Long-term potentiation (LTP) may be the long-lasting increase of signals across a connection between brain cells. This LTP apparently underlies an individual’s ability to remember over time and learn. In an attempt to understand this, scientists from the Duke University Medical Center discovered a cascade of signaling molecules that allows a usually very brief signal to last for tens of minutes. The cascade can probably provide the brain framework for stronger connections (synapses) that can summon a memory for a period of months or even years.
This research finds out the apparent way synapses change the strength of connections and can have a bearing on Alzheimer’s disease, autism as well as mental retardation. Researchers apparently found a biochemical process that lasts for a long time. This process was allegedly noted while examining the signaling molecules that control actin cytoskeleton, which serves as the structural framework of synapses. LTP is known as a long-lasting set of electrical impulses in nerve cells that’s triggered by a transient increase of calcium (Ca2+) ions within a synapse.
Experiments were undertaken to ascertain exactly how the short Ca2+ signal, which lasts only for approximately 0.1s, is translated into long-lasting (more than an hour) change in synaptic transmission. For this a two-photon microscopy technique was put to use. The employed technique may aid in visualizing molecular signaling within single synapses that undergo LTP. The microscopy method may have allowed scientists to scrutinize molecular activity within single synapses and measure the synapses for increase in their volume and strength of the connections.
“The signaling molecules could help to rearrange the framework, and give more volume and strength to the synapses,” Ryohei Yasuda, PhD, assistant professor of neurobiology and senior investigator said. “We reasoned that a long-lasting memory could possibly come from changes in the building block assemblies.”
Signaling molecules Rho and Cdc42 appear as regulators of the actin cytoskeleton and are activated by CaMKII. They probably relay a CaMKII signal into signals lasting many minutes that are vital for maintaining long-lasting plasticity of synapses. Since abnormal Rho and Cdc42 signals are supposedly linked with mental retardation and Alzheimer’s disease, understanding the signaling molecules can help analyze the diseases.
The research was published in the March 20 issue of Nature.