The GABA Developmental Shift Is Abolished by Maternal Immune Activation Already at Birth
| Autor: | Camille Dumon, Nail Burnashev, Amandine Fernandez, Paolo Bonifazi, Yehezkel Ben-Ari, Natalia Lozovaya, Diana C. Ferrari, Damien Guimond, Roman Tyzio |
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| Rok vydání: | 2018 |
| Předmět: |
endocrine system diseases
Postsynaptic Current Cognitive Neuroscience Hippocampus Glutamic Acid Biology Hippocampal formation 050105 experimental psychology Membrane Potentials 03 medical and health sciences Cellular and Molecular Neuroscience Glutamatergic 0302 clinical medicine Pregnancy medicine Animals Solute Carrier Family 12 Member 2 0501 psychology and cognitive sciences gamma-Aminobutyric Acid Pyramidal Cells 05 social sciences Antagonist Depolarization Dendrites CA3 Region Hippocampal Mice Inbred C57BL Poly I-C nervous system Excitatory postsynaptic potential Female Neuroscience 030217 neurology & neurosurgery Bumetanide medicine.drug |
| Zdroj: | Cerebral cortex (New York, N.Y. : 1991). 29(9) |
| ISSN: | 1460-2199 |
| Popis: | Epidemiological and experimental studies suggest that maternal immune activation (MIA) leads to developmental brain disorders, but whether the pathogenic mechanism impacts neurons already at birth is not known. We now report that MIA abolishes in mice the oxytocin-mediated delivery γ-aminobutyric acid (GABA) shift from depolarizing to hyperpolarizing in CA3 pyramidal neurons, and this is restored by the NKCC1 chloride importer antagonist bumetanide. Furthermore, MIA hippocampal pyramidal neurons at birth have a more exuberant apical arbor organization and increased apical dendritic length than age-matched controls. The frequency of spontaneous glutamatergic postsynaptic currents is also increased in MIA offspring, as well as the pairwise correlation of the synchronized firing of active cells in CA3. These alterations produced by MIA persist, since at P14–15 GABA action remains depolarizing, produces excitatory action, and network activity remains elevated with a higher frequency of spontaneous glutamatergic postsynaptic currents. Therefore, the pathogenic actions of MIA lead to important morphophysiological and network alterations in the hippocampus already at birth. |
| Databáze: | OpenAIRE |
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