Jan 4, 2007
A cellular molecule in the brain's hippocampus is responsible, according to a group led by Liliana Minichiello at the European Molecular Biology Laboratory in Monterotondo, Italy, together with Agnès Gruart from the Universidad Pablo de Olavide in Spain.
"Obviously, mental illnesses can better be cured when you know what molecules are involved. Right now, these drugs in existence, they do something, but very little. And I think that is because of a lack of knowledge about the molecular mechanism. It is not the first target to make a drug, but (our discovery) definitely will aid the people that do that work," said Minichiello.
Scientists have long known that neurons in the brain (http://news.com.com/Blueprinting+the+human+brain/2100-11393_3-6071061.html) communicate via electrical signals. A particularly strong and long-lasting signal to a brain cell is believed to be an indication of new information. Long-term protentation (LTP), the term for this phenomenon, is believed by scientists to be the origination of learning and recall at the molecular level.
In order to study this process as it is happening, scientists must be able to monitor the brain while it is learning. Minichiello and her group were able to monitor mice while they learned and recalled that new knowledge. Through this, the group tested whether a receptor molecule called TrkB, which is found in some hippocampus cells, may be central for the LTP process to take place.
"Other studies in our lab said that this molecule was significant. This went deeper and produced more evidence. We measured the LTP while the mouse was conscious and learning. The mouse was alive," Minichiello said.
Minichiello's group determined that mice with defective TrkB molecules were unable to activate an important signaling pathway, and were also unable to learn. In addition, they found that the cells with defective TrkB molecules were unable to generate a normal LTP recall response (remembering) when presented with a familiar situation.
In other words, the ability to learn, and the ability to recall something that had been learned, was impaired in mice without healthy TrkB molecules.
"We established that while the mouse is learning, there are changes in the hippocampus that do not happen if you mutate the receptor. It helps us to understand the molecular pathway for learning, but also for generating LTP," Minichiello said.
The discovery is significant in that it is the first time scientists have been able to prove that TrkB and the signaling pathway it activates are essential to learning and memory, according to Minichiello.