PHOTOLYTIC RELEASE OF NITRIC-OXIDE MODULATES NMDA RECEPTOR-MEDIATED TRANSMISSION BUT DOES NOT INDUCE LONG-TERM POTENTIATION AT HIPPOCAMPAL SYNAPSES

We have investigated the effects of photolytic release of nitric oxide (NO) on synaptic transmission in the hippocampal slice. Intracellular and extracellular recording techniques were used to monitor synaptic transmission in area CAI of slices prepared from young rats and maintained in an interface chamber at 24 degrees C. N-methyl-D-aspartate (NMDA) receptor-mediated transmission was depressed, in a concentration- and haemoglobin-dependent manner, by NO released from perfusion fluid containing an inert photosensitive precursor, K2Ru(NO)Cl-5, following exposure to flash of near-UV light. However, conjunction of photolytic release of NO together with either weak high frequency stimulation, or strong stimulation in the presence of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (D(-)AP5), did not lead to a persistent enhancement of synaptic efficacy. These results establish that photolytically released NO can affect NMDA receptor-mediated transmission but do not support a role for NO as a retrograde messenger at CA1 synapses.