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https://www.readbyqxmd.com/read/27872870/nanoscale-organization-of-synaptic-adhesion-proteins-revealed-by-single-molecule-localization-microscopy
#1
Ingrid Chamma, Florian Levet, Jean-Baptiste Sibarita, Matthieu Sainlos, Olivier Thoumine
The advent of superresolution imaging has created a strong need for both optimized labeling strategies and analysis methods to probe the nanoscale organization of complex biological structures. We present a thorough description of the distribution of synaptic adhesion proteins at the nanoscopic scale, namely presynaptic neurexin-[Formula: see text] ([Formula: see text]), and its two postsynaptic binding partners neuroligin-1 (Nlg1) and leucine-rich-repeat transmembrane protein 2 (LRRTM2). We monitored these proteins in the membrane of neurons by direct stochastic optical reconstruction microscopy, after live surface labeling with Alexa647-conjugated monomeric streptavidin...
October 2016: Neurophotonics
https://www.readbyqxmd.com/read/27869801/direct-dorsal-hippocampal-prelimbic-cortex-connections-strengthen-fear-memories
#2
Xiaojing Ye, Dana Kapeller-Libermann, Alessio Travaglia, M Carmen Inda, Cristina M Alberini
The ability to regulate the consolidation and strengthening of memories for threatening experiences is critical for mental health, and its dysregulation may lead to psychopathologies. Re-exposure to the context in which the threat was experienced can either increase or decrease fear response through distinct processes known, respectively, as reconsolidation or extinction. Using a context retrieval-dependent memory-enhancement model in rats, we report that memory strengthens through activation of direct projections from dorsal hippocampus to prelimbic (PL) cortex and activation of critical PL molecular mechanisms that are not required for extinction...
November 21, 2016: Nature Neuroscience
https://www.readbyqxmd.com/read/27865048/neuroligin-2-nonsense-variant-associated-with-anxiety-autism-intellectual-disability-hyperphagia-and-obesity
#3
Daniel J Parente, Caryn Garriga, Berivan Baskin, Ganka Douglas, Megan T Cho, Gabriel C Araujo, Marwan Shinawi
Neuroligins are post-synaptic, cellular adhesion molecules implicated in synaptic formation and function. NLGN2 is strongly linked to inhibitory, GABAergic signaling and is crucial for maintaining the excitation-inhibition balance in the brain. Disruption of the excitation-inhibition balance is associated with neuropsychiatric disease. In animal models, altered NLGN2 expression causes anxiety, developmental delay, motor discoordination, social impairment, aggression, and sensory processing defects. In humans, mutations in NLGN3 and NLGN4 are linked to autism and schizophrenia; NLGN2 missense variants are implicated in schizophrenia...
November 16, 2016: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/27805570/distinct-roles-for-extracellular-and-intracellular-domains-in-neuroligin-function-at-inhibitory-synapses
#4
Quynh-Anh Nguyen, Meryl E Horn, Roger A Nicoll
Neuroligins (NLGNs) are postsynaptic cell adhesion molecules that interact trans-synaptically with neurexins to mediate synapse development and function. NLGN2 is only at inhibitory synapses while NLGN3 is at both excitatory and inhibitory synapses. We found that NLGN3 function at inhibitory synapses in rat CA1 depends on the presence of NLGN2 and identified a domain in the extracellular region that accounted for this functional difference between NLGN2 and 3 specifically at inhibitory synapses. We further show that the presence of a cytoplasmic tail (c-tail) is indispensible, and identified two domains in the c-tail that are necessary for NLGN function at inhibitory synapses...
November 2, 2016: ELife
https://www.readbyqxmd.com/read/27782075/association-analysis-of-noncoding-variants-in-neuroligins-3-and-4x-genes-with-autism-spectrum-disorder-in-an-italian-cohort
#5
Martina Landini, Ivan Merelli, M Elisabetta Raggi, Nadia Galluccio, Francesca Ciceri, Arianna Bonfanti, Serena Camposeo, Angelo Massagli, Laura Villa, Erika Salvi, Daniele Cusi, Massimo Molteni, Luciano Milanesi, Anna Marabotti, Alessandra Mezzelani
Since involved in synaptic transmission and located on X-chromosome, neuroligins 3 and 4X have been studied as good positional and functional candidate genes for autism spectrum disorder pathogenesis, although contradictory results have been reported. Here, we performed a case-control study to assess the association between noncoding genetic variants in NLGN3 and NLGN4X genes and autism, in an Italian cohort of 202 autistic children analyzed by high-resolution melting. The results were first compared with data from 379 European healthy controls (1000 Genomes Project) and then with those from 1061 Italian controls genotyped by Illumina single nucleotide polymorphism (SNP) array 1M-duo...
