Document Detail

Role of nitric oxide in long-term potentiation of the rat medial vestibular nuclei.
MedLine Citation:
PMID:  11068144     Owner:  NLM     Status:  MEDLINE    
In rat brainstem slices, we investigated the role of nitric oxide in long-term potentiation induced in the ventral portion of the medial vestibular nuclei by high-frequency stimulation of the primary vestibular afferents. The nitric oxide scavenger [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide ] and the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester were administered before and after induction of potentiation. Both drugs completely prevented long-term potentiation, whereas they did not impede the potentiation build-up, or affect the already established potentiation. These results demonstrate that the induction, but not the maintenance of vestibular long-term potentiation, depends on the synthesis and release into the extracellular medium of nitric oxide. In addition, we analysed the effect of the nitric oxide donor sodium nitroprusside on vestibular responses. Sodium nitroprusside induced long-term potentiation, as evidenced through the field potential enhancement and unit peak latency decrease. This potentiation was impeded by D, L-2-amino-5-phosphonopentanoic acid, and was reduced under blockade of synaptosomal platelet-activating factor receptors by ginkgolide B and group I metabotropic glutamate receptors by (R,S)-1-aminoindan-1, 5-dicarboxylic acid. When reduced, potentiation fully developed following the washout of antagonist, demonstrating an involvement of platelet-activating factor and group I metabotropic glutamate receptors in its full development. Potentiation induced by sodium nitroprusside was also associated with a decrease in the paired-pulse facilitation ratio, which persisted under ginkgolide B, indicating that nitric oxide increases glutamate release independently of platelet-activating factor-mediated presynaptic events. We suggest that nitric oxide, released after the activation of N-methyl-D-aspartate receptors, acts as a retrograde messenger leading to an enhancement of glutamate release to a sufficient level for triggering potentiation. Once the synaptic efficacy has changed, it becomes a long-lasting phenomenon only through a subsequent action of platelet-activating factor.
S Grassi; V E Pettorossi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Neuroscience     Volume:  101     ISSN:  0306-4522     ISO Abbreviation:  Neuroscience     Publication Date:  2000  
Date Detail:
Created Date:  2001-01-12     Completed Date:  2001-02-15     Revised Date:  2009-11-03    
Medline Journal Info:
Nlm Unique ID:  7605074     Medline TA:  Neuroscience     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  157-64     Citation Subset:  IM    
Department of Internal Medicine, Section of Human Physiology, University of Perugia, I-06100 Perugia, Italy.
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MeSH Terms
Action Potentials / drug effects,  physiology
Benzoates / pharmacology
Electric Stimulation
Imidazoles / pharmacology
Long-Term Potentiation / drug effects,  physiology*
NG-Nitroarginine Methyl Ester / pharmacology
Neurons / cytology,  drug effects*,  metabolism
Nitric Oxide / metabolism*
Nitroprusside / pharmacology
Platelet Activating Factor / drug effects,  metabolism
Rats, Wistar
Signal Transduction / drug effects,  physiology
Synaptic Transmission / drug effects,  physiology
Vestibular Nuclei / cytology,  drug effects*,  metabolism
Reg. No./Substance:
0/Benzoates; 0/Imidazoles; 0/Platelet Activating Factor; 10102-43-9/Nitric Oxide; 145757-47-7/1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole; 15078-28-1/Nitroprusside; 50903-99-6/NG-Nitroarginine Methyl Ester

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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