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Synaptic Plasticity and Diseases 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 October 2023) | Viewed by 3238

Special Issue Editor


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Guest Editor
Graduate School of Dentistry, Osaka University, Suita, Japan
Interests: synaptic transmission; synaptic plasticity; ion channel; electrophysiology; cortex; trigeminal system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Synaptic plasticity is a basic process in the brain that allows humans and animals to adapt to changes in their environment and is considered the neural basis of learning and memory as well as brain disorders, including Alzheimer's disease, Parkinson's disease, autism, schizophrenia, mental retardation, chronic pain and drug addiction. Long-term potentiation (LTP) and long-term depression (LTD) are the most intensively studied forms of activity-dependent synaptic plasticity. It is now clear that that LTP and LTD are involved in many physiological functions and are linked to various brain disorders. An understanding of the cellular and molecular mechanisms in synaptic plasticity could aid the development of effective treatments for brain disorders. This Special Issue will be of interest to basic and clinical researchers involved in studies that focus on synaptic plasticity and diseases.

Dr. Hiroki Toyoda
Guest Editor

Manuscript Submission Information

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Keywords

  • synaptic plasticity
  • long-term potentiation
  • long-term depression
  • learning
  • memory
  • brain disorders

Published Papers (2 papers)

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16 pages, 3204 KiB  
Article
Dopamine-Dependent Ketamine Modulation of Glutamatergic Synaptic Plasticity in the Prelimbic Cortex of Adult Rats Exposed to Acute Stress
by Lia Forti, Elona Ndoj, Jessica Mingardi, Emanuele Secchi, Tiziana Bonifacino, Emanuele Schiavon, Giulia Carini, Luca La Via, Isabella Russo, Marco Milanese, Massimo Gennarelli, Giambattista Bonanno, Maurizio Popoli, Alessandro Barbon and Laura Musazzi
Int. J. Mol. Sci. 2023, 24(10), 8718; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24108718 - 13 May 2023
Cited by 2 | Viewed by 1539
Abstract
Traumatic stress is the main environmental risk factor for the development of psychiatric disorders. We have previously shown that acute footshock (FS) stress in male rats induces rapid and long-lasting functional and structural changes in the prefrontal cortex (PFC), which are partly reversed [...] Read more.
Traumatic stress is the main environmental risk factor for the development of psychiatric disorders. We have previously shown that acute footshock (FS) stress in male rats induces rapid and long-lasting functional and structural changes in the prefrontal cortex (PFC), which are partly reversed by acute subanesthetic ketamine. Here, we asked if acute FS may also induce any changes in glutamatergic synaptic plasticity in the PFC 24 h after stress exposure and whether ketamine administration 6 h after stress may have any effect. We found that the induction of long-term potentiation (LTP) in PFC slices of both control and FS animals is dependent on dopamine and that dopamine-dependent LTP is reduced by ketamine. We also found selective changes in ionotropic glutamate receptor subunit expression, phosphorylation, and localization at synaptic membranes induced by both acute stress and ketamine. Although more studies are needed to understand the effects of acute stress and ketamine on PFC glutamatergic plasticity, this first report suggests a restoring effect of acute ketamine, supporting the potential benefit of ketamine in limiting the impact of acute traumatic stress. Full article
(This article belongs to the Special Issue Synaptic Plasticity and Diseases 2.0)
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11 pages, 1544 KiB  
Article
Genetic Background Influence on Hippocampal Synaptic Plasticity: Frequency-Dependent Variations between an Inbred and an Outbred Mice Strain
by Candice M. Roux, Pierre Lecouflet, Jean-Marie Billard, Elise Esneault, Marianne Leger, Pascale Schumann-Bard and Thomas Freret
Int. J. Mol. Sci. 2023, 24(5), 4304; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054304 - 21 Feb 2023
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Abstract
For almost half a century, acute hippocampal slice preparations have been widely used to investigate anti-amnesic (or promnesic) properties of drug candidates on long-term potentiation (LTP)—a cellular substrate that supports some forms of learning and memory. The large variety of transgenic mice models [...] Read more.
For almost half a century, acute hippocampal slice preparations have been widely used to investigate anti-amnesic (or promnesic) properties of drug candidates on long-term potentiation (LTP)—a cellular substrate that supports some forms of learning and memory. The large variety of transgenic mice models now available makes the choice of the genetic background when designing experiments crucially important. Furthermore, different behavioral phenotypes were reported between inbred and outbred strains. Notably, some differences in memory performance were emphasized. Despite this, investigations, unfortunately, did not explore electrophysiological properties. In this study, two stimulation paradigms were used to compare LTP in the hippocampal CA1 area of both inbred (C57BL/6) and outbred (NMRI) mice. High-frequency stimulation (HFS) revealed no strain difference, whereas theta-burst stimulation (TBS) resulted in significantly reduced LTP magnitude in NMRI mice. Additionally, we demonstrated that this reduced LTP magnitude (exhibited by NMRI mice) was due to lower responsiveness to theta-frequency during conditioning stimuli. In this paper, we discuss the anatomo-functional correlates that may explain such hippocampal synaptic plasticity divergence, although straightforward evidence is still lacking. Overall, our results support the prime importance of considering the animal model related to the intended electrophysiological experiments and the scientific issues to be addressed. Full article
(This article belongs to the Special Issue Synaptic Plasticity and Diseases 2.0)
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