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Photolytically released nitric oxide produces a delayed but persistent suppression of LTP in area CA1 of the rat hippocampal slice
Author(s) -
Murphy K. P. S. J.,
Bliss T. V. P.
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.453ac.x
Subject(s) - long term potentiation , nmda receptor , chemistry , nitric oxide , neurotransmission , hippocampal formation , ltp induction , long term depression , neuroscience , biophysics , glutamate receptor , receptor , ampa receptor , biology , biochemistry , organic chemistry
1 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. 2 Photolytically released NO (1–4.5 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. 3 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 ≈ 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. 4 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.

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