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Special Issue "Synaptic Transmission and Protein Interaction"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 30 September 2021.

Special Issue Editors

Dr. Julie Perroy
E-Mail Website
Guest Editor
IGF, University of Montpellier, CNRS, INSERM, Montpellier, France
Interests: Synapse; Protein-protein interaction; Glutame receptosome; Synaptic transmission; Cell signaling; Plasticity; Neuronal networks; Autism Spectrum Disorder
Dr. Enora Moutin
E-Mail Website
Guest Editor
IGF, University of Montpellier, CNRS, INSERM, Montpellier, France
Interests: Synapse; Protein-protein interaction; Glutame receptosome; Synaptic transmission; Cell signaling; Plasticity; Neuronal networks; Autism Spectrum Disorder

Special Issue Information

Dear Colleagues,

This Special Issue is devoted to Synaptic Transmission and Protein Interaction.

Synaptic transmission between two neurons includes all the molecular processes allowing the release of neurotransmitters by the presynaptic element, the stimulation of post-synaptic receptors, and the initiation of signaling pathways to transmit the activation of the post-synaptic element. All these molecular mechanisms rely on the ability of proteins to interact, to form functional protein complexes. Protein–protein interactions within these complexes are regulated by environmental stimuli that multiply the number of functional signaling platforms generated from a limited number of proteins, which in turn finely control synaptic transmission. This Special Issue aims to bring together recent advances in our understanding of the dynamics and fundamental roles of protein–protein interactions in synaptic transmission.

Articles offering innovative insights into the multifaceted functions of proteins depending on their interactions are welcome. This Special Issue may include but is not limited to: original research articles focusing on nanodomain organization (receptors multimerization, scaffold interactions, signaling cascades, protein interactomes, etc.), dynamics of protein–protein interaction, further characterization of functional signaling platforms, studies using protein–protein interactions as therapeutic targets, and review articles which summarize and highlight recent advances in the field.

Dr. Julie Perroy
Dr. Enora Moutin
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Synapse
  • Protein-protein interaction
  • Nanodomain
  • Receptosome
  • Scaffold complexes
  • Synaptic transmission
  • Cell signaling
  • Interactome

Published Papers (3 papers)

