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Researchers Uncover Key Step In Manufacture of Memory Protein

s, resembling prongs. These prongs fit into a corresponding indentation on CPE, analogous to the way a plug for an electric appliance fits into an electric wall outlet, Dr. Loh said.

The golgi apparatus then encases the lipid rafts ?along with proBDNF ?in bubble-like structures known as vesicles. Within these vesicles, proBDNF is converted to mBDNF by other enzymes. The vesicles are then transported to the cell’s outer membrane, where they remain until they are ready to be secreted. Once the cell receives an electrical signal from another neuron, these vesicles fuse with the cell’s outer membrane, open up, and release mBDNF.

During their research, Dr. Loh and her colleagues observed mice genetically incapable of producing CPE. In these mice, proBDNF could not be delivered into the lipid raft-rich vesicles for conversion to mBDNF. Instead, it appeared to leak out of the golgi apparatus, where it leached through the cell membrane without first having been converted to active mBDNF. Because they cannot make mBDNF, CPE-deficient mice have poor long-term memory.

Dr. Loh added that, in the near future, an understanding of the chemical mechanism she and her colleagues deciphered in the current study may provide insight into long-term memory deficits. She explained that other researchers have learned that some human beings lack normal CPE due to mutations in the CPE gene. Future research may determine if the CPE mutation affects these individuals?long-term memory.


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Source:NIH


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