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Photolytically released nitric oxide produces a delayed but persistent suppression of LTP in area CA1 of the rat hippocampal slice
Ist Teil von
The Journal of physiology, 1999-03, Vol.515 (2), p.453-462
Ort / Verlag
Oxford, UK: The Physiological Society
Erscheinungsjahr
1999
Quelle
Wiley-Blackwell Journals
Beschreibungen/Notizen
We have used flash photolysis of a caged form of nitric oxide (NO), potassium pentachloronitrosylruthenate (K 2 Ru(NO)Cl 5 ), to apply known concentrations of NO, with a high degree of temporal resolution, to hippocampal slices prepared from juvenile
male rats maintained in an interface recording chamber.
Photolytically released NO (1â4.5 μM) from bath applied caged NO reduced the magnitude of long-term potentiation (LTP) in
a concentration-dependent manner. This effect was abolished in the presence of the NO scavenger haemoglobin. NO had no effect
on pre-established LTP.
Exposure to photolytically released NO had no effect on normal fast synaptic transmission, but did result in depression of
N -methyl-D-aspartate (NMDA) receptor-mediated transmission recorded using extracellular electrodes. The onset of NO-induced
depression was relatively slow, taking >40 s to manifest itself, and several minutes to achieve maximum depression ( t ½ â 70 s). NO-induced depression persisted for more than 2 h after photolysis. The time courses of the action of NO on NMDA
receptor-mediated responses and its action on the induction of LTP were similar.
These results suggest that released NO may play a role in determining the subsequent threshold for the induction of LTP at
Schaffer-commissural synapses through a reduction in the efficacy of NMDA receptor function when repeated conditioning trains
are used.