Washington: New research from the Lisman Laboratory has pointed to a molecule that is central to the process by which memories are stored in the brain.
The brain is composed of neurons that communicate with each other through structures called synapses, the contact point between neurons. Synapses convey electrical signals from the “sender” neuron to the “receiver” neuron. Importantly, a synapse can vary in strength; a strong synapse has a large effect on its target cell, a weak synapse has little effect.
New research by John Lisman, professor of biology and the Zalman Abraham Kekst chair in neuroscience, helped in explaining how memories are stored at synapses. His work builds on previous studies showing that changes in the strength of these synapses are critical in the process of learning and memory.
“It is now quite clear that memory is encoded not by the change in the number of cells in the brain, but rather by changes in the strength of synapses,” said Lisman.
“You can actually now see that when learning occurs, some synapses become stronger and others become weaker,” added Lisman.
Lisman’s team is showed that the synaptic strength is controlled by the complex of CaMKII.
John Lisman with another molecule called the NMDAR-type glutamate receptor (NMDAR). His lab has discovered that the amount of this molecular complex (called the CaMKII/NMDAR complex) actually determines how strong a synapse is, and, most likely, how well a memory is stored.
A key finding in their experiment used a procedure that reduced the amount of this complex. When the complex was reduced, the synapse became weaker. This weakening was persistent, indicating that the memory stored at that synapse was erased.
The study is detailed in the Journal of Neuroscience.