New Haven, Conn. — A family of proteins that help build the cytoskeleton, or the bones of the cell, also play an important role in learning and memory, according to a study published this month in The Journal of Neuroscience.
Marina Picciotto, associate professor of psychiatry, pharmacology and neurobiology at Yale School of Medicine, and the senior author of the study, studied mice missing one of these proteins—ί–adducin—and found the cytoskeleton developed normally. However, the mice were impaired during fear conditioning and memory exercises.
“We were hoping to find a mechanism that cells use to make short term changes in nerve cell communication permanent, but we were surprised that losing ί–adducin made such a big change in both the nerve cell communication and in behavioral measures of memory,” Picciotto said.
The focus of the study is long–term potentiation, which is a form of neuronal plasticity and may form the biological basis for some kinds of memory. Long–term potentiation refers to the fact that if two neurons in the hippocampus are active at the same time, the connection between them can be strengthened. This change, or potentiation, can last for hours to days. This may serve to lay a foundation for more permanent changes, such as the construction of new connections, or synapses, between the neurons.
“If you learn to do something new, your neurons have to adapt and change to create a stronger, more direct pathway between neurons,” Picciotto said. “The protein ί–adducin appears to be important for making those new connections.”
In this study, the mice that did not have the protein were not able to strengthen a synapse in the hippocampus, which is the area of the brain that enables us to remember people, places and things. “If the mice don’t have ί–adducin, they can’t make a new map,” Picciotto said. “It’s not enough to just have the electrical properties, the skeleton is very important in making long–lasting changes between nerve cells that result in learning.”
Citation: Journal of Neuroscience 25: 2138–2145 (February–2005)
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