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Wenqin Luo - One of the best experts on this subject based on the ideXlab platform.
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aversive learning increases Release probability of olfactory sensory neurons
Current Biology, 2020Co-Authors: Janardhan P Bhattarai, Mary Schreck, Andrew H Moberly, Wenqin LuoAbstract:Summary Predicting danger from previously associated sensory stimuli is essential for survival. Contributions from altered peripheral sensory inputs are implicated in this process, but the underlying mechanisms remain elusive. Here, we use the mammalian olfactory system to investigate such mechanisms. Primary olfactory sensory neurons (OSNs) project their axons directly to the olfactory bulb (OB) glomeruli, where their Synaptic Release is subject to local and cortical influence and neuromodulation. Pairing optogenetic activation of a single glomerulus with foot shock in mice induces freezing to light stimulation alone during fear retrieval. This is accompanied by an increase in OSN Release probability and a reduction in GABAB receptor expression in the conditioned glomerulus. Furthermore, freezing time is positively correlated with the Release probability of OSNs in fear-conditioned mice. These results suggest that aversive learning increases peripheral olfactory inputs at the first synapse, which may contribute to the behavioral outcome.
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aversive learning increases Release probability of olfactory sensory neurons
bioRxiv, 2019Co-Authors: Janardhan P Bhattarai, Mary Schreck, Andrew H Moberly, Wenqin LuoAbstract:Abstract Predicting danger from previously associated sensory stimuli is essential for survival. Contributions from altered peripheral sensory inputs are implicated in this process, but the underlying mechanisms remain elusive. Here we use the mammalian olfactory system to investigate such mechanisms. Primary olfactory sensory neurons (OSNs) project their axons directly to the olfactory bulb (OB) glomeruli where their Synaptic Release is subject to local and cortical influence and neuromodulation. Pairing optogenetic activation of a single glomerulus with foot shock in mice induces freezing to the light stimulation alone during fear retrieval. This is accompanied by an increase in OSN Release probability and a reduction in GABAB receptor expression in the conditioned glomerulus. Furthermore, freezing time is positively correlated with the Release probability of OSNs in fear conditioned mice. These results suggest that aversive learning increases peripheral olfactory inputs at the first synapse, which may contribute to the behavioral outcome.
Kalina T Haas - One of the best experts on this subject based on the ideXlab platform.
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pre post Synaptic alignment through neuroligin 1 tunes Synaptic transmission efficiency
eLife, 2018Co-Authors: Dolors Grillobosch, Kalina T Haas, Benjamin Compans, Mathieu Letellier, Thomas M Bartol, Terrence J. SejnowskiAbstract:The nanoscale organization of neurotransmitter receptors regarding pre-Synaptic Release sites is a fundamental determinant of the Synaptic transmission amplitude and reliability. How modifications in the pre- and post-Synaptic machinery alignments affects Synaptic currents, has only been addressed with computer modelling. Using single molecule super-resolution microscopy, we found a strong spatial correlation between AMPA receptor (AMPAR) nanodomains and the post-Synaptic adhesion protein neuroligin-1 (NLG1). Expression of a truncated form of NLG1 disrupted this correlation without affecting the intrinsic AMPAR organization, shifting the pre-Synaptic Release machinery away from AMPAR nanodomains. Electrophysiology in dissociated and organotypic hippocampal rodent cultures shows these treatments significantly decrease AMPAR-mediated miniature and EPSC amplitudes. Computer modelling predicts that ~100 nm lateral shift between AMPAR nanoclusters and glutamate Release sites induces a significant reduction in AMPAR-mediated currents. Thus, our results suggest the synapses necessity to Release glutamate precisely in front of AMPAR nanodomains, to maintain a high Synaptic responses efficiency.
