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Synaptic Transmission and Protein Interaction

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

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 33582

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Special Issue Editors

Dr. Julie Perroy

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Guest Editor

IGF, University of Montpellier, CNRS, INSERM, 34094 Montpellier, France
Interests: synapse; protein-protein interaction; glutame receptosome; synaptic transmission; cell signaling; plasticity; neuronal networks; autism spectrum disorder
Special Issues, Collections and Topics in MDPI journals

Dr. Enora Moutin

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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

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Keywords

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

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Published Papers (9 papers)

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Research

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23 pages, 70853 KiB

Open AccessArticle

Cell Types and Synapses Expressing the SNARE Complex Regulating Proteins Complexin 1 and Complexin 2 in Mammalian Retina

by Uwe Thorsten Lux, Johanna Ehrenberg, Anneka Joachimsthaler, Jenny Atorf, Bianca Pircher, Kerstin Reim, Jan Kremers, Andreas Gießl and Johann Helmut Brandstätter

Int. J. Mol. Sci. 2021, 22(15), 8131; https://doi.org/10.3390/ijms22158131 - 29 Jul 2021

Cited by 2 | Viewed by 2778

Abstract

Complexins (Cplxs) 1 to 4 are components of the presynaptic compartment of chemical synapses where they regulate important steps in synaptic vesicle exocytosis. In the retina, all four Cplxs are present, and while we know a lot about Cplxs 3 and 4, little is known about Cplxs 1 and 2. Here, we performed in situ hybridization experiments and bioinformatics and exploited Cplx 1 and Cplx 2 single-knockout mice combined with immunocytochemistry and light microscopy to characterize in detail the cell type and synapse-specific distribution of Cplx 1 and Cplx 2. We found that Cplx 2 and not Cplx 1 is the main isoform expressed in normal and displaced amacrine cells and ganglion cells in mouse retinae and that amacrine cells seem to operate with a single Cplx isoform at their conventional chemical synapses. Surprising was the finding that retinal function, determined with electroretinographic recordings, was altered in Cplx 1 but not Cplx 2 single-knockout mice. In summary, the results provide an important basis for future studies on the function of Cplxs 1 and 2 in the processing of visual signals in the mammalian retina. Full article

(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)

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16 pages, 5417 KiB

Open AccessArticle

FMRP Interacts with RARα in Synaptic Retinoic Acid Signaling and Homeostatic Synaptic Plasticity

by Esther Park, Anthony G. Lau, Kristin L. Arendt and Lu Chen

Int. J. Mol. Sci. 2021, 22(12), 6579; https://doi.org/10.3390/ijms22126579 - 19 Jun 2021

Cited by 8 | Viewed by 2800

Abstract

The fragile X syndrome (FXS) is an X-chromosome-linked neurodevelopmental disorder with severe intellectual disability caused by inactivation of the fragile X mental retardation 1 (FMR1) gene and subsequent loss of the fragile X mental retardation protein (FMRP). Among the various types of abnormal synaptic function and synaptic plasticity phenotypes reported in FXS animal models, defective synaptic retinoic acid (RA) signaling and subsequent defective homeostatic plasticity have emerged as a major synaptic dysfunction. However, the mechanism underlying the defective synaptic RA signaling in the absence of FMRP is unknown. Here, we show that RARα, the RA receptor critically involved in synaptic RA signaling, directly interacts with FMRP. This interaction is enhanced in the presence of RA. Blocking the interaction between FMRP and RARα with a small peptide corresponding to the critical binding site in RARα abolishes RA-induced increases in excitatory synaptic transmission, recapitulating the phenotype seen in the Fmr1 knockout mouse. Taken together, these data suggest that not only are functional FMRP and RARα necessary for RA-dependent homeostatic synaptic plasticity, but that the interaction between these two proteins is essential for proper transcription-independent RA signaling. Our results may provide further mechanistic understanding into FXS synaptic pathophysiology. Full article

(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)

