Abstract
Nitric oxide (NO) signaling is required for the induction of long-term depression (LTD) in parallel fiber/Purkinje cell synapses in the cerebellum: NO is released following climbing fiber stimulation and blockade of this NO signal suppresses LTD in slices. However, NO is not obligatory for inducing LTD in cultured Purkinje cells or in slices treated with fluorocitrate, a gliotoxic metabolic inhibitor. Various possibilities about the roles of NO in cerebellar synaptic plasticity are discussed: NO may enable LTD by removing some inherent glial suppression on neural plasticity; it may work as an integrated signal producing some decision-making ability to cerebellar neural networks; and it may coordinate quick adaptation and life-time stability in cerebellar motor learning.
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