L’enzyme de la glycolyse GAPDH joue un double rôle dans la neurotransmission GABAergique et l’épilepsie humaine

Jacques Laschet; René Pumain

doi:doi:10.1051/medsci/20072389687

Accès gratuit

Numéro		Med Sci (Paris) Volume 23, Numéro 8-9, Août-Septembre 2007


Page(s)		687 - 689
Section		Nouvelles
DOI		http://dx.doi.org/10.1051/medsci/20072389687
Publié en ligne		15 August 2007

Smart, TG, Thomas P, Brandon NJ, Moss SJ. Heterologous regulation of GABA_A receptors: protein phosphorylation. In : Pharmacology of GABA and glycine neurotransmission. Berlin : Springer-Verlag, 2001 : 195–225.
Sweetnam PM, Lloyd J, Gallombardo P, et al. Phosphorylation of the GABAa/benzodiazepine receptor alpha subunit by a receptor-associated protein kinase. J Neurochem 1988; 51 : 1274–84.
Bureau, MH, Laschet JJ. Endogenous phosphorylation of distinct gamma-aminobutyric acid type A receptor polypeptides by Ser/Thr and Tyr kinase activities associated with the purified receptor. J Biol Chem 1995; 270 : 26482–7.
Stelzer A, Kay AR, Wong RKS. GABA_A-receptor function in hippocampal cells is maintained by phosphorylation factors. Science 1988; 241 : 339–41.
Kawamoto RM, Caswell AH. Autophosphorylation of glyceraldehydephosphate dehydrogenase and phosphorylation of protein from skeletal muscle microsomes. Biochemistry 1986; 25 : 657–61.
Laschet JJ, Minier F, Kurcewicz I, et al. Glyceraldehyde-3-phosphate dehydrogenase is a GABA_A receptor kinase linking glycolysis to neuronal inhibition. J Neurosci 2004; 24 : 7614–22.
Minier F, Laschet JJ, Evrard B, Bureau MH. Endogenous phosphorylation of the GABA_A receptor protein is counteracted by a membrane-associated phosphatase. Neurochem Int 2000; 36 : 499–506.
Laschet JJ, Kurcewicz I, Minier F, et al. Dysfunction of GABAA receptor glycolysis-dependent modulation in human partial epilepsy. Proc Natl Acad Sci USA 2007; 104 : 3472–7.
Ryvlin P, Bouvard S, Le Bars D, et al. Clinical utility of flumazenil-PET versus [18F]fluorodeoxyglucose-PET and MRI in refractory partial epilepsy. A prospective study in 100 patients. Brain 1998; 121 : 2067–81.
Peyron R, Le Bars D, Cinotti L, et al. Effects of GABA_A receptors activation on brain glucose metabolism in normal subjects and temporal lobe epilepsy (TLE) patients. A positron emission tomography (PET) study. Part I: brain glucose metabolism is increased after GABA_A receptors activation. Epilepsy Res 1994; 19 : 45–54.
Peyron R, Cinotti L, Le Bars D, et al. Effects of GABA_A receptors activation on brain glucose metabolism in normal subjects and temporal lobe epilepsy (TLE) patients. A positron emission tomography (PET) study. Part II: the focal hypometabolism is reactive to GABA_A agonist administration in TLE. Epilepsy Res 1994; 19 : 55–62.

[1] Smart, TG, Thomas P, Brandon NJ, Moss SJ. Heterologous regulation of GABA_A receptors: protein phosphorylation. In : Pharmacology of GABA and glycine neurotransmission. Berlin : Springer-Verlag, 2001 : 195–225.

[2] Sweetnam PM, Lloyd J, Gallombardo P, et al. Phosphorylation of the GABAa/benzodiazepine receptor alpha subunit by a receptor-associated protein kinase. J Neurochem 1988; 51 : 1274–84.

[3] Bureau, MH, Laschet JJ. Endogenous phosphorylation of distinct gamma-aminobutyric acid type A receptor polypeptides by Ser/Thr and Tyr kinase activities associated with the purified receptor. J Biol Chem 1995; 270 : 26482–7.

[4] Stelzer A, Kay AR, Wong RKS. GABA_A-receptor function in hippocampal cells is maintained by phosphorylation factors. Science 1988; 241 : 339–41.

[5] Kawamoto RM, Caswell AH. Autophosphorylation of glyceraldehydephosphate dehydrogenase and phosphorylation of protein from skeletal muscle microsomes. Biochemistry 1986; 25 : 657–61.

[6] Laschet JJ, Minier F, Kurcewicz I, et al. Glyceraldehyde-3-phosphate dehydrogenase is a GABA_A receptor kinase linking glycolysis to neuronal inhibition. J Neurosci 2004; 24 : 7614–22.

[7] Minier F, Laschet JJ, Evrard B, Bureau MH. Endogenous phosphorylation of the GABA_A receptor protein is counteracted by a membrane-associated phosphatase. Neurochem Int 2000; 36 : 499–506.

[8] Laschet JJ, Kurcewicz I, Minier F, et al. Dysfunction of GABAA receptor glycolysis-dependent modulation in human partial epilepsy. Proc Natl Acad Sci USA 2007; 104 : 3472–7.

[9] Ryvlin P, Bouvard S, Le Bars D, et al. Clinical utility of flumazenil-PET versus [18F]fluorodeoxyglucose-PET and MRI in refractory partial epilepsy. A prospective study in 100 patients. Brain 1998; 121 : 2067–81.

[10] Peyron R, Le Bars D, Cinotti L, et al. Effects of GABA_A receptors activation on brain glucose metabolism in normal subjects and temporal lobe epilepsy (TLE) patients. A positron emission tomography (PET) study. Part I: brain glucose metabolism is increased after GABA_A receptors activation. Epilepsy Res 1994; 19 : 45–54.

[11] Peyron R, Cinotti L, Le Bars D, et al. Effects of GABA_A receptors activation on brain glucose metabolism in normal subjects and temporal lobe epilepsy (TLE) patients. A positron emission tomography (PET) study. Part II: the focal hypometabolism is reactive to GABA_A agonist administration in TLE. Epilepsy Res 1994; 19 : 55–62.

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