[article]
| Titre : |
Enzymes in the glutamate-glutamine cycle in the anterior cingulate cortex in postmortem brain of subjects with autism |
| Type de document : |
Texte imprimé et/ou numérique |
| Auteurs : |
Chie SHIMMURA, Auteur ; Katsuaki SUZUKI, Auteur ; Yasuhide IWATA, Auteur ; Kenji J. TSUCHIYA, Auteur ; Koji OHNO, Auteur ; Hideo MATSUZAKI, Auteur ; Keiko IWATA, Auteur ; Yosuke KAMENO, Auteur ; Taro TAKAHASHI, Auteur ; Tomoyasu WAKUDA, Auteur ; Kazuhiko NAKAMURA, Auteur ; Kenji HASHIMOTO, Auteur ; Norio MORI, Auteur |
| Année de publication : |
2013 |
| Article en page(s) : |
7 p. |
| Langues : |
Anglais (eng) |
| Mots-clés : |
Autism Glutamate Glutaminase Glutamate-glutamine cycle Anterior cingulate cortex |
| Index. décimale : |
PER Périodiques |
| Résumé : |
BACKGROUND:Accumulating evidence suggests that dysfunction in the glutamatergic system may underlie the pathophysiology of autism. The anterior cingulate cortex (ACC) has been implicated in autism as well as in glutamatergic neurotransmission. We hypothesized that alterations in the glutamate-glutamine cycle in the ACC might play a role in the pathophysiology of autism.METHODS:We performed Western blot analyses for the protein expression levels of enzymes in the glutamate-glutamine cycle, including glutamine synthetase, kidney-type glutaminase, liver-type glutaminase, and glutamate dehydrogenases 1 and 2, in the ACC of postmortem brain of individuals with autism (n=7) and control subjects (n=13).RESULTS:We found that the protein levels of kidney-type glutaminase, but not those of the other enzymes measured, in the ACC were significantly lower in subjects with autism than in controls.CONCLUSION:The results suggest that reduced expression of kidney-type glutaminase may account for putative alterations in glutamatergic neurotransmission in the ACC in autism. |
| En ligne : |
http://dx.doi.org/10.1186/2040-2392-4-6 |
| Permalink : |
https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202 |
in Molecular Autism > (March 2013) . - 7 p.
[article] Enzymes in the glutamate-glutamine cycle in the anterior cingulate cortex in postmortem brain of subjects with autism [Texte imprimé et/ou numérique] / Chie SHIMMURA, Auteur ; Katsuaki SUZUKI, Auteur ; Yasuhide IWATA, Auteur ; Kenji J. TSUCHIYA, Auteur ; Koji OHNO, Auteur ; Hideo MATSUZAKI, Auteur ; Keiko IWATA, Auteur ; Yosuke KAMENO, Auteur ; Taro TAKAHASHI, Auteur ; Tomoyasu WAKUDA, Auteur ; Kazuhiko NAKAMURA, Auteur ; Kenji HASHIMOTO, Auteur ; Norio MORI, Auteur . - 2013 . - 7 p. Langues : Anglais ( eng) in Molecular Autism > (March 2013) . - 7 p.
| Mots-clés : |
Autism Glutamate Glutaminase Glutamate-glutamine cycle Anterior cingulate cortex |
| Index. décimale : |
PER Périodiques |
| Résumé : |
BACKGROUND:Accumulating evidence suggests that dysfunction in the glutamatergic system may underlie the pathophysiology of autism. The anterior cingulate cortex (ACC) has been implicated in autism as well as in glutamatergic neurotransmission. We hypothesized that alterations in the glutamate-glutamine cycle in the ACC might play a role in the pathophysiology of autism.METHODS:We performed Western blot analyses for the protein expression levels of enzymes in the glutamate-glutamine cycle, including glutamine synthetase, kidney-type glutaminase, liver-type glutaminase, and glutamate dehydrogenases 1 and 2, in the ACC of postmortem brain of individuals with autism (n=7) and control subjects (n=13).RESULTS:We found that the protein levels of kidney-type glutaminase, but not those of the other enzymes measured, in the ACC were significantly lower in subjects with autism than in controls.CONCLUSION:The results suggest that reduced expression of kidney-type glutaminase may account for putative alterations in glutamatergic neurotransmission in the ACC in autism. |
| En ligne : |
http://dx.doi.org/10.1186/2040-2392-4-6 |
| Permalink : |
https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202 |
|
Enzymes in the glutamate-glutamine cycle in the anterior cingulate cortex in postmortem brain of subjects with autism in Molecular Autism, (March 2013)
