Animal nervous systems remodel following stress. Although global stress-dependent changes are well documented, contributions of individual neuron remodeling events to animal behavior modification are challenging to study. In response to environmental insults, C. elegans become stress-resistant dauers. Dauer entry induces amphid sensory organ remodeling in which bilateral AMsh glial cells expand and fuse, allowing embedded AWC chemosensory neurons to extend sensory receptive endings. We show that amphid remodeling correlates with accelerated dauer exit upon exposure to favorable conditions and identify a G protein-coupled receptor, REMO-1, driving AMsh glia fusion, AWC neuron remodeling, and dauer exit. REMO-1 is expressed in and localizes to AMsh glia tips, is dispensable for other remodeling events, and promotes stress-induced expression of the remodeling receptor tyrosine kinase VER-1. Our results demonstrate how single-neuron structural changes affect animal behavior, identify key glial roles in stress-induced nervous system plasticity, and demonstrate that remodeling primes animals to respond to favorable conditions.
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http://dx.doi.org/10.1016/j.celrep.2020.108607 | DOI Listing |
Gamma oscillations are disrupted in various neurological disorders, including Alzheimer's disease (AD). In AD mouse models, non-invasive audiovisual stimulation (AuViS) at 40 Hz enhances gamma oscillations, clears amyloid-beta, and improves cognition. We investigated mechanisms of circuit remodeling underlying these restorative effects by leveraging the sensitivity of hippocampal neurogenesis to activity in middle-aged wild-type mice.
View Article and Find Full Text PDFBrief monocular deprivation during a developmental critical period, but not thereafter, alters the receptive field properties (tuning) of neurons in visual cortex, but the characteristics of neural circuitry that permit this experience-dependent plasticity are largely unknown. We performed repeated calcium imaging at neuronal resolution to track the tuning properties of populations of excitatory layer 2/3 neurons in mouse visual cortex during or after the critical period, as well as in mutant mice that sustain critical-period plasticity as adults. The instability of tuning for populations of neurons was greater in juvenile mice and adult mutant mice.
View Article and Find Full Text PDFNat Commun
January 2025
School of Future Technology, University of Chinese Academy of Sciences, 100190, Beijing, PR China.
In bioneuronal systems, the synergistic interaction between mechanosensitive piezo channels and neuronal synapses can convert and transmit pressure signals into complex temporal plastic pulses with excitatory and inhibitory features. However, existing artificial tactile neuromorphic systems struggle to replicate the elaborate temporal plasticity observed between excitatory and inhibitory features in biological systems, which is critical for the biomimetic processing and memorizing of tactile information. Here we demonstrate a mechano-gated iontronic piezomemristor with programmable temporal-tactile plasticity.
View Article and Find Full Text PDFVitam Horm
January 2025
Department Normal Physiology, Yaroslavl State Medical University, Yaroslavl, Russia. Electronic address:
The hypothalamus, in addition to controlling the main body's vital functions, is also involved in aging regulation. The aging process in the hypothalamus is accompanied by disturbed intracellular pathways, including Ca signaling and neuronal excitability in the brain. Intrinsic electrophysiological properties of individual neurons and synaptic transmission between cells is disrupted in the central nervous system of old animals.
View Article and Find Full Text PDFChronic stress profoundly affects the structure and function of the prefrontal cortex (PFC), a brain region critical for executive functions and emotional regulation. This review synthesizes current knowledge on stress-induced PFC plasticity, encompassing structural, functional, and molecular changes. We examine how chronic stress leads to dendritic atrophy, spine loss, and alterations in neuronal connectivity within the PFC, particularly affecting the medial PFC.
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