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31 pages, 11604 KiB

Open AccessArticle

Role of Satb1 and Satb2 Transcription Factors in the Glutamate Receptors Expression and Ca²⁺ Signaling in the Cortical Neurons In Vitro

by Egor A. Turovsky, Maria V. Turovskaya, Evgeniya I. Fedotova, Alexey A. Babaev, Victor S. Tarabykin and Elena G. Varlamova

Int. J. Mol. Sci. 2021, 22(11), 5968; https://doi.org/10.3390/ijms22115968 - 31 May 2021

Cited by 15 | Viewed by 3834

Abstract

Transcription factors Satb1 and Satb2 are involved in the processes of cortex development and maturation of neurons. Alterations in the expression of their target genes can lead to neurodegenerative processes. Molecular and cellular mechanisms of regulation of neurotransmission by these transcription factors remain poorly understood. In this study, we have shown that transcription factors Satb1 and Satb2 participate in the regulation of genes encoding the NMDA-, AMPA-, and KA- receptor subunits and the inhibitory GABA(A) receptor. Deletion of gene for either Satb1 or Satb2 homologous factors induces the expression of genes encoding the NMDA receptor subunits, thereby leading to higher amplitudes of Ca²⁺-signals in neurons derived from the Satb1-deficient (Satb1^fl/+ * Nex^Cre/+) and Satb1-null mice (Satb1^fl/fl * Nex^Cre/+) in response to the selective agonist reducing the EC50 for the NMDA receptor. Simultaneously, there is an increase in the expression of the Gria2 gene, encoding the AMPA receptor subunit, thus decreasing the Ca²⁺-signals of neurons in response to the treatment with a selective agonist (5-Fluorowillardiine (FW)). The Satb1 deletion increases the sensitivity of the KA receptor to the agonist (domoic acid), in the cortical neurons of the Satb1-deficient mice but decreases it in the Satb1-null mice. At the same time, the Satb2 deletion decreases Ca²⁺-signals and the sensitivity of the KA receptor to the agonist in neurons from the Satb1-null and the Satb1-deficient mice. The Satb1 deletion affects the development of the inhibitory system of neurotransmission resulting in the suppression of the neuron maturation process and switching the GABAergic responses from excitatory to inhibitory, while the Satb2 deletion has a similar effect only in the Satb1-null mice. We show that the Satb1 and Satb2 transcription factors are involved in the regulation of the transmission of excitatory signals and inhibition of the neuronal network in the cortical cell culture. Full article

(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)

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19 pages, 4698 KiB

Open AccessArticle

Serine/Threonine Phosphatases in LTP: Two B or Not to Be the Protein Synthesis Blocker-Induced Impairment of Early Phase

by Alexander V. Maltsev, Natalia V. Bal and Pavel M. Balaban

Int. J. Mol. Sci. 2021, 22(9), 4857; https://doi.org/10.3390/ijms22094857 - 4 May 2021

Cited by 2 | Viewed by 3099

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 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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11 pages, 2426 KiB

Open AccessArticle

Lithium Enhances the GABAergic Synaptic Activities on the Hypothalamic Preoptic Area (hPOA) Neurons

by Santosh Rijal, Seon Hui Jang, Soo Joung Park and Seong Kyu Han

Int. J. Mol. Sci. 2021, 22(8), 3908; https://doi.org/10.3390/ijms22083908 - 9 Apr 2021

Cited by 7 | Viewed by 3264

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 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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17 pages, 4044 KiB

Open AccessReview

Stable and Flexible Synaptic Transmission Controlled by the Active Zone Protein Interactions

by Sumiko Mochida

Int. J. Mol. Sci. 2021, 22(21), 11775; https://doi.org/10.3390/ijms222111775 - 29 Oct 2021

Cited by 5 | Viewed by 2775

Abstract

An action potential triggers neurotransmitter release from synaptic vesicles docking to a specialized release site of the presynaptic plasma membrane, the active zone. The active zone is a highly organized structure with proteins that serves as a platform for synaptic vesicle exocytosis, mediated by SNAREs complex and Ca²⁺ sensor proteins, within a sub-millisecond opening of nearby Ca²⁺ channels with the membrane depolarization. In response to incoming neuronal signals, each active zone protein plays a role in the release-ready site replenishment with synaptic vesicles for sustainable synaptic transmission. The active zone release apparatus provides a possible link between neuronal activity and plasticity. This review summarizes the mostly physiological role of active zone protein interactions that control synaptic strength, presynaptic short-term plasticity, and homeostatic synaptic plasticity. Full article

