Abstract
The role of nitric oxide (NO) in the induction of longterm depression (LTD) in the cerebellum was explored using a new, organic, membrane-impermeant form of caged NO. NO photolytically released inside Purkinje neurons mimicked parallel fiber (PF) activity in synergizing with brief postsynaptic depolarization to induce LTD. Such LTD required a delay of <50 ms between the end of photolysis and the onset of depolarization, was prevented by intracellular Ca 2+ chelation, and was mutually occlusive with LTD conventionally produced by PF activation plus depolarization. Bath application of NO synthase inhibitor or of myoglobin, a NO trap, prevented LTD induction via PF stimulation, but not that from intracellular uncaged NO, whereas intracellular myoglobin blocked both protocols. NO is therefore an anterograde transmitter in LTD induction. A biochemical requirement forsimultaneous NO and elevation of intracellular free Ca 2+ would explain why PF activity must coincide with postsynaptic action potentials.
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