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Neuroscience_topics
Neuroscience: CNS disease, pain, brain research, ion channels, synaptic transmission, channelopathies, neuronal network
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Scooped by Julien Hering, PhD
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The mechanisms and functions of spontaneous neurotransmitter release

The mechanisms and functions of spontaneous neurotransmitter release | Neuroscience_topics | Scoop.it

Fast synaptic communication in the brain requires synchronous vesicle fusion that is evoked by action potential-induced Ca2+ influx. However, synaptic terminals also release neurotransmitters by spontaneous vesicle fusion, which is independent of presynaptic action potentials. A functional role for spontaneous neurotransmitter release events in the regulation of synaptic plasticity and homeostasis, as well as the regulation of certain behaviours, has been reported. In addition, there is evidence that the presynaptic mechanisms underlying spontaneous release of neurotransmitters and their postsynaptic targets are segregated from those of evoked neurotransmission. These findings challenge current assumptions about neuronal signalling and neurotransmission, as they indicate that spontaneous neurotransmission has an autonomous role in interneuronal communication that is distinct from that of evoked release.(...) -  by David Holcman & Rafael Yuste, Nature Reviews Neuroscience,  16, 5–16 (2015)

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The Number and Organization of Ca2+ Channels in the Active Zone Shapes Neurotransmitter Release from Schaffer Collateral Synapses

The Number and Organization of Ca2+ Channels in the Active Zone Shapes Neurotransmitter Release from Schaffer Collateral Synapses | Neuroscience_topics | Scoop.it
[Abstract] Fast synaptic transmission requires tight colocalization of Ca2+ channels and neurotransmitter vesicles. It is generally thought that Ca2+ channels are expressed abundantly in presynaptic active zones, that vesicles within the same active zone have similar release properties, and that significant vesicle depletion only occurs at synapses with high release probability. Here we show, at excitatory CA3→CA1 synapses in mouse hippocampus, that release from individual vesicles is generally triggered by only one Ca2+ channel and that only few functional Ca2+ channels may be spread in the active zone at variable distances to neighboring neurotransmitter vesicles. Using morphologically realistic Monte Carlo simulations, we show that this arrangement leads to a widely heterogeneous distribution of release probability across the vesicles docked at the active zone, and that depletion of the vesicles closest to Ca2+ channels can account for the Ca2+ dependence of short-term plasticity at these synapses. These findings challenge the prevailing view that efficient synaptic transmission requires numerous presynaptic Ca2+ channels in the active zone, and indicate that the relative arrangement of Ca2+ channels and vesicles contributes to the heterogeneity of release probability within and across synapses and to vesicle depletion at small central synapses with low average release probability. - by Scimemi A. & Diamond J.S., The Journal of Neuroscience, 12 December 2012, 32(50): 18157-18176
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[Review] Neurotransmitter Transporters: Structure Meets Function

[Review] Neurotransmitter Transporters: Structure Meets Function | Neuroscience_topics | Scoop.it
Highlights
  • Review of sodium coupling and conformational change in neurotransmitter transporter
  • Side-by-side structural comparison of transporter homologs GltPh and LeuT
  • Relating crystal structures of GltPh and LeuT to functional data and simulations
  • Structural and functional implications of sodium coupling in these transporters

(...) - by Focke PJ et al.StructureVolume 21, Issue 5, 694-705, 7 May 2013

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Glycine receptors support excitatory neurotransmitter release in developing mouse visual cortex

[Abstract] Glycine receptors (GlyRs) are found in most areas of the brain, and their dysfunction can cause severe neurological disorders. While traditionally thought of as inhibitory receptors, presynaptic-acting GlyRs (preGlyRs) can also facilitate glutamate release under certain circumstances, although the underlying molecular mechanisms are unknown. In the current study, we sought to better understand the role of GlyRs in the facilitation of excitatory neurotransmitter release in mouse visual cortex. Using whole-cell recordings, we found that preGlyRs facilitate glutamate release in developing, but not adult, visual cortex. The glycinergic enhancement of neurotransmitter release in early development depends on the high intracellular to extracellular Cl− gradient maintained by the Na+–K+–2Cl− cotransporter and requires Ca2+ entry through voltage-gated Ca2+ channels. The glycine transporter 1, localized to glial cells, regulates extracellular glycine concentration and the activation of these preGlyRs. Our findings demonstrate a developmentally regulated mechanism for controlling excitatory neurotransmitter release in the neocortex. - by Kunz PA et al., November 15, 2012, The Journal of Physiology, 590, 5749-5764

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