Astrocyte-derived neurons provide excitatory input to the adult striatal circuitry
| Autor: | María Díaz-Moreno, Gilad Silberberg, Jannis Kalkitsas, Christian Göritz, David O. Dias, Eduardo L Guimarães, Daniel Holl, Matthijs C. Dorst |
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| Rok vydání: | 2021 |
| Předmět: |
Dendritic spine
Population Glutamic Acid Mice Transgenic Striatum Nitric Oxide Synthase Type I Biology Glutamatergic Mice Interneurons Connexin 30 Premovement neuronal activity Animals GABAergic Neurons education Neurons Recombination Genetic education.field_of_study Multidisciplinary Neurogenesis Cell Differentiation Biological Sciences Deoxyuridine Electrophysiological Phenomena Luminescent Proteins Tamoxifen nervous system Gene Expression Regulation Astrocytes Excitatory postsynaptic potential GABAergic Neuroscience |
| Zdroj: | Proc Natl Acad Sci U S A |
| ISSN: | 1091-6490 |
| Popis: | Astrocytes have emerged as a potential source for new neurons in the adult mammalian brain. In mice, adult striatal neurogenesis can be stimulated by local damage, which recruits striatal astrocytes into a neurogenic program by suppression of active Notch signaling (J. P. Magnusson et al., Science 346, 237-241 [2014]). Here, we induced adult striatal neurogenesis in the intact mouse brain by the inhibition of Notch signaling in astrocytes. We show that most striatal astrocyte-derived neurons are confined to the anterior medial striatum, do not express established striatal neuronal markers, and exhibit dendritic spines, which are atypical for striatal interneurons. In contrast to striatal neurons generated during development, which are GABAergic or cholinergic, most adult astrocyte-derived striatal neurons possess distinct electrophysiological properties, constituting the only glutamatergic striatal population. Astrocyte-derived neurons integrate into the adult striatal microcircuitry, both receiving and providing synaptic input. The glutamatergic nature of these neurons has the potential to provide excitatory input to the striatal circuitry and may represent an efficient strategy to compensate for reduced neuronal activity caused by aging or lesion-induced neuronal loss. |
| Databáze: | OpenAIRE |
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