Final Report Summary - INTERPLASTICITY (Long-term synaptic plasticity in interneurons: mechanisms and computational significance) The connections among excitatory neurons are known to be modifiable, and this plasticity is thought to underlie memory encoding. However, synapses innervating inhibitory cells are also modifiable, but far less is known about the mechanisms underlying this phenomenon, and its consequences for maintaining normal circuit function, generating the rhythms of the brain, and storing memories. We have shown that synaptic plasticity in inhibitory cells follows different rules than synaptic plasticity in excitatory cells, and even operates in different ways among distinct populations of inhibitory cells. We also uncovered how individual sources of calcium interact to trigger plasticity in inhibitory cells, and also how individual calcium channels trigger the release of neurotransmitter from small synapses. The roles of distinct receptors for the excitatory neurotransmitter glutamate imply that strengthening and weakening of synapses may occur in response to different conjunctions of signals. We have begun to integrate this information at a molecular and cellular level to understand how inhibitory signalling permits entire brain regions to function. The population rhythms of whole brain areas are co-ordinated, and this is widely thought to allow the selective transmission of signals across long distances. We have shown that information can indeed be encoded in the oscillatory firing of large populations of neurons, and retrieved using simple networks of inhibitory cells interacting with excitatory neurons. We have also shown how a local circuit of excitatory and inhibitory cells can be made to fire in step with an oscillatory input, thereby allows synchronization in long-distance connections in the brain.
