Spike timing precision in response to a subthreshold stimulation can be enhanced by noise in ensembles of neurons [X. Pei, L. Wilkens, and F. Moss, Phys. Rev. Lett. 77, 4679 (1996)]. We elucidate the mechanism underlying this phenomenon by computing the membrane potential distributions of ensembles of Hodgkin-Huxley neuron models. For small noise amplitudes, the membrane potential distribution takes on a Gaussian form centered on the resting potential, while for large fluctuations, there is a significant spread to lower potentials. These two regimes are separated by a relatively narrow band where the distributions transit rapidly from the Gaussian-like shapes to the spread ones. We argue that the optimal noise that maximizes the spike timing precision is situated close to this boundary.
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http://dx.doi.org/10.1103/physreve.60.7235 | DOI Listing |
Brain
January 2025
Translational Neuroimaging Laboratory, Montreal Neurological Institute, H3A 2B4, Montreal, Canada.
Plasma phosphorylated tau biomarkers open unprecedented opportunities for identifying carriers of Alzheimer's disease pathophysiology in early disease stages using minimally invasive techniques. Plasma p-tau biomarkers are believed to reflect tau phosphorylation and secretion. However, it remains unclear to what extent the magnitude of plasma p-tau abnormalities reflects neuronal network disturbance in the form of cognitive impairment.
View Article and Find Full Text PDFSci Transl Med
January 2025
University of Strasbourg, INSERM, Strasbourg Translational Neuroscience & Psychiatry STEP-CRBS, UMR-S 1329, 67000 Strasbourg, France.
Sleep alterations have been described in several neurodegenerative diseases yet are currently poorly characterized in amyotrophic lateral sclerosis (ALS). This study investigates sleep macroarchitecture and related hypothalamic signaling disruptions in ALS. Using polysomnography, we found that both patients with ALS as well as asymptomatic and mutation carriers exhibited increased wakefulness and reduced non-rapid eye movement sleep.
View Article and Find Full Text PDFPLoS Comput Biol
January 2025
Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
Theoretical neuroscientists and machine learning researchers have proposed a variety of learning rules to enable artificial neural networks to effectively perform both supervised and unsupervised learning tasks. It is not always clear, however, how these theoretically-derived rules relate to biological mechanisms of plasticity in the brain, or how these different rules might be mechanistically implemented in different contexts and brain regions. This study shows that the calcium control hypothesis, which relates synaptic plasticity in the brain to the calcium concentration ([Ca2+]) in dendritic spines, can produce a diverse array of learning rules.
View Article and Find Full Text PDFPLoS Comput Biol
January 2025
Kavli Institute for Systems Neuroscience and Centre for Algorithms in the Cortex, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
Persistent homology applied to the activity of grid cells in the Medial Entorhinal Cortex suggests that this activity lies on a toroidal manifold. By analyzing real data and a simple model, we show that neural oscillations play a key role in the appearance of this toroidal topology. To quantitatively monitor how changes in spike trains influence the topology of the data, we first define a robust measure for the degree of toroidality of a dataset.
View Article and Find Full Text PDFJ Vis Exp
January 2025
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, Harvard Medical School;
A method to quantitate the stabilization of Mitochondria-Associated endoplasmic reticulum Membranes (MAMs) in a 3-dimensional (3D) neural model of Alzheimer's disease (AD) is presented here. To begin, fresh human neuro progenitor ReN cells expressing β-amyloid precursor protein (APP) containing familial Alzheimer's disease (FAD) or naïve ReN cells are grown in thin (1:100) Matrigel-coated tissue culture plates. After the cells reach confluency, these are electroporated with expression plasmids encoding red fluorescence protein (RFP)-conjugated mitochondria-binding sequence of AKAP1(34-63) (Mito-RFP) that detects mitochondria or constitutive MAM stabilizers MAM 1X or MAM 9X that stabilize tight (6 nm ± 1 nm gap width) or loose (24 nm ± 3 nm gap width) MAMs, respectively.
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