Synaptic Function and Energy Use

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 15 February 2026 | Viewed by 854

Special Issue Editor


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Guest Editor
Department of Drug Discovery Medicine, Kyoto University Graduate School of Medicine, Kyoto 606-8397, Japan
Interests: neuron; synapses; neurobiology; synaptic plasticity; electrophysiology; neural plasticity; neuropharmacology; inflammation; neurobiology and brain physiology; neurophysiology; neuropsychiatry
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Special Issue Information

Dear Colleagues, 

Synapses are metabolically costly to operate. Research over the years has shed light on how synaptic function is sustained through dynamic, activity-dependent coupling with ATP synthesis, mitochondrial function, and motility, glia, and vasculature. Critically, dysfunction in such coupling, which arises in a number of neurological disorders, impairs cognitive function. Furthermore, an accumulating body of evidence has found that synaptic function and energy use is sensitive to nutrient and caloric intake, as well as to metabolic factors including ketone bodies, leptin, and insulin. Thus, the metabolically expensive synapse is regulated closely by the peripheral metabolic state.

This purpose of this Special Issue is to provide an up-to-date understanding of the link between synaptic function and energy use, its relation to peripheral metabolic state and nutrient status, and its relevance to cognitive function and neurological disorders. It is open to original articles, reviews, and perspectives that cover any element of these key aspects. 

Prof. Dr. Gen Ohtsuki
Guest Editor

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Keywords

  • presynapse
  • postsynapse
  • ATP
  • mitochondria
  • glia
  • pericyte
  • vasculature
  • fatty acids
  • ketone bodies
  • leptin
  • insulin
  • glucose
  • lactate

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Published Papers (1 paper)

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Review

17 pages, 427 KB  
Review
New Insights on Mitochondria-Targeted Neurological Drugs
by Silvia Lores-Arnaiz
Biology 2026, 15(3), 228; https://doi.org/10.3390/biology15030228 - 26 Jan 2026
Abstract
Aging and neurodegenerative diseases are characterized by common features involving bioenergetics deficiencies, oxidative stress and alterations of calcium buffering. Mechanisms of mitochondrial-targeted drugs include the modulation of electron transport chain and oxidative phosphorylation, the binding to mitochondrial lipids, free-radical scavenging, calcium signaling, and [...] Read more.
Aging and neurodegenerative diseases are characterized by common features involving bioenergetics deficiencies, oxidative stress and alterations of calcium buffering. Mechanisms of mitochondrial-targeted drugs include the modulation of electron transport chain and oxidative phosphorylation, the binding to mitochondrial lipids, free-radical scavenging, calcium signaling, and possible effects on mitochondrial biogenesis and dynamics and on the regulation of mitophagic pathways. One of the main sites of action of mitochondria-targeted drugs is the interaction with respiratory chain components. Mitochondrial-targeted compounds such as Mito-Q, and Mito-apocynin have been developed by conjugating triphenylphosphonium (TPP+) lipophilic cation group with natural molecules, therefore obtaining promising drugs for reestablishing the correct functioning of the mitochondrial respiratory chain. Stabilization of cardiolipin at the inner mitochondrial membrane by elamipretide or SkQ1 and mitochondria-targeted ROS scavengers can also offer a therapeutic approach to prevent bioenergetic impairment associated with several diseases. In addition, the modulation of calcium signaling can be achieved using both MCU agonists and antagonists representing another mitochondrial target for drug therapies development. Finally, potential strategies for treating neurodegenerative diseases based on the modulation of mitochondrial biogenesis, dynamics and/or mitophagic pathways are discussed. Full article
(This article belongs to the Special Issue Synaptic Function and Energy Use)
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