Dendritic excitability and synaptic plasticity in hippocampal pyramidal neurons

It is now clear that most neurons do not integrate synaptic inputs passively. Rather, voltage-gated channels are present in dendrites and the resulting currents actively influence synaptic integration. We have shown that dendritic voltage-gated channels allow for active backpropagation of action potentials initiated in the dendrites, as well as active initiation of sodium and calcium spikes in the dendrites. Much of our current research is focused on understanding how these active properties of dendrites contribute to synaptic integration and plasticity.

Targeted inhibition and dendritic integration

Integration of synaptic inputs in dendrites involves not only excitatory events, but also inhibition. Specific classes of interneurons in the hippocampus target different regions of the dendrites very precisely. We are taking a combined computational and experimental approach to understanding how inhibition targeting different regions of hippocampal neurons (e.g. soma vs. distal dendrites) is uniquely involved in synaptic integration.

Mechanisms of action potential bursting in hippocampal pyramidal neurons

Neurons signal to their network targets via action potentials traveling down the axon. These signals may be generated alone or in hig-frequency clusters called bursts. In the hippocampus, pyramidal neurons in subiculum burst much more robustly than those in CA1. We are therefore studying the mechanisms responsible for action potential bursting in these two regions of the hippocampus. Furthermore, we have found that action potential bursting in subiculum is frequency and activity dependent. Ongoing work is directed at understanding the mechanisms that regulate switches between regular-spiking and burst-spiking modes in these neurons.

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