October 22, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27725662/developmental-plasticity-shapes-synaptic-phenotypes-of-autism-associated-neuroligin-3-mutations-in-the-calyx-of-held
#6
B Zhang, E Seigneur, P Wei, O Gokce, J Morgan, T C Südhof
Neuroligins are postsynaptic cell-adhesion molecules that bind to presynaptic neurexins. Mutations in neuroligin-3 predispose to autism, but how such mutations affect synaptic function remains incompletely understood. Here we systematically examined the effect of three autism-associated mutations, the neuroligin-3 knockout, the R451C knockin, and the R704C knockin, on synaptic transmission in the calyx of Held, a central synapse ideally suited for high-resolution analyses of synaptic transmission. Surprisingly, germline knockout of neuroligin-3 did not alter synaptic transmission, whereas the neuroligin-3 R451C and R704C knockins decreased and increased, respectively, synaptic transmission...
October 11, 2016: Molecular Psychiatry
https://www.readbyqxmd.com/read/27717669/the-lgi1-adam22-protein-complex-in-synaptic-transmission-and-synaptic-disorders
#7
Yuko Fukata, Norihiko Yokoi, Yuri Miyazaki, Masaki Fukata
Physiological functioning of the brain requires fine-tuned synaptic transmission, and its dysfunction causes various brain disorders such as autism, dementia, and epilepsy. It is therefore extremely important to identify and characterize key regulators of synaptic function. In particular, disease-related synaptic proteins, such as autism-related neurexin-neuroligin and psychiatric disorder-related NMDA receptor, have attracted considerable attention. Recent basic and clinical research has highlighted critical roles of a ligand-receptor complex, LGI1-ADAM22, in synaptic transmission and brain function, as mutations in the LGI1 gene cause autosomal dominant lateral temporal lobe epilepsy and autoantibodies to LGI1 cause limbic encephalitis which is characterized by memory loss and seizures...
October 4, 2016: Neuroscience Research
https://www.readbyqxmd.com/read/27697534/emerging-roles-of-the-neurotrophin-receptor-trkc-in-synapse-organization
#8
Yusuke Naito, Alfred Kihoon Lee, Hideto Takahashi
Tropomyosin-receptor-kinase (Trk) receptors have been extensively studied for their roles in kinase-dependent signaling cascades in nervous system development. Synapse organization is coordinated by trans-synaptic interactions of various cell adhesion proteins, a representative example of which is the neurexin-neuroligin complex. Recently, a novel role for TrkC as a synapse organizing protein has been established. Post-synaptic TrkC binds to pre-synaptic type-IIa receptor-type protein tyrosine phosphatase sigma (PTPσ)...
September 30, 2016: Neuroscience Research
https://www.readbyqxmd.com/read/27664583/functions-of-synapse-adhesion-molecules-neurexin-neuroligins-and-neurodevelopmental-disorders
#9
Xueshan Cao, Katsuhiko Tabuchi
Neurexins and neuroligins are two distinct families of single-pass transmembrane proteins localized at pre- and postsynapses, respectively. They trans-synaptically interact with each other and induce synapse formation and maturation. Common variants and rare mutations, including copy number variations, short deletions, and single or small nucleotide changes in neurexin and neuroligin genes have been linked to the neurodevelopmental disorders, such as autism spectrum disorders (ASDs). In this review, we summarize the structure and basic synaptic function of neurexins and neuroligins, followed by behaviors and synaptic phenotypes of knock-in and knock-out mouse of these family genes...
September 21, 2016: Neuroscience Research
https://www.readbyqxmd.com/read/27608760/altered-cortical-dynamics-and-cognitive-function-upon-haploinsufficiency-of-the-autism-linked-excitatory-synaptic-suppressor-mdga2
#10
Steven A Connor, Ina Ammendrup-Johnsen, Allen W Chan, Yasushi Kishimoto, Chiaki Murayama, Naokazu Kurihara, Atsushi Tada, Yuan Ge, Hong Lu, Ryan Yan, Jeffrey M LeDue, Hirotaka Matsumoto, Hiroshi Kiyonari, Yutaka Kirino, Fumio Matsuzaki, Toshiharu Suzuki, Timothy H Murphy, Yu Tian Wang, Tohru Yamamoto, Ann Marie Craig
Mutations in a synaptic organizing pathway contribute to autism. Autism-associated mutations in MDGA2 (MAM domain containing glycosylphosphatidylinositol anchor 2) are thought to reduce excitatory/inhibitory transmission. However, we show that mutation of Mdga2 elevates excitatory transmission, and that MDGA2 blocks neuroligin-1 interaction with neurexins and suppresses excitatory synapse development. Mdga2(+/-) mice, modeling autism mutations, demonstrated increased asymmetric synapse density, mEPSC frequency and amplitude, and altered LTP, with no change in measures of inhibitory synapses...