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pre post Synaptic alignment through neuroligin tunes Synaptic transmission efficiency
bioRxiv, 2017Co-Authors: Eric Hosy, Dolors Grillobosch, Kalina T Haas, Benjamin Compans, Mathieu Letellier, Thomas M Bartol, Terrence J. Sejnowski, Daniel Choquet, Olivier ThoumineAbstract:The nanoscale organization of neurotransmitter receptors relative to pre-Synaptic Release sites is a fundamental determinant of both amplitude and reliability of Synaptic transmission. How modifications in the alignment between pre- and post-Synaptic machineries affect Synaptic current properties has only been addressed with computer modeling, and therefore remains hypothetical. Using dual-color single molecule based super-resolution microscopy, we found a strong spatial correlation between AMPA receptor (AMPAR) nanodomains and the post-Synaptic adhesion protein neuroligin-1 (NLG1). Expression of a C-terminal truncated form of NLG1 disrupted this correlation without affecting the intrinsic organization of AMPAR nanodomains. Moreover, this NLG1 dominant-negative mutant significantly shifted the pre-Synaptic Release machinery from AMPAR Synaptic clusters. Electrophysiology and computer modeling show that this physical shift is sufficient to induce a significant decrease in Synaptic transmission. Thus, our results suggest the necessity for synapses to Release glutamate in front of AMPAR nanodomains, to maintain a high efficiency of Synaptic responses.
Dolors Grillobosch - One of the best experts on this subject based on the ideXlab platform.
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pre post Synaptic alignment through neuroligin 1 tunes Synaptic transmission efficiency
eLife, 2018Co-Authors: Dolors Grillobosch, Kalina T Haas, Benjamin Compans, Mathieu Letellier, Thomas M Bartol, Terrence J. SejnowskiAbstract:The nanoscale organization of neurotransmitter receptors regarding pre-Synaptic Release sites is a fundamental determinant of the Synaptic transmission amplitude and reliability. How modifications in the pre- and post-Synaptic machinery alignments affects Synaptic currents, has only been addressed with computer modelling. Using single molecule super-resolution microscopy, we found a strong spatial correlation between AMPA receptor (AMPAR) nanodomains and the post-Synaptic adhesion protein neuroligin-1 (NLG1). Expression of a truncated form of NLG1 disrupted this correlation without affecting the intrinsic AMPAR organization, shifting the pre-Synaptic Release machinery away from AMPAR nanodomains. Electrophysiology in dissociated and organotypic hippocampal rodent cultures shows these treatments significantly decrease AMPAR-mediated miniature and EPSC amplitudes. Computer modelling predicts that ~100 nm lateral shift between AMPAR nanoclusters and glutamate Release sites induces a significant reduction in AMPAR-mediated currents. Thus, our results suggest the synapses necessity to Release glutamate precisely in front of AMPAR nanodomains, to maintain a high Synaptic responses efficiency.
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pre post Synaptic alignment through neuroligin tunes Synaptic transmission efficiency
bioRxiv, 2017Co-Authors: Eric Hosy, Dolors Grillobosch, Kalina T Haas, Benjamin Compans, Mathieu Letellier, Thomas M Bartol, Terrence J. Sejnowski, Daniel Choquet, Olivier ThoumineAbstract:The nanoscale organization of neurotransmitter receptors relative to pre-Synaptic Release sites is a fundamental determinant of both amplitude and reliability of Synaptic transmission. How modifications in the alignment between pre- and post-Synaptic machineries affect Synaptic current properties has only been addressed with computer modeling, and therefore remains hypothetical. Using dual-color single molecule based super-resolution microscopy, we found a strong spatial correlation between AMPA receptor (AMPAR) nanodomains and the post-Synaptic adhesion protein neuroligin-1 (NLG1). Expression of a C-terminal truncated form of NLG1 disrupted this correlation without affecting the intrinsic organization of AMPAR nanodomains. Moreover, this NLG1 dominant-negative mutant significantly shifted the pre-Synaptic Release machinery from AMPAR Synaptic clusters. Electrophysiology and computer modeling show that this physical shift is sufficient to induce a significant decrease in Synaptic transmission. Thus, our results suggest the necessity for synapses to Release glutamate in front of AMPAR nanodomains, to maintain a high efficiency of Synaptic responses.
