A Role for Protein in Learning and Memory

Researchers have identified a protein crucial for understanding both dendritic remodeling and dendritic pruning. This protein and associated pathways are likely one of the primary systems underlying changes in synaptic efficacy, one of the most fundamental aspects of learning.

As a result of neural activity, intracellular stores of calcium increase. This process is known to be involved in long term depression and long term potentiation, the two processes often cited in computational models as the biological agents of unit connection "weight changes." This new research helps elucidate exactly how this process may occur, as a result of dephosphorylation (and hence activation) of a protein called MEF2 which is a negative regulator of synapse formation.

When activated, MEF2 promotes the transcription of several genes known to restrict synapse number. This finding is somewhat counterintuitive, since it means that under conditions of learning new synapses are not generated, but instead the brain remodels those synapses already available to it (although MEF2 has the opposite effect if it's sumoylated, as opposed to phosphorylated, which in turn appears to depend on its location in the brain). Several other other calcium-dependent proteins are also generated (including CREST and CREB) which are known to be involved in the formation of new synapses. The precise nature of the interactions between these conflicting activity-dependent proteins is still a mystery.

For more freely-available information, see this press release.

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