Molecular Mechanisms of Presynaptic Membrane Retrieval and Synaptic Vesicle Reformation

Kononenko, Natalia L.; Haucke, Volker

doi:10.1016/j.neuron.2014.12.016

Cited by 176 publications

(206 citation statements)

References 149 publications

(245 reference statements)

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“…Although ITSN1 has been linked to endocytosis at synapses (25,(31)(32)(33), defective Reelin signaling in absence of ITSN1 does not appear to arise from impaired endocytosis of either VLDLR or ApoER2 or from altered expression of these receptors on the neuronal surface (Fig. S8).…”

Section: Discussionmentioning

confidence: 99%

“…cell signaling (30), exocytosis/endocytosis (25,27,28,(31)(32)(33), development of dendritic spines (29,34), cortical midline connectivity (35), and spatial learning (35), its precise physiological function in the mammalian central nervous system in vivo remains incompletely understood. Here we identify ITSN1 as a component of Reelin signaling that acts predominantly by facilitating the VLDLR-Dab1 axis to direct neuronal migration in the forebrain and to augment synaptic plasticity.…”

Section: Significancementioning

confidence: 99%

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Intersectin 1 is a component of the Reelin pathway to regulate neuronal migration and synaptic plasticity in the hippocampus

Jakob

Kochlamazashvili

Jäpel

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Brain development and function depend on the directed and coordinated migration of neurons from proliferative zones to their final position. The secreted glycoprotein Reelin is an important factor directing neuronal migration. Loss of Reelin function results in the severe developmental disorder lissencephaly and is associated with neurological diseases in humans. Reelin signals via the lipoprotein receptors very low density lipoprotein receptor (VLDLR) and apolipoprotein E receptor 2 (ApoER2), but the exact mechanism by which these receptors control cellular function is poorly understood. We report that loss of the signaling scaffold intersectin 1 (ITSN1) in mice leads to defective neuronal migration and ablates Reelin stimulation of hippocampal long-term potentiation (LTP). Knockout (KO) mice lacking ITSN1 suffer from dispersion of pyramidal neurons and malformation of the radial glial scaffold, akin to the hippocampal lamination defects observed in VLDLR or ApoER2 mutants. ITSN1 genetically interacts with Reelin receptors, as evidenced by the prominent neuronal migration and radial glial defects in hippocampus and cortex seen in double-KO mice lacking ITSN1 and ApoER2. These defects were similar to, albeit less severe than, those observed in Reelin-deficient or VLDLR/ ApoER2 double-KO mice. Molecularly, ITSN1 associates with the VLDLR and its downstream signaling adaptor Dab1 to facilitate Reelin signaling. Collectively, these data identify ITSN1 as a component of Reelin signaling that acts predominantly by facilitating the VLDLR-Dab1 axis to direct neuronal migration in the cortex and hippocampus and to augment synaptic plasticity.Reelin signaling | hippocampus | synaptic plasticity | endocytosis | multidomain scaffold

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Section: Discussionmentioning

confidence: 99%

Section: Significancementioning

confidence: 99%

Intersectin 1 is a component of the Reelin pathway to regulate neuronal migration and synaptic plasticity in the hippocampus

Jakob

Kochlamazashvili

Jäpel

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…It has been proposed that different endocytotic pathways can coexist in one single synapse [69]. It therefore seems that different pathways are perhaps not different for neuronal subtypes in general, but that use of CME or fast membrane retrieval may be dependent on synaptic activity.…”

Section: [ 4 5 5 _ T D $ D I F F ] A-synuclein -A Possible Role In Slmentioning

confidence: 99%

α-Synuclein – Regulator of Exocytosis, Endocytosis, or Both?

Lautenschläger

Kaminski

Schierle

2017

Trends in Cell Biology

119

124

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a-Synuclein is known as a presynaptic protein that binds to small synaptic vesicles. Recent studies suggest that a-synuclein is not only attracted to these tiny and therewith highly curved membranes, but that in fact the sensing and regulation of membrane curvature is part of its physiological function. Moreover, recent studies have suggested that a-synuclein plays a role in the endocytosis of synaptic vesicles, and have provided support for a function of a-synuclein during exo-and endocytosis in which curvature sensing and membrane stabilization are crucial steps. This review aims to highlight recent research in the field and adds a new picture on the function of a-synuclein in maintaining synaptic homeostasis upon intense and repetitive neuronal activity.

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“…Exocytic membrane fusion has to be coupled to compensatory membrane retrieval to prevent membrane expansion and loss of tension, as well as to recycle vesicle or granule components. In neurons, fast and slow mechanisms of local presynaptic membrane retrieval and vesicle reformation have been described (Kononenko and Haucke, 2015). In contrast, much less is known about how granule membrane components are retrieved post-fusion in endocrine cells and how exo-endocytic coupling may occur.…”

mentioning

confidence: 99%

“…In neurons, exocytosis of neurotransmitter from synaptic vesicles occurs at specialized so-called active zones and is spatiotemporally coupled to the rapid retrieval of exocytosed vesicle proteins from the surrounding periactive zone area (Haucke et al, 2011) by clathrin-independent as well as clathrin-dependent endocytosis (CME) mechanisms (Kononenko and Haucke, 2015). Such close coupling of regulated exo-and endocytosis at synapses is crucial for sustained neurotransmission, e.g., to clear release sites of previously exocytosed material and to maintain the fusion competence of recycled synaptic vesicles (Hosoi et al, 2009).…”

mentioning

confidence: 99%