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GABAergic

Differential Vulnerability of Adult Neurogenic Niches to Dosage of the Neurodevelopmental-Disorder Linked Gene Foxg1

[Molecular Psychiatry] The authors reported that FOXG1 was expressed in the main adult neurogenic niches in mice, i.e. the hippocampal dentate gyrus and the subependymal zone/olfactory bulb system, where neurogenesis of glutamatergic and GABAergic neurons persisted into adulthood.

Microglia Regulate Chandelier Cell Axo-Axonic Synaptogenesis

[Proceedings of the National Academy of Sciences of the United States of America] Scientists identifed a synaptogenic/growth-promoting role for microglia in regulating pyramidal neuron axon initial segment (AIS) synapse formation by chandelier cells, a unique interneuron subtype whose axonal terminals, called cartridges, selectively targeted the AIS.

Cross-Talk between GABAergic Postsynapse and Microglia Regulate Synapse Loss after Brain Ischemia

[Science Advances] Scientists reported that at 24 hours after ischemia, microglia released brain-derived neurotrophic factor to downregulate glutamatergic and GABAergic synapses within the peri-infarct area.

Autism Genes Converge on Asynchronous Development of Shared Neuron Classes

[Nature] Scientists used organoid models of the human cerebral cortex to identify cell-type-specific developmental abnormalities that result from haploinsufficiency in three autism spectrum disorder risk genes—SUV420H1, ARID1B and CHD8—in multiple cell lines from different donors.

Human Stem Cell-Derived GABAergic Neurons Functionally Integrate into Human Neuronal Networks

[Scientific Reports] Researchers provided a proof-of-concept that human embryonic stem cell-derived neurons could integrate and modulate the activity of a human host neuronal network.

Caught in Vicious Circles: A Perspective on Dynamic Feed-Forward Loops Driving Oxidative Stress in Schizophrenia

[Molecular Psychiatry] Scientists review the existing experimental and translational research pinpointing the complex dynamics of oxidative stress mechanisms and their modulation in relation to schizophrenia pathophysiology.

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