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Emerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and DiseaseDefective neuromuscular synaptogenesis in agrin-deficient mutant miceDevelopmental expression of two-pore domain K+ channels, TASK-1 and TREK-1, in the rat cochleaPostnatal changes in TASK-1 and TREK-1 expression in rat brain stem and cerebellum43K protein and acetylcholine receptors colocalize during the initial stages of neuromuscular synapse formation in vivoA rat model of ataxia-telangiectasia: evidence for a neurodegenerative phenotype.Rats with a missense mutation in Atm display neuroinflammation and neurodegeneration subsequent to accumulation of cytosolic DNA following unrepaired DNA damage.Functional decline at the aging neuromuscular junction is associated with altered laminin-α4 expression.Myocardial deletion of Smad4 using a novel α skeletal muscle actin Cre recombinase transgenic mouse causes misalignment of the cardiac outflow tractGenetic deficiency of GABA differentially regulates respiratory and non-respiratory motor neuron development.Targeting of the ETS factor GABPalpha disrupts neuromuscular junction synaptic function.Clustering and immobilization of acetylcholine receptors by the 43-kD protein: a possible role for dystrophin-related protein.Structural and functional characterization of dendritic arbors and GABAergic synaptic inputs on interneurons and principal cells in the rat basolateral amygdala.Neural agrin: a synaptic stabiliser.Tick holocyclotoxins trigger host paralysis by presynaptic inhibition.Marked changes in dendritic structure and spine density precede significant neuronal death in vulnerable cortical pyramidal neuron populations in the SOD1(G93A) mouse model of amyotrophic lateral sclerosisDevelopmental changes in the morphology of mouse hypoglossal motor neuronsDysregulation of the complement cascade in the hSOD1G93A transgenic mouse model of amyotrophic lateral sclerosis.The C5a anaphylatoxin receptor CD88 is expressed in presynaptic terminals of hippocampal mossy fibres.Cortical synaptic and dendritic spine abnormalities in a presymptomatic TDP-43 model of amyotrophic lateral sclerosis.Neuregulin-1 potentiates agrin-induced acetylcholine receptor clustering through muscle-specific kinase phosphorylation.Neural agrin increases postsynaptic ACh receptor packing by elevating rapsyn protein at the mouse neuromuscular synapse.IGF-I and insulin activate mitogen-activated protein kinase via the type 1 IGF receptor in mouse embryonic stem cells.Rapsyn interaction with calpain stabilizes AChR clusters at the neuromuscular junction.Failure of postsynaptic specialization to develop at neuromuscular junctions of rapsyn-deficient mice.Cross-ethnic meta-analysis identifies association of the GPX3-TNIP1 locus with amyotrophic lateral sclerosis.Loss of laminin-α4 results in pre- and postsynaptic modifications at the neuromuscular junction.Role for terminal complement activation in amyotrophic lateral sclerosis disease progression.Solving the alpha-conotoxin folding problem: efficient selenium-directed on-resin generation of more potent and stable nicotinic acetylcholine receptor antagonists.Glycinergic and GABAergic synaptic activity differentially regulate motoneuron survival and skeletal muscle innervation.Motor Areas Show Altered Dendritic Structure in an Amyotrophic Lateral Sclerosis Mouse Model.Investigating Methodological Differences in the Assessment of Dendritic Morphology of Basolateral Amygdala Principal Neurons-A Comparison of Golgi-Cox and Neurobiotin Electroporation Techniques.Defects in synaptic transmission at the neuromuscular junction precedes motor deficits in a TDP-43Q331K transgenic mouse model of amyotrophic lateral sclerosis.Regulated Alternative Splicing of DrosophilaDscam2 Is Necessary for Attaining the Appropriate Number of Photoreceptor Synapses.Glycinergic Neurotransmission: A Potent Regulator of Embryonic Motor Neuron Dendritic Morphology and Synaptic Plasticity.Identification of RNA bound to the TDP-43 ribonucleoprotein complex in the adult mouse brain.Pharmacological inhibition of complement C5a-C5a1 receptor signalling ameliorates disease pathology in the hSOD1G93A mouse model of amyotrophic lateral sclerosis.Motor cortex layer V pyramidal neurons exhibit dendritic regression, spine loss, and increased synaptic excitation in the presymptomatic hSOD1(G93A) mouse model of amyotrophic lateral sclerosis.Alterations in hypoglossal motor neurons due to GAD67 and VGAT deficiency in mice.Genetic absence of the vesicular inhibitory amino acid transporter differentially regulates respiratory and locomotor motor neuron development.
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description
researcher
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wetenschapper
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Noakes PG
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Noakes PG
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Peter G. Noakes
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Noakes PG
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Noakes PG
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Peter G. Noakes
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Noakes PG
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Noakes PG
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Noakes PG
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Peter G. Noakes
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P108
P106
P31
P496
0000-0001-9821-8478