Nitric oxide-induced potentiation of CA1 hippocampal synaptic transmissionduring baseline stimulation is strictly frequency-dependent

Nitric oxide (NO) has been hypothesised to serve a signalling role in certa in types of synaptic plasticity. If so, exogenously applied NO should be ab le to elicit those same plastic changes under appropriate conditions. In th e case of hippocampal long-term potentiation (LTP), however, existing evide nce is discrepant. Field recordings of synaptic transmission in the CA1 are a of rat hippocampal slices were used to re-examine this issue. Under 0.2 H z afferent fibre stimulation, NO (delivered using two different NONOates) p roduced, concentration-dependently, a depression of synaptic transmission. On washout of NO, the depression gave way to a persistent potentiation, the amplitude of which was also graded with NONOate concentration. Tetanus-ind uced LTP, induced an hour after washout, was occluded in proportion to the degree of prior NO-induced potentiation. At a lower stimulation frequency o f 0.033 Hz, the depression was unaltered but no rebound potentiation took p lace and subsequent tetanus-induced LTP was normal. Tests indicated that th ere is a clear time-window during which 0.2 Hz stimulation needs to be appl ied relative to the delivery of NO to produce a potentiation. The findings explain previous divergent results and indicate that exogenous NO-triggered potentiation depends critically on the frequency of synaptic transmission. (C) 2001 Elsevier Science Ltd. All rights reserved.