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MINIREVIEW

Action Potentials: To the Nucleus and Beyond

Laboratory of Neurobiology, National Institute of Environmental Health Services, National Institutes of Health, Research Triangle Park, North Carolina 27709

To whom requests for reprints should be addressed at ¹ Synaptic and Developmental Plasticity Group, Laboratory of Neurobiology, NIEHS, 111 Alexander Drive, Research Triangle Park, NC 27709. E-mail: dudek{at}niehs.nih.gov

The neuronal nucleus is now widely accepted as playing a vital role in maintaining long-term changes in synaptic effectiveness. To act, however, the nucleus must be appropriately relayed with information regarding the latest round of synaptic plasticity. Several constraints of doing so in a neuron pertain to the often significant spatial distance of synapses from the nucleus and the number of synapses required for such a signal to reach functional levels in the nucleus. Largely based on the sensitivity of transcriptional responses to NMDA receptor antagonists, it has been postulated that the signals are physically relayed by biochemical messengers from the synapse to the nucleus. Alternatively, a second, less often considered but equally viable method of signal transduction may be initiated by action potentials generated proximal to the nucleus, wherefrom the signal can be relayed directly by calcium or indirectly by biochemical second messengers. We consider action potential-dependent signaling to the nucleus to have its own computational advantages over the synapse-to-nucleus signal for some functions. This minireview summarizes the logic and experimental support for these two modes of signaling and attempts to validate the action potential model as playing an important role in transcriptional regulation relating specifically to long-term synaptic plasticity.

Key Words: action potentials • Ca2+ • synaptic plasticity • LTP • LTD