Oligodendrocyte lineage cells (oligodendroglia) and neurons engage in bidirectional communication throughout life to support healthy brain function. Recent work shows that changes in neuronal activity can modulate proliferation, differentiation, and myelination to support the formation and function of neural circuits. While oligodendroglia express a diverse collection of receptors for growth factors, signaling molecules, neurotransmitters and neuromodulators, our knowledge of the intracellular signaling pathways that are regulated by neuronal activity remains largely incomplete. Many of the pathways that modulate oligodendroglia behavior are driven by changes in intracellular calcium signaling, which may differentially affect cytoskeletal dynamics, gene expression, maturation, integration, and axonal support. Additionally, activity-dependent neuron-oligodendroglia communication plays an integral role in the recovery from demyelinating injuries. In this review, we summarize the modalities of communication between neurons and oligodendroglia and explore possible roles of activity-dependent calcium signaling in mediating cellular behavior and myelination.
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http://dx.doi.org/10.1016/j.neulet.2020.134916 | DOI Listing |
Proc Natl Acad Sci U S A
January 2025
Bioelectricity Laboratory, Department of Physiology and Biophysics, School of Medicine, University of California, Irvine, CA 92697.
Loss-of-function sequence variants in , which encodes the voltage-gated potassium channel Kv1.1, cause Episodic Ataxia Type 1 (EA1) and epilepsy. Due to a paucity of drugs that directly rescue mutant Kv1.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Helen Wills Neuroscience Institute, University of California Berkeley, Berkeley, CA 94720.
Norepinephrine in vertebrates and its invertebrate analog, octopamine, regulate the activity of neural circuits. We find that, when hungry, larvae switch activity in type II octopaminergic motor neurons (MNs) to high-frequency bursts, which coincide with locomotion-driving bursts in type I glutamatergic MNs that converge on the same muscles. Optical quantal analysis across hundreds of synapses simultaneously reveals that octopamine potentiates glutamate release by tonic type Ib MNs, but not phasic type Is MNs, and occurs via the G-coupled octopamine receptor (OAMB).
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Brain Sciences, Weizmann Institute of Science, Rehovot 7610001, Israel.
Retinal ganglion cells (RGCs) typically respond to light stimulation over their spatially restricted receptive field. Using large-scale recordings in the mouse retina, we show that a subset of non- direction-selective (DS) RGCs exhibit asymmetric activity, selective to motion direction, in response to a stimulus crossing an area far beyond the classic receptive field. The extraclassical response arises via inputs from an asymmetric distal zone and is enhanced by desensitization mechanisms and an inherent DS component, creating a network of neurons responding to motion toward the optic disc.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Neurophysiology, Medical Faculty, Ruhr University Bochum, Bochum 44780, Germany.
The novelty, saliency, and valency of ongoing experiences potently influence the firing rate of the ventral tegmental area (VTA) and the locus coeruleus (LC). Associative experience, in turn, is recorded into memory by means of hippocampal synaptic plasticity that is regulated by noradrenaline sourced from the LC, and dopamine, sourced from both the VTA and LC. Two persistent forms of synaptic plasticity, long-term potentiation (LTP), and long-term depression (LTD) support the encoding of different kinds of spatial experience.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Key Laboratory of Mental Disorders, The Second Hospital of Shandong University, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, 250012, China.
Major depressive disorder (MDD) is usually considered associate with immune inflammation and synaptic injury within specific brain regions. However, the molecular mechanisms underlying the neural deterioration resulting in depression remain unclear. Here, it is found that miR-204-5p is markedly downregulated in the ventromedial prefrontal cortex (vmPFC) in a chronic unpredictable mild stress (CUMS) induce rat model of depression.
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