The generation of spikes by neurons is energetically a costly process and the evaluation of the metabolic energy required to maintain the signaling activity of neurons a challenge of practical interest. Neuron models are frequently used to represent the dynamics of real neurons but hardly ever to evaluate the electrochemical energy required to maintain that dynamics. This paper discusses the interpretation of a Hodgkin-Huxley circuit as an energy model for real biological neurons and uses it to evaluate the consumption of metabolic energy in the transmission of information between neurons coupled by electrical synapses, i.e., gap junctions. We show that for a single postsynaptic neuron maximum energy efficiency, measured in bits of mutual information per molecule of adenosine triphosphate (ATP) consumed, requires maximum energy consumption. For groups of parallel postsynaptic neurons we determine values of the synaptic conductance at which the energy efficiency of the transmission presents clear maxima at relatively very low values of metabolic energy consumption. Contrary to what could be expected, the best performance occurs at a low energy cost.
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http://dx.doi.org/10.1103/PhysRevE.83.031912 | DOI Listing |
Plant Physiol Biochem
January 2025
Laboratory of Microbial Genetics, Department of Botany, Institute of Science, Banaras Hindu University, Varanasi, 221005, India. Electronic address:
Nitric oxide synthases (NOSs) are heme-based monooxygenases that catalyze the NADPH-dependent oxidation of L-arginine to produce NO and L-citrulline. Over the past five years, the identification and characterization of NOS homologs in cyanobacteria have significantly advanced our understanding of these enzymes. However, the precise mechanisms through which NOS-derived NO influences nitrogen metabolism remain incompletely elucidated.
View Article and Find Full Text PDFPlant Physiol Biochem
January 2025
Department of Botany and Microbiology, College of Science, King Saud University, Riyadh, 11451, Saudi Arabia.
Melatonin (Mel) is a tryptophan-derived (N-acetyl-5-methoxytryptamine) molecule. In the present study, role of Mel in the regulation of various anaplerotic enzymes is discussed in relation to N metabolism and H-ATPase activity in mung bean under Cd stress. The application of Mel to the Cd-stressed mung bean seedlings was remarkable in improving the activity of hexokinase (35.
View Article and Find Full Text PDFPLoS One
January 2025
CFD Research Corporation, Huntsville, AL, United States of America.
Purpose: To assess physiological metrics during the use of a commercially available bilateral active ankle exoskeleton during a challenging military-relevant task and if use of the exoskeleton during this task influences: metabolic load, physiological measures or rate of perceived exertion.
Methods: Nine healthy volunteers (5M, 4F) completed this randomized cross-over design trial, with a baseline visit and two randomized test sessions (with/without the exoskeleton). Variables included impact on time to exhaustion during walking on a treadmill at varying speeds and gradients (0-15%) at 26.
Proc Natl Acad Sci U S A
January 2025
Department of Chemistry, New York University, New York, NY 10003.
Frameshifting is an essential mechanism employed by many viruses including coronaviruses to produce viral proteins from a compact RNA genome. It is facilitated by specific RNA folds in the frameshift element (FSE), which has emerged as an important therapeutic target. For SARS-CoV-2, a specific 3-stem pseudoknot has been identified to stimulate frameshifting.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Yusuf Hamied Department of Chemistry, Centre for Misfolding Diseases, University of Cambridge, Cambridge CB2 1EW, United Kingdom.
The onset and development of Alzheimer's disease is linked to the accumulation of pathological aggregates formed from the normally monomeric amyloid-β peptide within the central nervous system. These Aβ aggregates are increasingly successfully targeted with clinical therapies at later stages of the disease, but the fundamental molecular steps in early stage disease that trigger the initial nucleation event leading to the conversion of monomeric Aβ peptide into pathological aggregates remain unknown. Here, we show that the Aβ peptide can form biomolecular condensates on lipid bilayers both in molecular assays and in living cells.
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