September 7, 2016: Neuron
https://www.readbyqxmd.com/read/27594578/syncams-from-axon-guidance-to-neurodevelopmental-disorders
#11
Jeannine A Frei, Esther T Stoeckli
Many cell adhesion molecules are located at synapses but only few of them can be considered synaptic cell adhesion molecules in the strict sense. Besides the Neurexins and Neuroligins, the LRRTMs (leucine rich repeat transmembrane proteins) and the SynCAMs/CADMs can induce synapse formation when expressed in non-neuronal cells and therefore are true synaptic cell adhesion molecules. SynCAMs (synaptic cell adhesion molecules) are a subfamily of the immunoglobulin superfamily of cell adhesion molecules. As suggested by their name, they were first identified as cell adhesion molecules at the synapse which were sufficient to trigger synapse formation...
September 1, 2016: Molecular and Cellular Neurosciences
https://www.readbyqxmd.com/read/27581450/neuroligins-are-selectively-essential-for-nmdar-signaling-in-cerebellar-stellate-interneurons
#12
Bo Zhang, Thomas C Südhof
UNLABELLED: Neuroligins are postsynaptic cell-adhesion molecules that contribute to synapse specification. However, many other postsynaptic cell-adhesion molecules are known and the relative contributions of neuroligins versus other such molecules in different types of synapses and neurons remains largely unknown. Here, we have studied the role of neuroligins in cerebellar stellate interneurons that participate in a well defined circuit that converges on Purkinje cells as the major output neurons of cerebellar cortex...
August 31, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27565350/proteomic-analysis-of-unbounded-cellular-compartments-synaptic-clefts
#13
Ken H Loh, Philipp S Stawski, Austin S Draycott, Namrata D Udeshi, Emily K Lehrman, Daniel K Wilton, Tanya Svinkina, Thomas J Deerinck, Mark H Ellisman, Beth Stevens, Steven A Carr, Alice Y Ting
Cellular compartments that cannot be biochemically isolated are challenging to characterize. Here we demonstrate the proteomic characterization of the synaptic clefts that exist at both excitatory and inhibitory synapses. Normal brain function relies on the careful balance of these opposing neural connections, and understanding how this balance is achieved relies on knowledge of their protein compositions. Using a spatially restricted enzymatic tagging strategy, we mapped the proteomes of two of the most common excitatory and inhibitory synaptic clefts in living neurons...
August 25, 2016: Cell
https://www.readbyqxmd.com/read/27473321/synaptic-adhesion-molecules-regulate-the-integration-of-new-granule-neurons-in-the-postnatal-mouse-hippocampus-and-their-impact-on-spatial-memory
#14
Marine Krzisch, Christine Fülling, Laura Jabinet, Jan Armida, Elias Gebara, Frédéric Cassé, Samia Habbas, Andrea Volterra, Jean-Pierre Hornung, Nicolas Toni
Postnatal hippocampal neurogenesis induces network remodeling and may participate to mechanisms of learning. In turn, the maturation and survival of newborn neurons is regulated by their activity. Here, we tested the effect of a cell-autonomous overexpression of synaptic adhesion molecules on the maturation and survival of neurons born postnatally and on hippocampal-dependent memory performances. Families of adhesion molecules are known to induce pre- and post-synaptic assembly. Using viral targeting, we overexpressed three different synaptic adhesion molecules, SynCAM1, Neuroligin-1B and Neuroligin-2A in newborn neurons in the dentate gyrus of 7- to 9-week-old mice...
July 29, 2016: Cerebral Cortex
https://www.readbyqxmd.com/read/27423632/hippocampal-and-motor-fronto-cortical-neuroligin1-is-increased-in-an-animal-model-of-depression
#15
Pingfu Feng, Afaf A Akladious, Yufen Hu
Neuroligins (NLGNs) regulate synaptic excitability, neuronal signaling and sleep. We hypothesize that alteration of NLGNs is involved in the pathology of depression and tested the hypothesis in a model of depression using Wistar Kyoto (WKy) rat and its control, the Wistar (Wis) rat. We first evaluated behavioral deficits using the forced swim test and then characterized alterations of NLGN1 and NLGN2 with RT-PCR and Western Blotting in the prefrontal cortex, motor frontal cortex and hippocampus. Compared with controls of Wis rats, (1) the WKy rats had significantly shorter swim time and longer immobile time; (2) NLGN1 mRNA levels was higher in the motor frontal cortex and hippocampus in the WKy model; (3) NLGN1 protein was significantly higher in the motor frontal cortex, the prefrontal cortex and the hippocampus in the WKy model; (4) NLGN2 mRNA was significantly higher in the motor frontal cortex but significantly lower in the hippocampus in the WKy model...
