Modulation of Postnatal Neurogenesis by Perinatal Asphyxia: Effect of D1 and D2 Dopamine Receptor Agonists
Autor: | E. Palacios, A Chiti-Morales, Ronald Perez-Lobos, Mario Herrera-Marschitz, Carolyne Lespay-Rebolledo, Paola Morales, Diego Bustamante, Valentina Vio, Andrea Tapia-Bustos |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
Agonist medicine.medical_specialty medicine.drug_class General Neuroscience Neurogenesis Subventricular zone Hippocampus Biology Toxicology 03 medical and health sciences 030104 developmental biology 0302 clinical medicine medicine.anatomical_structure Quinpirole Endocrinology nervous system Dopamine receptor Dopamine Dopamine receptor D2 Internal medicine medicine 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Neurotoxicity Research. 31:109-121 |
ISSN: | 1476-3524 1029-8428 |
Popis: | Perinatal asphyxia (PA) is associated to delayed cell death, affecting neurocircuitries of basal ganglia and hippocampus, and long-term neuropsychiatric disabilities. Several compensatory mechanisms have been suggested to take place, including cell proliferation and neurogenesis. There is evidence that PA can increase postnatal neurogenesis in hippocampus and subventricular zone (SVZ), modulated by dopamine, by still unclear mechanisms. We have studied here the effect of selective dopamine receptor agonists on cell death, cell proliferation and neurogenesis in organotypic cultures from control and asphyxia-exposed rats. Hippocampus and SVZ sampled at 1–3 postnatal days were cultured for 20–21 days. At day in vitro (DIV) 19, cultures were treated either with SKF38393 (10 and 100 µM, a D1 agonist), quinpirole (10 µM, a D2 agonist) or sulpiride (10 μM, a D2 antagonist) + quinpirole (10 μM) and BrdU (10 μM, a mitosis marker) for 24 h. At DIV 20–21, cultures were processed for immunocytochemistry for microtubule-associated protein-2 (MAP-2, a neuronal marker), and BrdU, evaluated by confocal microscopy. Some cultures were analysed for cell viability at DIV 20–21 (LIVE/DEAD kit). PA increased cell death, cell proliferation and neurogenesis in hippocampus and SVZ cultures. The increase in cell death, but not in cell proliferation, was inhibited by both SKF38393 and quinpirole treatment. Neurogenesis was increased by quinpirole, but only in hippocampus, in cultures from both asphyxia-exposed and control-animals, effect that was antagonised by sulpiride, leading to the conclusion that dopamine modulates neurogenesis in hippocampus, mainly via D2 receptors. |
Databáze: | OpenAIRE |
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