When we learn new information we use only a tiny fraction of the neurons in our brain for that particular memory trace. In order to allow the molecular study of those specific neurons we combined elements of the tet system with a promoter that is activated by high level neural activity (the cfos promoter) to generate mice in which a genetic tag can be introduced into neurons that are active at a given point in time. The tag can be maintained for a prolonged period, creating a precise record of the neural activity pattern at a specific point in time. Using fear conditioning we found that the same neurons activated during learning were reactivated when the animal recalled the fearful event. We also found that these neurons were no longer activated following memory extinction, consistent with the idea that extinction modifies a component of the original memory trace.
That quote is from an abstract for a talk by Mark Mayford that will be given next week at UCSD. However, the following paper seems to report those results:
Leon G. Reijmers, Brian L. Perkins, Naoki Matsuo, Mark Mayford. Localization of a Stable Neural Correlate of Associative Memory. Science 31 August 2007: Vol. 317. no. 5842, pp. 1230 – 1233.
In addition, here’s the rest of the talk abstract, which seems to report new results:
One fundamental question in memory research has been how this nuclear to synaptic communication occurs. Using the cfos transgenic approach to specifically focus on activated circuits, we found in a recent study that glutamate receptors get specifically targeted to synapses that are altered with learning. That is, learning produces a sort of molecular tag at certain synapses that allows them to capture the newly synthesized receptors arriving from the nucleus hours after the learning event. Thus, the synapses that are altered in strength to produce a short-term memory must be primed, or tagged, to receive new receptor in order for that memory to be maintained long-term.