. "If we could identify the underpinnings of this mechanism, we may be able to target the specific mechanism to affect or reverse the aging process in human neurons."
To record the electrical and physiological properties of single neurons, the scientists created a new method and applied it to the marine snail Aplysia californica, a widely used animal model. Many Aplysia gene expression signatures have counterparts in the human genome.
Using this methodology, which was published in the Journal of Visualized Experiments, the scientists were then able to focus on neuron R15, a burst firing neuron that is implicated in the regulation of water content and reproduction, showing how its response to the neurotransmitter acetylcholine and gene expression changed with age.
In a study published in the journal PLOS ONE, the team described specific changes in burst firing and action potentialswhich play a central role in cell-to-cell communicationduring the aging of R15, suggesting that changes in the response to acetylcholine during aging has been conserved
|Contact: Eric Sauter|
Scripps Research Institute