Roger A. Nicoll - One of the best experts on this subject based on the ideXlab platform.
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Kainate receptors depress excitatory Synaptic transmission at CA3right-arrowCA1 synapses in the hippocampus via a direct preSynaptic action
2013Co-Authors: Matthew Frerking, Dietmar Schmitz, Qiang Zhou, Joshua Johansen, Roger A. NicollAbstract:Kainate receptor activation depresses Synaptic Release of neurotransmitter at a number of synapses in the CNS. The mechanism underlying this depression is controversial, and both ionotropic and metabotropic mechanisms have been suggested. We report here that the AMPA/kainate receptor agonists domoate (DA) and kainate (KA) cause a preSynaptic depression of glutamatergic transmission at CA33CA1 synapses in the hippocampus, which is not blocked by the AMPA receptor antagonist GYKI 53655 but is blocked by the AMPA/KA receptor antagonist CNQX. Neither a blockade of interneuronal discharge nor antagonists of several neuromodulators affect the depression, suggesting that it is not the result of indirect excitation and subsequent Release of a neuromodulator. PreSynaptic depolarization, achieved via increasing extracellular K � , caused a depression of the preSynaptic fiber volley and a
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Vesicular glutamate transporters 1 and 2 target to functionally distinct Synaptic Release sites.
Science (New York N.Y.), 2004Co-Authors: Robert T. Fremeau, Roger A. Nicoll, Kaiwen Kam, Tayyaba Qureshi, Juliette Johnson, David R. Copenhagen, Jon Storm-mathisen, Farrukh A. Chaudhry, Robert H. EdwardsAbstract:Vesicular glutamate transporters (VGLUTs) 1 and 2 show a mutually exclusive distribution in the adult brain that suggests specialization for synapses with different properties of Release. Consistent with this distribution, inactivation of the VGLUT1 gene silenced a subset of excitatory neurons in the adult. However, the same cell populations exhibited VGLUT1-independent transmission early in life. Developing hippocampal neurons transiently coexpressed VGLUT2 and VGLUT1 at distinct Synaptic sites with different short-term plasticity. The loss of VGLUT1 also reduced the reserve pool of Synaptic vesicles. Thus, VGLUT1 plays an unanticipated role in membrane trafficking at the nerve terminal.
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Synaptic activation of preSynaptic kainate receptors on hippocampal mossy fiber synapses
Neuron, 2000Co-Authors: Dietmar Schmitz, Matthew Frerking, Roger A. NicollAbstract:Kainate receptors (KARs) are a poorly understood family of ionotropic glutamate receptors. A role for these receptors in the preSynaptic control of transmitter Release has been proposed but remains controversial. Here, KAR agonists are shown to enhance fiber excitability, and a number of experiments show that this is a direct effect of KARs on the preSynaptic fibers. In addition, KAR activation inhibits evoked transmitter Release from mossy fiber synapses. Synaptic Release of glutamate from either neighboring mossy fiber synapses or associational/commisural (A/C) synapses results in the activation of these preSynaptic ionotropic KARs. These results, along with previous studies, indicate that KARs, through the endogenous Release of glutamate, mediate excitatory postSynaptic potentials (EPSPs), alter preSynaptic excitability, and modulate transmitter Release.