(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)

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23 pages, 2289 KiB

Open AccessReview

NMDARs, Coincidence Detectors of Astrocytic and Neuronal Activities

by Mark W. Sherwood, Stéphane H. R. Oliet and Aude Panatier

Int. J. Mol. Sci. 2021, 22(14), 7258; https://doi.org/10.3390/ijms22147258 - 6 Jul 2021

Cited by 14 | Viewed by 4325

Abstract

Synaptic plasticity is an extensively studied cellular correlate of learning and memory in which NMDARs play a starring role. One of the most interesting features of NMDARs is their ability to act as a co-incident detector. It is unique amongst neurotransmitter receptors in this respect. Co-incident detection is possible because the opening of NMDARs requires membrane depolarisation and the binding of glutamate. Opening of NMDARs also requires a co-agonist. Although the dynamic regulation of glutamate and membrane depolarization have been well studied in coincident detection, the role of the co-agonist site is unexplored. It turns out that non-neuronal glial cells, astrocytes, regulate co-agonist availability, giving them the ability to influence synaptic plasticity. The unique morphology and spatial arrangement of astrocytes at the synaptic level affords them the capacity to sample and integrate information originating from unrelated synapses, regardless of any pre-synaptic and post-synaptic commonality. As astrocytes are classically considered slow responders, their influence at the synapse is widely recognized as modulatory. The aim herein is to reconsider the potential of astrocytes to participate directly in ongoing synaptic NMDAR activity and co-incident detection. Full article

(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)

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29 pages, 3502 KiB

Open AccessReview

RGS14 Regulation of Post-Synaptic Signaling and Spine Plasticity in Brain

by Nicholas H. Harbin, Sara N. Bramlett, Carolina Montanez-Miranda, Gizem Terzioglu and John R. Hepler

Int. J. Mol. Sci. 2021, 22(13), 6823; https://doi.org/10.3390/ijms22136823 - 25 Jun 2021

Cited by 16 | Viewed by 5455

Abstract

The regulator of G-protein signaling 14 (RGS14) is a multifunctional signaling protein that regulates post synaptic plasticity in neurons. RGS14 is expressed in the brain regions essential for learning, memory, emotion, and stimulus-induced behaviors, including the basal ganglia, limbic system, and cortex. Behaviorally, RGS14 regulates spatial and object memory, female-specific responses to cued fear conditioning, and environmental- and psychostimulant-induced locomotion. At the cellular level, RGS14 acts as a scaffolding protein that integrates G protein, Ras/ERK, and calcium/calmodulin signaling pathways essential for spine plasticity and cell signaling, allowing RGS14 to naturally suppress long-term potentiation (LTP) and structural plasticity in hippocampal area CA2 pyramidal cells. Recent proteomics findings indicate that RGS14 also engages the actomyosin system in the brain, perhaps to impact spine morphogenesis. Of note, RGS14 is also a nucleocytoplasmic shuttling protein, where its role in the nucleus remains uncertain. Balanced nuclear import/export and dendritic spine localization are likely essential for RGS14 neuronal functions as a regulator of synaptic plasticity. Supporting this idea, human genetic variants disrupting RGS14 localization also disrupt RGS14’s effects on plasticity. This review will focus on the known and unexplored roles of RGS14 in cell signaling, physiology, disease and behavior. Full article

(This article belongs to the Special Issue Synaptic Transmission and Protein Interaction)

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14 pages, 1551 KiB

Open AccessReview

Adrenoceptors Modulate Cholinergic Synaptic Transmission at the Neuromuscular Junction

by Ellya Bukharaeva, Venera Khuzakhmetova, Svetlana Dmitrieva and Andrei Tsentsevitsky

Int. J. Mol. Sci. 2021, 22(9), 4611; https://doi.org/10.3390/ijms22094611 - 28 Apr 2021

Cited by 11 | Viewed by 3793

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 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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