Calcium good for more than strong bones

When memories are made and learning occurs, the connections between brain cells change. Scientists know that an influx of calcium is critical to this process. A theoretical model developed by a research team from Brown University, Providence, R.I., shows that cells' ability to fine-tune this calcium flow not only sparks changes in synapses, but allows cells to maintain a working state of equilibrium.

Luk Chong Yeung, a neuroscience research associate, and her colleagues have come up with a concept that hinges on calcium control. Certain receptors, which act like gates, allow calcium to rush into brain cells that receive memory-making information. Once inside these cells, calcium sets off chemical reactions that change the connections between neurons, or synapses. That malleability, known as synaptic plasticity, is believed to be the fundamental basis of memory, learning, and brain development.

Yeung has demonstrated that the control of these receptors not only makes synapses stronger or weaker, but stabilizes them--without interfering with the richness of the cellular response to signals sent from neighboring cells. "The beauty of the brain is that it is plastic and robust at the same time," Yeung explains. "If the model is verified experimentally, we've solved an important piece of the puzzle of how these seemingly antagonistic properties can and, in fact, must coexist in the cell."

Scientists previously had developed a model where N-methyl-D-aspartate receptors control the flow of calcium into signal-receiving neutrons. The model unified several observations of synaptic plasticity and, after being tested in labs, it is seen as the standard model by many researchers in the field. It had a flaw, however. Although explaining how synapses get stronger or weaker, it did not account for how they stabilize. Without homeostasis, synapses could grow indefinitely--an impossible scenario.

Yeung's team based their model on experimental data as well as mathematical equations. Then the model was applied to a stimulated brain cell receiving signals from competing synapses. The theory held up: Regulating the flow of calcium into cells allows for rapid synaptic changes that capture the transient features of the signal and slows homeostatic control that returns the cell to a steady state.

"The key feature of the model is that, unlike many neural learning theories, it is built on real quantities that can be measured in the lab," Yeung points out. "But the basic principles are universal enough to be applied to any stable plasticity model."

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