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the role of the synthetic enzyme gad65 in the control of neuronal γ aminobutyric acid Release
Proceedings of the National Academy of Sciences of the United States of America, 1999Co-Authors: Ning Tian, David R. Copenhagen, Carl C H Petersen, Shera F Kash, Steinunn Baekkeskov, Roger A. NicollAbstract:We have studied GABAergic Synaptic transmission in retinal ganglion cells and hippocampal pyramidal cells to determine, at a cellular level, what is the effect of the targeted disruption of the gene encoding the synthetic enzyme GAD65 on the Synaptic Release of γ-aminobutyric acid (GABA). Neither the size nor the frequency of GABA-mediated spontaneous inhibitory postSynaptic currents (IPSCs) were reduced in retina or hippocampus in GAD65−/− mice. However, the Release of GABA during sustained Synaptic activation was substantially reduced. In the retina both electrical- and K+-induced increases in IPSC frequency were depressed without a change in IPSC amplitude. In the hippocampus the transient increase in the probability of inhibitory transmitter Release associated with posttetanic potentiation was absent in the GAD65−/− mice. These results indicate that during and immediately after sustained stimulation the increase in the probability of transmitter Release is not maintained in GAD65−/− mice. Such a finding suggests a decrease in the size or refilling kinetics of the releasable pool of vesicles, and various mechanisms are discussed that could account for such a defect.
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the opioid peptide dynorphin mediates heteroSynaptic depression of hippocampal mossy fibre synapses and modulates long term potentiation
Nature, 1993Co-Authors: Marc G Weisskopf, Robert A Zalutsky, Roger A. NicollAbstract:The mossy fibre pathway in the hippocampus uses glutamate as a neurotransmitter, but also contains the opioid peptide dynorphin. Synaptic Release of dynorphin causes a preSynaptic inhibition of neighbouring mossy fibres and inhibits the induction and expression of mossy fibre long-term potentiation. These findings demonstrate a physiological role for a neuropeptide in the central nervous system, provide a functional basis for the coexistence of a neuropeptide with classic neurotransmitters and demonstrate the very different roles played by these two classes of signalling molecules.
Janardhan P Bhattarai - One of the best experts on this subject based on the ideXlab platform.
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aversive learning increases Release probability of olfactory sensory neurons
Current Biology, 2020Co-Authors: Janardhan P Bhattarai, Mary Schreck, Andrew H Moberly, Wenqin LuoAbstract:Summary Predicting danger from previously associated sensory stimuli is essential for survival. Contributions from altered peripheral sensory inputs are implicated in this process, but the underlying mechanisms remain elusive. Here, we use the mammalian olfactory system to investigate such mechanisms. Primary olfactory sensory neurons (OSNs) project their axons directly to the olfactory bulb (OB) glomeruli, where their Synaptic Release is subject to local and cortical influence and neuromodulation. Pairing optogenetic activation of a single glomerulus with foot shock in mice induces freezing to light stimulation alone during fear retrieval. This is accompanied by an increase in OSN Release probability and a reduction in GABAB receptor expression in the conditioned glomerulus. Furthermore, freezing time is positively correlated with the Release probability of OSNs in fear-conditioned mice. These results suggest that aversive learning increases peripheral olfactory inputs at the first synapse, which may contribute to the behavioral outcome.
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aversive learning increases Release probability of olfactory sensory neurons
bioRxiv, 2019Co-Authors: Janardhan P Bhattarai, Mary Schreck, Andrew H Moberly, Wenqin LuoAbstract:Abstract Predicting danger from previously associated sensory stimuli is essential for survival. Contributions from altered peripheral sensory inputs are implicated in this process, but the underlying mechanisms remain elusive. Here we use the mammalian olfactory system to investigate such mechanisms. Primary olfactory sensory neurons (OSNs) project their axons directly to the olfactory bulb (OB) glomeruli where their Synaptic Release is subject to local and cortical influence and neuromodulation. Pairing optogenetic activation of a single glomerulus with foot shock in mice induces freezing to the light stimulation alone during fear retrieval. This is accompanied by an increase in OSN Release probability and a reduction in GABAB receptor expression in the conditioned glomerulus. Furthermore, freezing time is positively correlated with the Release probability of OSNs in fear conditioned mice. These results suggest that aversive learning increases peripheral olfactory inputs at the first synapse, which may contribute to the behavioral outcome.