September 30, 2016: Psychiatry Research
https://www.readbyqxmd.com/read/27375445/odor-experiences-during-preimaginal-stages-cause-behavioral-and-neural-plasticity-in-adult-honeybees
#16
Gabriela Ramírez, Carol Fagundez, Juan P Grosso, Pablo Argibay, Andrés Arenas, Walter M Farina
In eusocial insects, experiences acquired during the development have long-term consequences on mature behavior. In the honeybee that suffers profound changes associated with metamorphosis, the effect of odor experiences at larval instars on the subsequent physiological and behavioral response is still unclear. To address the impact of preimaginal experiences on the adult honeybee, colonies containing larvae were fed scented food. The effect of the preimaginal experiences with the food odor was assessed in learning performance, memory retention and generalization in 3-5- and 17-19 day-old bees, in the regulation of their expression of synaptic-related genes and in the perception and morphology of their antennae...
2016: Frontiers in Behavioral Neuroscience
https://www.readbyqxmd.com/read/27300699/prenatal-exposure-to-histone-deacetylase-inhibitors-affects-gene-expression-of-autism-related-molecules-and-delays-neuronal-maturation
#17
Takuya Kawanai, Yukio Ago, Ryo Watanabe, Aya Inoue, Atsuki Taruta, Yusuke Onaka, Shigeru Hasebe, Hitoshi Hashimoto, Toshio Matsuda, Kazuhiro Takuma
Valproic acid (VPA) is a multi-target drug and an inhibitor of histone deacetylase (HDAC). We have previously demonstrated that prenatal exposure to VPA at embryonic day 12.5 (E12.5), but not at E14.5, causes autism-like behavioral abnormalities in male mouse offspring. We have also found that prenatal VPA exposure causes transient histone hyperacetylation in the embryonic brain, followed by decreased neuronal cell numbers in the prefrontal and somatosensory cortices after birth. In the present study, we examined whether prenatal HDAC inhibition affects neuronal maturation in primary mouse cortical neurons...
June 14, 2016: Neurochemical Research
https://www.readbyqxmd.com/read/27252060/er-stress-induced-aberrant-neuronal-maturation-and-neurodevelopmental-disorders
#18
Koichi Kawada, Takaaki Iekumo, Masayuki Kaneko, Yasuyuki Nomura, Yasunobu Okuma
Neurodevelopmental disorders, which include autism spectrum disorder, are congenital impairments in the growth and development of the central nervous system. They are mainly accentuated during infancy and childhood. Autism spectrum disorder may be caused by environmental factors, genomic imprinting of chromosome 15q11-q13 regions, and gene defects such as those in genes encoding neurexin and neuroligin, which are involved in synaptogenesis and synaptic signaling. However, regardless of the many reports on neurodevelopmental disorders, the pathogenic mechanism and treatment of neurodevelopmental disorders remain unclear...
2016: Yakugaku Zasshi: Journal of the Pharmaceutical Society of Japan
https://www.readbyqxmd.com/read/27240195/a-split-horseradish-peroxidase-for-the-detection-of-intercellular-protein-protein-interactions-and-sensitive-visualization-of-synapses
#19
Jeffrey D Martell, Masahito Yamagata, Thomas J Deerinck, Sébastien Phan, Carolyn G Kwa, Mark H Ellisman, Joshua R Sanes, Alice Y Ting
Intercellular protein-protein interactions (PPIs) enable communication between cells in diverse biological processes, including cell proliferation, immune responses, infection, and synaptic transmission, but they are challenging to visualize because existing techniques have insufficient sensitivity and/or specificity. Here we report a split horseradish peroxidase (sHRP) as a sensitive and specific tool for the detection of intercellular PPIs. The two sHRP fragments, engineered through screening of 17 cut sites in HRP followed by directed evolution, reconstitute into an active form when driven together by an intercellular PPI, producing bright fluorescence or contrast for electron microscopy...
July 2016: Nature Biotechnology
https://www.readbyqxmd.com/read/27225763/synapse-formation-in-monosynaptic-sensory-motor-connections-is-regulated-by-presynaptic-rho-gtpase-cdc42
#20
Fumiyasu Imai, David R Ladle, Jennifer R Leslie, Xin Duan, Tilat A Rizvi, Georgianne M Ciraolo, Yi Zheng, Yutaka Yoshida
UNLABELLED: Spinal reflex circuit development requires the precise regulation of axon trajectories, synaptic specificity, and synapse formation. Of these three crucial steps, the molecular mechanisms underlying synapse formation between group Ia proprioceptive sensory neurons and motor neurons is the least understood. Here, we show that the Rho GTPase Cdc42 controls synapse formation in monosynaptic sensory-motor connections in presynaptic, but not postsynaptic, neurons. In mice lacking Cdc42 in presynaptic sensory neurons, proprioceptive sensory axons appropriately reach the ventral spinal cord, but significantly fewer synapses are formed with motor neurons compared with wild-type mice...
May 25, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
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