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Titolo:
Exogenous nitric oxide causes potentiation of hippocampal synaptic transmission during low-frequency stimulation via the endogenous nitric oxide-cGMPpathway
Autore:
Bon, CLM; Garthwaite, J;
Indirizzi:
Univ Coll London, Wolfson Inst Biomed Res, London WC1E 6BT, England Univ Coll London London England WC1E 6BT d Res, London WC1E 6BT, England
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 4, volume: 14, anno: 2001,
pagine: 585 - 594
SICI:
0953-816X(200108)14:4<585:ENOCPO>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; TRANSIENT FOREBRAIN ISCHEMIA; SENSITIVE GUANYLYL CYCLASE; CENTRAL-NERVOUS-SYSTEM; CA1 PYRAMIDAL NEURONS; RAT HIPPOCAMPUS; CEREBRAL-ISCHEMIA; AREA CA1; DEPRESSION; ADENOSINE;
Keywords:
hippocampus; long-term potentiation; nitric oxide; rat; soluble guanylyl cyclase; synaptic plasticity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
66
Recensione:
Indirizzi per estratti:
Indirizzo: Garthwaite, J Univ Coll London, Wolfson Inst Biomed Res, Gower St, London WC1E 6BT, England Univ Coll London Gower St London England WC1E 6BT , England
Citazione:
C.L.M. Bon e J. Garthwaite, "Exogenous nitric oxide causes potentiation of hippocampal synaptic transmission during low-frequency stimulation via the endogenous nitric oxide-cGMPpathway", EUR J NEURO, 14(4), 2001, pp. 585-594

Abstract

Nitric oxide (NO) is a putative participant in synaptic plasticity and demonstrations that exogenous NO can elicit the same plastic changes have beentaken to support such a role. The experiments, carried out on the CA1 region of rat hippocampal slices, were aimed at testing this interpretation. A major component of tetanus-induced long-term potentiation (LTP) was lost inresponse to L-nitroarginine, which inhibits NO synthase, and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), which inhibits NO-sensitive soluble guanylyl cyclase (sGC). At 0.2 Hz afferent fibre stimulation, exogenous NO produced, concentration-dependently, a synaptic depression that reverted on washout to a persistent potentiation that occluded tetanus-induced LTP. TheNO concentrations necessary (estimated in the 100-nM range), however, weremostly supramaximal for stimulating hippocampal slice sGC activity. Nevertheless the potentiation, but not the preceding depression, was blocked by ODQ. L-nitroarginine and an NMDA antagonist were similarly effective, indicating mediation by the endogenous NMDA receptor-NO synthase-sGC pathway. At a concentration normally too low to affect synaptic transmission but sufficient to stimulate sGC (estimated to be 50 nM), exogenous NO reversed the effect of L-nitroarginine and caused a potentiation which was blocked by ODQ. At a concentration inducing the depression/potentiation sequence, NO partially inhibited hippocampal slice oxygen consumption. It is concluded that, at physiological levels, exogenous NO can directly elicit a potentiation ofsynaptic transmission through sGC, provided that the synapses are suitablyprimed. At higher concentrations, NO inhibits mitochondrial respiration, which can result in an enduring synaptic potentiation due to secondary activation of the endogenous NO-cGMP pathway.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 10:35:55