about
Latrophilin 1 and its endogenous ligand Lasso/teneurin-2 form a high-affinity transsynaptic receptor pair with signaling capabilitiesThe multiple actions of black widow spider toxins and their selective use in neurosecretion studiesDifferential triggering of spontaneous glutamate release by P/Q-, N- and R-type Ca2+ channels.Independent regulation of basal neurotransmitter release efficacy by variable Ca²+ influx and bouton size at small central synapses.Lambert-Eaton syndrome IgG inhibits transmitter release via P/Q Ca2+ channels.Calmodulin as a major calcium buffer shaping vesicular release and short-term synaptic plasticity: facilitation through buffer dislocationDifferent transporter systems regulate extracellular GABA from vesicular and non-vesicular sourcesAction potential broadening in a presynaptic channelopathy.Nanoscale-targeted patch-clamp recordings of functional presynaptic ion channels.Is levetiracetam different from other antiepileptic drugs? Levetiracetam and its cellular mechanism of action in epilepsy revisited.alpha-Latrotoxin, acting via two Ca2+-dependent pathways, triggers exocytosis of two pools of synaptic vesicles.Functional expression of alpha-latrotoxin in baculovirus system.Low Stress Ion Conductance Microscopy of Sub-Cellular Stiffness.Functional cross-interaction of the fragments produced by the cleavage of distinct adhesion G-protein-coupled receptors.Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization.CaMKII translocation requires local NMDA receptor-mediated Ca2+ signaling.Mutant alpha-latrotoxin (LTXN4C) does not form pores and causes secretion by receptor stimulation: this action does not require neurexins.Structure of alpha-latrotoxin oligomers reveals that divalent cation-dependent tetramers form membrane pores.Presynaptic fluctuations and release-independent depression.The alpha-latrotoxin mutant LTXN4C enhances spontaneous and evoked transmitter release in CA3 pyramidal neurons.Alternative Splicing of P/Q-Type Ca2+ Channels Shapes Presynaptic Plasticity.Latrophilin, Neurexin, and Their Signaling-deficient Mutants Facilitate α-Latrotoxin Insertion into Membranes but Are Not Involved in Pore FormationTetramerisation of α-latrotoxin by divalent cations is responsible for toxin-induced non-vesicular release and contributes to the Ca2+-dependent vesicular exocytosis from synaptosomesAlpha-latrotoxin modulates the secretory machinery via receptor-mediated activation of protein kinase CSynaptotagmin 1 oligomers clamp and regulate different modes of neurotransmitter releasePreparation of dissociated mouse primary neuronal cultures from long-term cryopreserved brain tissue
P50
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P50
description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Kirill E Volynski
@ast
Kirill E Volynski
@es
Kirill E Volynski
@nl
Kirill E Volynski
@sl
Kirill Volynski
@de
Kirill Volynski
@en
Кирилл Евгеньевич Волынский
@ru
type
label
Kirill E Volynski
@ast
Kirill E Volynski
@es
Kirill E Volynski
@nl
Kirill E Volynski
@sl
Kirill Volynski
@de
Kirill Volynski
@en
Кирилл Евгеньевич Волынский
@ru
altLabel
Kirill E Volynski
@en
Kirill Jewgenjewitsch Wolynski
@de
Kirill Volynsky
@en
Kirill Wolynski
@de
Kirll Yevgenyevich Volynsky
@en
prefLabel
Kirill E Volynski
@ast
Kirill E Volynski
@es
Kirill E Volynski
@nl
Kirill E Volynski
@sl
Kirill Volynski
@de
Kirill Volynski
@en
Кирилл Евгеньевич Волынский
@ru
P106
P21
P31
P496
0000-0001-8208-1905