Protein tyrosine phosphatase receptor type R is required for Purkinje cell responsiveness in cerebellar long-term depression

Erkens, Mirthe; Tanaka-Yamamoto, Keiko; Chéron, Guy; Márquez-Ruiz, Javier; Prigogine, Cynthia; Schepens, Jan; Kasri, Nael Nadif; Augustine, George J; Hendriks, Wiljan

doi:10.1186/s13041-014-0092-8

Cited by 62 publications

(67 citation statements)

References 67 publications

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“…We thus asked whether neuronal AKHR was also required for starvation-induced increase in food consumption. We first examined food consumption during the course of a single meal, by using a capillary-based feeding assay named the MAFE ( MA nual FE eding) assay ( Qi et al, 2015 ) ( Figure 3d ). We found that starvation could significantly increase food consumption, and that neuronal knock-down of AKHR did not affect starvation-induced increase in meal size ( Figure 3f ).…”

Section: Resultsmentioning

confidence: 99%

Regulation of starvation-induced hyperactivity by insulin and glucagon signaling in adult Drosophila

Huang

et al. 2016

eLife

126

177

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Starvation induces sustained increase in locomotion, which facilitates food localization and acquisition and hence composes an important aspect of food-seeking behavior. We investigated how nutritional states modulated starvation-induced hyperactivity in adult Drosophila. The receptor of the adipokinetic hormone (AKHR), the insect analog of glucagon, was required for starvation-induced hyperactivity. AKHR was expressed in a small group of octopaminergic neurons in the brain. Silencing AKHR+ neurons and blocking octopamine signaling in these neurons eliminated starvation-induced hyperactivity, whereas activation of these neurons accelerated the onset of hyperactivity upon starvation. Neither AKHR nor AKHR+ neurons were involved in increased food consumption upon starvation, suggesting that starvation-induced hyperactivity and food consumption are independently regulated. Single cell analysis of AKHR+ neurons identified the co-expression of Drosophila insulin-like receptor (dInR), which imposed suppressive effect on starvation-induced hyperactivity. Therefore, insulin and glucagon signaling exert opposite effects on starvation-induced hyperactivity via a common neural target in Drosophila.DOI: http://dx.doi.org/10.7554/eLife.15693.001

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Section: Resultsmentioning

confidence: 99%

Regulation of starvation-induced hyperactivity by insulin and glucagon signaling in adult Drosophila

Huang

et al. 2016

eLife

126

177

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“…It has also appeared difficult to study each step independently, many studies focusing on the global cytotoxicity resulting from aggregates internalization 16 20 27 31 . The binding step can be studied in vitro using artificial liposomes 11 22 32 33 34 , but this strategy neglects the prominent role of membrane proteins and the extracellular matrix in fibrils binding 10 13 17 35 . In this work we demonstrate, by measuring the binding of fibrils displaying identical structures and physico-chemical properties but different lengths to lipid vesicles and cultured cells, that fibril ends are not a prime determinant of the binding process of αSyn and HTTExon1 assemblies.…”

Section: Discussionmentioning

confidence: 99%

“…Different mechanisms have been proposed. The binding could be passive 10 , mediated by an interaction with the membrane lipids 11 , and/or with specific protein partners 12 13 14 . The efficiency of the binding seems to depend both on the aggregates characteristics, such as their charge or conformation 10 15 , and on the properties of the membrane, with an emphasis on the role of a specific lipid composition 16 17 or of the membrane curvature 18 19 .…”

mentioning

confidence: 99%

α-Synuclein and huntingtin exon 1 amyloid fibrils bind laterally to the cellular membrane

Monsellier¹,

Bousset²,

Melki³

2016

Sci Rep

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Fibrillar aggregates involved in neurodegenerative diseases have the ability to spread from one cell to another in a prion-like manner. The underlying molecular mechanisms, in particular the binding mode of the fibrils to cell membranes, are poorly understood. In this work we decipher the modality by which aggregates bind to the cellular membrane, one of the obligatory steps of the propagation cycle. By characterizing the binding properties of aggregates made of α-synuclein or huntingtin exon 1 protein displaying similar composition and structure but different lengths to mammalian cells we demonstrate that in both cases aggregates bind laterally to the cellular membrane, with aggregates extremities displaying little or no role in membrane binding. Lateral binding to artificial liposomes was also observed by transmission electron microscopy. In addition we show that although α-synuclein and huntingtin exon 1 fibrils bind both laterally to the cellular membrane, their mechanisms of interaction differ. Our findings have important implications for the development of future therapeutic tools that aim to block protein aggregates propagation in the brain.

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“…On the postsynaptic side, the endosomal system is involved in the insertion of integral neurotransmitter receptors in the plasma membrane, which is a mechanism of synaptic plasticity (see review 18 ). For example, depletion of the endosomal sorting protein VPS35 leads to decreased levels of glutamate receptors in the plasma membrane, reducing glutamatergic neurotransmission 19 – 21 . The glutamate ionotropic receptor AMPA type subunit 1 (gene GRIA1, Supplementary Table S2 , Supplementary Fig.…”

Section: Discussionmentioning

confidence: 99%

The endosomal protein sorting nexin 4 is a synaptic protein

Vázquez-Sánchez

Gonzalez‐Lozano

Walfenzao

et al. 2020

Sci Rep

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Sorting nexin 4 (SNX4) is an evolutionary conserved protein that mediates recycling from endosomes back to the plasma membrane in yeast and mammalian cells. SNX4 is expressed in the brain. Altered protein levels are associated with Alzheimer’s disease, but the neuronal localization and function of SNX4 have not been addressed. Using a new antibody, endogenous neuronal SNX4 co-localized with both early and recycling endosome markers, similar to the reported localization of SNX4 in non-neuronal cells. Neuronal SNX4 accumulated specifically in synaptic areas, with a predominant localization to presynaptic terminals. Acute depletion of neuronal SNX4 using independent short hairpin RNAs did not affect the levels of the transferrin receptor, a canonical SNX4 cargo. Quantitative mass spectrometry revealed that upon SNX4 knockdown the class of proteins involved in neurotransmission was the most dysregulated. This included integral membrane proteins at both the presynaptic and postsynaptic side of the synapse that participate in diverse synaptic processes such as synapse assembly, neurotransmission and the synaptic vesicle cycle. These data suggest that SNX4 is implicated in a variety of synaptic processes.

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Protein tyrosine phosphatase receptor type R is required for Purkinje cell responsiveness in cerebellar long-term depression

Cited by 62 publications

References 67 publications

Regulation of starvation-induced hyperactivity by insulin and glucagon signaling in adult Drosophila

Regulation of starvation-induced hyperactivity by insulin and glucagon signaling in adult Drosophila

α-Synuclein and huntingtin exon 1 amyloid fibrils bind laterally to the cellular membrane

The endosomal protein sorting nexin 4 is a synaptic protein

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