Long-term potentiation (LTP) refers to the long-lasting increase of electrical impulses across a connection among brain cells.
LTP signifies humans’ ability to remember things over time and the capacity to learn. But, the logic behind long-term memory remains as a question in neuroscience. Hence, a research team at the Duke University Medical Center has discovered a group of signaling molecules, which controls the actin cytoskeleton that serves as framework of synapses. These signaling molecules enable a very elaborate brain signal to last for 10 minutes.
Dendritic Spine Formation in Single Synapse During Long-Term Potentiation. Signaling activity is color coded (red = high activity of Cdc42, blue = low activity). Activity is high only in the growing spine, and this shows Cdc42 helps to strengthen a synapse for long-term memory storage.
The team has been exploring the signaling molecules that can aid in rearranging the structural framework and provide additional strength and capacity to the synapses. Assistant professor of neurobiology, Ryohei Yasuda, states that Duke researchers’ findings show how the change in brain connections’ strength by synapses would have an effect on autism, mental retardation, and Alzheimer's disease. He also adds that the findings suggest that a biochemical process that continues for some time produces memory storage.
It is known that an increase of calcium ions (Ca2+) present in a single synapse activates long-lasting electrical signals in nerve cells, LTP. Hence, the scientists from Duke University Medical Center conducted experiments to understand precisely, the conversion of short Ca2+ impulse (lasts approximately 0.1s) into long -lasting signal in a synaptic transmission.
In order to explore LTP of signaling molecules in a single synapse, the researchers have utilized a 2-photon microscopy method. This technique helps to visualize molecular activity within a single synapse. In addition, it allows measurement of the synapses for strength and volume increase.
The team has found that CaMKII triggers the Cdc42 and Rho signaling molecules and transmit a CaMKII signal into long-lasting signals. These signals play a major role in retaining plasticity of synapses that are long-lasting and play an important role in the brain’s capability to change while memorizing and learning. Thus, the findings of Duke researchers will offer several insights into diseases such as Alzheimer's disease and mental retardation.
Source: http://www.dukemednews.org/