ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    facet.materialart.
    Unknown
    Oxytocin-mediated GABA inhibition during delivery attenuates autism pathogenesis in rodent offspring (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-02-08
    Description: We report that the oxytocin-mediated neuroprotective gamma-aminobutyric acid (GABA) excitatory-inhibitory shift during delivery is abolished in the valproate and fragile X rodent models of autism. During delivery and subsequently, hippocampal neurons in these models have elevated intracellular chloride levels, increased excitatory GABA, enhanced glutamatergic activity, and elevated gamma oscillations. Maternal pretreatment with bumetanide restored in offspring control electrophysiological and behavioral phenotypes. Conversely, blocking oxytocin signaling in naive mothers produced offspring having electrophysiological and behavioral autistic-like features. Our results suggest a chronic deficient chloride regulation in these rodent models of autism and stress the importance of oxytocin-mediated GABAergic inhibition during the delivery process. Our data validate the amelioration observed with bumetanide and oxytocin and point to common pathways in a drug-induced and a genetic rodent model of autism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tyzio, Roman -- Nardou, Romain -- Ferrari, Diana C -- Tsintsadze, Timur -- Shahrokhi, Amene -- Eftekhari, Sanaz -- Khalilov, Ilgam -- Tsintsadze, Vera -- Brouchoud, Corinne -- Chazal, Genevieve -- Lemonnier, Eric -- Lozovaya, Natalia -- Burnashev, Nail -- Ben-Ari, Yehezkel -- New York, N.Y. -- Science. 2014 Feb 7;343(6171):675-9. doi: 10.1126/science.1247190.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24503856" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/*chemically induced/*genetics/metabolism ; Behavior, Animal ; Bumetanide/administration & dosage ; Chlorides/metabolism ; *Cytoprotection ; Disease Models, Animal ; Female ; Fragile X Mental Retardation Protein/genetics ; Maternal-Fetal Exchange ; Mice ; Oxytocin/*metabolism ; Parturition ; Pregnancy ; Rats ; Valproic Acid/pharmacology ; gamma-Aminobutyric Acid/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    Response to Comment on "Oxytocin-mediated GABA inhibition during delivery attenuates autism pathogenesis in rodent offspring" (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-10-11
    Description: Bambini-Junior et al. questioned whether our treatment in two rodent models of autism has a long-lasting effect into adulthood. In response, we show that bumetanide treatment around delivery attenuates autistic behavioral features in adult offspring. Therefore, the polarity of gamma-aminobutyric acid (GABA) actions during delivery exerts long-lasting priming actions after birth.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eftekhari, Sanaz -- Shahrokhi, Amene -- Tsintsadze, Vera -- Nardou, Romain -- Brouchoud, Corinne -- Conesa, Magali -- Burnashev, Nail -- Ferrari, Diana C -- Ben-Ari, Yehezkel -- New York, N.Y. -- Science. 2014 Oct 10;346(6206):176. doi: 10.1126/science.1256009.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France. UMR 901, Aix-Marseille University, Marseille, France. Neurochlore, Campus Scientifique de Luminy, 163 Route de Luminy, Marseille, France. On leave from Iran University of Medical Sciences, Tehran, Iran. ; Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France. UMR 901, Aix-Marseille University, Marseille, France. Neurochlore, Campus Scientifique de Luminy, 163 Route de Luminy, Marseille, France. On leave from Tehran University of Medical Sciences, Tehran, Iran. ; Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France. UMR 901, Aix-Marseille University, Marseille, France. ; Neurochlore, Campus Scientifique de Luminy, 163 Route de Luminy, Marseille, France. ; Mediterranean Institute of Neurobiology (INMED), U901, INSERM, Marseille, France. UMR 901, Aix-Marseille University, Marseille, France. Neurochlore, Campus Scientifique de Luminy, 163 Route de Luminy, Marseille, France. yehezkel.ben-ari@inserm.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25301611" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/*chemically induced/*genetics ; *Cytoprotection ; Female ; Oxytocin/*metabolism ; Pregnancy ; gamma-Aminobutyric Acid/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...