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Research

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Open AccessArticle
Serine/Threonine Phosphatases in LTP: Two B or Not to Be the Protein Synthesis Blocker-Induced Impairment of Early Phase
Int. J. Mol. Sci. 2021, 22(9), 4857; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094857 - 04 May 2021
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Abstract
Dephosphorylation of target proteins at serine/threonine residues is one of the most crucial mechanisms regulating their activity and, consequently, the cellular functions. The role of phosphatases in synaptic plasticity, especially in long-term depression or depotentiation, has been reported. We studied serine/threonine phosphatase activity [...] Read more.
Dephosphorylation of target proteins at serine/threonine residues is one of the most crucial mechanisms regulating their activity and, consequently, the cellular functions. The role of phosphatases in synaptic plasticity, especially in long-term depression or depotentiation, has been reported. We studied serine/threonine phosphatase activity during the protein synthesis blocker (PSB)-induced impairment of long-term potentiation (LTP). Established protein phosphatase 2B (PP2B, calcineurin) inhibitor cyclosporin A prevented the LTP early phase (E-LTP) decline produced by pretreatment of hippocampal slices with cycloheximide or anisomycin. For the first time, we directly measured serine/threonine phosphatase activity during E-LTP, and its significant increase in PSB-treated slices was demonstrated. Nitric oxide (NO) donor SNAP also heightened phosphatase activity in the same manner as PSB, and simultaneous application of anisomycin + SNAP had no synergistic effect. Direct measurement of the NO production in hippocampal slices by the NO-specific fluorescent probe DAF-FM revealed that PSBs strongly stimulate the NO concentration in all studied brain areas: CA1, CA3, and dentate gyrus (DG). Cyclosporin A fully abolished the PSB-induced NO production in the hippocampus, suggesting a close relationship between nNOS and PP2B activity. Surprisingly, cyclosporin A alone impaired short-term plasticity in CA1 by decreasing paired-pulse facilitation, which suggests bi-directionality of the influences of PP2B in the hippocampus. In conclusion, we proposed a minimal model of signaling events that occur during LTP induction in normal conditions and the PSB-treated slices. Full article
(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)
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Open AccessArticle
Lithium Enhances the GABAergic Synaptic Activities on the Hypothalamic Preoptic Area (hPOA) Neurons
Int. J. Mol. Sci. 2021, 22(8), 3908; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083908 - 09 Apr 2021
Viewed by 390
Abstract
Lithium (Li+) salt is widely used as a therapeutic agent for treating neurological and psychiatric disorders. Despite its therapeutic effects on neurological and psychiatric disorders, it can also disturb the neuroendocrine axis in patients under lithium therapy. The hypothalamic area contains [...] Read more.
Lithium (Li+) salt is widely used as a therapeutic agent for treating neurological and psychiatric disorders. Despite its therapeutic effects on neurological and psychiatric disorders, it can also disturb the neuroendocrine axis in patients under lithium therapy. The hypothalamic area contains GABAergic and glutamatergic neurons and their receptors, which regulate various hypothalamic functions such as the release of neurohormones, control circadian activities. At the neuronal level, several neurotransmitter systems are modulated by lithium exposure. However, the effect of Li+ on hypothalamic neuron excitability and the precise action mechanism involved in such an effect have not been fully understood yet. Therefore, Li+ action on hypothalamic neurons was investigated using a whole-cell patch-clamp technique. In hypothalamic neurons, Li+ increased the GABAergic synaptic activities via action potential independent presynaptic mechanisms. Next, concentration-dependent replacement of Na+ by Li+ in artificial cerebrospinal fluid increased frequencies of GABAergic miniature inhibitory postsynaptic currents without altering their amplitudes. Li+ perfusion induced inward currents in the majority of hypothalamic neurons independent of amino-acids receptor activation. These results suggests that Li+ treatment can directly affect the hypothalamic region of the brain and regulate the release of various neurohormones involved in synchronizing the neuroendocrine axis. Full article
(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)
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Review

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Open AccessReview
Adrenoceptors Modulate Cholinergic Synaptic Transmission at the Neuromuscular Junction
Int. J. Mol. Sci. 2021, 22(9), 4611; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094611 - 28 Apr 2021
Viewed by 272
Abstract
Adrenoceptor activators and blockers are widely used clinically for the treatment of cardiovascular and pulmonary disorders. More recently, adrenergic agents have also been used to treat neurodegenerative diseases. Recent studies indicate a location of sympathetic varicosities in close proximity to neuromuscular junctions. The [...] Read more.
Adrenoceptor activators and blockers are widely used clinically for the treatment of cardiovascular and pulmonary disorders. More recently, adrenergic agents have also been used to treat neurodegenerative diseases. Recent studies indicate a location of sympathetic varicosities in close proximity to neuromuscular junctions. The pressing question is whether there could be any effects of endo- or exogenous catecholamines on cholinergic neuromuscular transmission. It was shown that the pharmacological stimulation of adrenoceptors, as well as sympathectomy, can affect both acetylcholine release from motor nerve terminals and the functioning of postsynaptic acetylcholine receptors. In this review, we discuss the recent data regarding the effects of adrenergic drugs on neurotransmission at the neuromuscular junction. The elucidation of the molecular mechanisms by which the clinically relevant adrenomimetics and adrenoblockers regulate quantal acetylcholine release from the presynaptic nerve terminals and postsynaptic sensitivity may help in the design of highly effective and well-tolerated sympathomimetics for treating a number of neurodegenerative diseases accompanied by synaptic defects. Full article
(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)
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