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Tiveron, M.-C.

Publications and source records attributed to Tiveron, M.-C..

3 recordsLinked to original sources

Gliogenesis from the subventricular zone modulates the extracellular matrix at the glial scar after brain ischemia

Activation of the subventricular zone (SVZ) following cerebral ischemia is one of the brains early responses to counteract neuron loss and minimize tissue damage. Impaired brain regions communicate with the SVZ through various chemotactic signals that promote cell migration and differentiation, primarily involving neural stem cells (NSC), neuroblasts, or glioblasts. However, the activation of gliogenesis and the role of newly formed astrocytes in the post-ischemic scenario remain subjects of debate. We have previously demonstrated that adenosine release after brain ischemia prompts the SVZ to generate new astrocytes. Here, we used transient brain ischemia in mice to identify the cellular origin of these astrocytes within the SVZ neurogenic niche and to investigate their role in the pathological process. By combining immunofluorescence, BrdU-tracing, and genetic cell labeling, we tracked the migration of newborn astrocytes, positive for the proteoglycan marker Thbs4, from the dorsal and medial SVZ to the perilesional barrier surrounding the ischemic core, known as the "glial scar". We found that these Thbs4-positive astrocytes modulate the dense extracellular matrix at the lesion border by both synthesizing and degrading hyaluronan. We also show that while the accumulation of hyaluronan at the lesion site is sufficient to recruit newborn astrocytes, its degradation at the SVZ correlates with gliogenesis. These findings suggest that newborn astrocytes could be a promising pharmacological target for modulating the glial scar after brain ischemia and facilitate tissue regeneration.

neuroscience↗

Sensory deprivation triggers phenotypic adjustment of dopaminergic interneurons in the mouse olfactory bulb

Olfactory sensory activity is a main factor factor controlling intergration and survival of neurons in the olfactory bulb. However, its impact on specific neuronal subtypes is unclear. Using reversible unilateral naris closure in concert with longitudinal in vivo imaging we show here that newborn GABAergic interneurons undergo significant cell death under sensory deprivation. In contrast, dopaminergic OB neurons survive under deprivation, but react with a reversible downregulation of tyrosine hydroxylase expression. long abstractNeurogenesis persists in the mammalian subventricular zone after birth, producing various populations of olfactory bulb (OB) interneurons. These include GABAergic and mixed dopaminergic/GABAergic double neurotransmitter neurons for the glomerular layer. While olfactory sensory activity is one of the main factors controlling newborn neuron integration, its effect on specific neuronal subtypes is far less clear. Here we use a reversible unilateral deprivation paradigm in combination with longitudinal in vivo imaging to characterize the behavior of newborn glomerular neurons. We find that a substantial fraction of purely GABAergic neurons die after four weeks of sensory deprivation. Tyrosine Hydroxylase (TH) positive dopaminergic/ GABAergic neurons show no signifficant cell death under deprivation, but react with an important decrease in TH expression levels. Importantly, this effect reverses after naris reopening, pointing to a specific adaptation of this neuron population to the level of sensory activity. We conclude that sensory deprivation induces adjustments in the excitation/inhibition balance of the OB implicating cell death and adaptation of neurotransmitter use in specific neuron types.

neuroscience↗

Neuronal integration in the adult olfactory bulb is a non-selective addition process

Adult neurogenesis is considered a competition in which neurons scramble during a critical period for integration and survival. Moreover, newborn neurons are thought to replace preexisting ones that die. Despite a wealth of evidence supporting this model, systematic in vivo observations of the process are still scarce. We used 2-photon imaging to study neuronal integration and survival directly in the olfactory bulb (OB) of living mice. Long-term tracking of over 1400 neurons demonstrated that cell-loss in the OB is virtually absent. Neuronal death resembling a critical period was induced by standard doses of BrdU or EdU, but disappeared when low doses of EdU were used, demonstrating toxicity. Finally, we demonstrate that the OB grows throughout life. This shows that neuronal selection during OB-neurogenesis does not occur during integration and argues against the existence of a critical period. Moreover, the OB is not a \"turnover\" system but shows lifelong neuronal addition.

neuroscience↗