Document Detail


Selective gamma-hydroxybutyric acid receptor ligands increase extracellular glutamate in the hippocampus, but fail to activate G protein and to produce the sedative/hypnotic effect of gamma-hydroxybutyric acid.
MedLine Citation:
PMID:  14535954     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Two gamma-hydroxybutyric acid (GHB) analogues, trans-gamma-hydroxycrotonic acid (t-HCA) and gamma-(p-methoxybenzyl)-gamma-hydroxybutyric acid (NCS-435) displaced [3H]GHB from GHB receptors with the same affinity as GHB but, unlike GHB, failed to displace [3H]baclofen from GABAB receptors. The effect of the GHB analogues, GHB and baclofen, on G protein activity and hippocampal extracellular glutamate levels was compared. While GHB and baclofen stimulated 5'-O-(3-[35S]thiotriphospate) [35S]GTPgammaS binding both in cortex homogenate and cortical slices, t-HCA and NCS-435 were ineffective up to 1 mm concentration. GHB and baclofen effect was suppressed by the GABAB antagonist CGP 35348 but not by the GHB receptor antagonist NCS-382. Perfused into rat hippocampus, 500 nm and 1 mm GHB increased and decreased extracellular glutamate levels, respectively. GHB stimulation was suppressed by NCS-382, while GHB inhibition by CGP 35348. t-HCA and NCS-435 (0.1-1000 microm) locally perfused into hippocampus increased extracellular glutamate; this effect was inhibited by NCS-382 (10 microm) but not by CGP 35348 (500 microm). The results indicate that GHB-induced G protein activation and reduction of glutamate levels are GABAB-mediated effects, while the increase of glutamate levels is a GHB-mediated effect. Neither t-HCA nor NCS-435 reproduced GHB sedative/hypnotic effect in mice, confirming that this effect is GABAB-mediated. The GHB analogues constitute important tools for understanding the physiological role of endogenous GHB and its receptor.
Authors:
M Paola Castelli; Luca Ferraro; Ignazia Mocci; Francesca Carta; Mauro A M Carai; Tiziana Antonelli; Sergio Tanganelli; Giorgio Cignarella; Gian Luigi Gessa
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  87     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  2003 Nov 
Date Detail:
Created Date:  2003-10-10     Completed Date:  2003-11-24     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  722-32     Citation Subset:  IM    
Affiliation:
Neuroscienze S.c.a r.l., Cagliari, Italy.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autoradiography
Benzocycloheptenes / pharmacology
Binding, Competitive / drug effects
Brain Chemistry
Extracellular Space / metabolism
GABA Antagonists / pharmacology
GTP-Binding Proteins / drug effects,  metabolism*
Glutamic Acid / metabolism*
Guanosine 5'-O-(3-Thiotriphosphate) / pharmacokinetics
Hippocampus / drug effects,  metabolism*
Hydroxybutyrates / pharmacology*
Hypnotics and Sedatives / pharmacology
Ligands
Male
Mice
Mice, Inbred DBA
Microdialysis
Organophosphorus Compounds / pharmacology
Rats
Rats, Sprague-Dawley
Receptors, Cell Surface / drug effects,  metabolism*
Reflex / drug effects
Chemical
Reg. No./Substance:
0/4-hydroxybutyric acid receptor; 0/Benzocycloheptenes; 0/GABA Antagonists; 0/Hydroxybutyrates; 0/Hypnotics and Sedatives; 0/Ligands; 0/Organophosphorus Compounds; 0/Receptors, Cell Surface; 0/gamma-(4-methoxybenzyl)-gamma-hydroxybutyric acid; 123690-79-9/CGP 35348; 131733-92-1/NCS 382; 37589-80-3/Guanosine 5'-O-(3-Thiotriphosphate); 4013-24-5/4-hydroxy-2-butenoic acid; 56-86-0/Glutamic Acid; 591-81-1/4-hydroxybutyric acid; EC 3.6.1.-/GTP-Binding Proteins

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


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