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in turncan causeneuronal damage by overactivating NMDA - type glutamate receptors and related signaling pathways
Hyperexcitability of neuronal networks ... in turncan causeneuronal damage by overactivating NMDA - type glutamate receptors and related signaling pathways
Hyperexcitability of neuronal networks ... in turncan causeneuronal damage by overactivating NMDA - type glutamate receptors and related signaling pathways
RON conformational change ... spontaneous dimerizationcausesconstitutive receptor phosphorylation and increased intracellular signaling activation
Alcoholinfluencesneurotransmitter systems in the brain , including glutamate receptors and the glutamate signaling pathway
synapsesinfluencessurface levels of glutamate receptors and synaptic function
synthesis ... synapsesinfluencessurface levels of glutamate receptors and synaptic function
energy failureleadingto high extracellular glutamate and over - activation of neuronal glutamate receptors
The activation of these receptorscausesan inhibitory effect on the release of neurotransmitters acetylcholine and glutamate
synaptic activityinfluencessynaptic development and glutamate receptor expression
synaptic activityinfluencessynaptic development and glutamate receptor expression ... and
Peripheral inflammationleadsto glutamate release from nociceptors and AMPA and NMDA receptor activation
Interaction with HLA - B or HLA - Eleadsto inhibition of FCER1A signaling and serotonin release
This Nootropic primarily affects the cholinergic and glutamatergic systemscausingan increased release of acetylcholine and glutamate neurotransmitters
the eventsresultingfrom ischemia and glutamate receptor activation
oxygen and glucose deprivation in organotypic hippocampal cultures(passive) caused byGlutamate and non - glutamate receptor mediated toxicity
the disinhibition of GABAergic interneuronscausesthe release of glutamate and the activation of glutamate receptors
the accumulation of glutamatewould ... resultin overstimulation of glutamate receptors and glutamate excitotoxicity
to be disturbed in breast cancerleadingto IGF1 receptor activation and uncontrolled tyrosine kinase signalling
This result could be usedto designpolarity indicators on the basis of the fluorescence signals
A poor diet ... omega-3 fatty acidsleadsto dysfunctions in insulin receptor signaling and cognition
Physiologic effectsresultfrom intracellular signaling of membrane receptors and ion channels
chromosomal rearrangements and mutationsresultin aberrant cytokine receptor and kinase signaling
various genesresultingfrom simultaneous stimulation of neurons by glutamate and a monoamine neurotransmitter
normalizing the corticosterone responseresultingin down - regulating of the pCaMKII and glutamate receptor levels
both by the binding of the chemoeffector ligand to the periplasmic domain and by methylation of specific glutamate residues on the cytoplasmic domain of the receptor(passive) are influencedSignaling outputs from chemotaxis receptors
The latter sitesinfluencethe signaling and function of receptors
In contrast , antagonistic ligands such as decorin could induce internalization via a caveolar - mediated pathwayleadingto attenuated signaling and intracellular proteolysis of the receptor
stress and lead to neuron damage(passive) can be caused byincreases in the neurotransmitter glutamate and the metabolite kynurenine
It is thoughtto influenceglutamate and acetylcholine receptors
It acts on a receptor in the brain called NMDA receptorto influenceneurotransmitter glutamate and GABA
to neuronal deathultimately leadingto neuronal death
to the pathogenesis of AD and glaucomacontributeto the pathogenesis of AD and glaucoma
some of the psychomotor and cognitive processes associated with schizophreniathereby may influencesome of the psychomotor and cognitive processes associated with schizophrenia
neurons to become more electrically excitedcausesneurons to become more electrically excited
to cell deathleadsto cell death
from reduced receptor internalization and resensitizationresultfrom reduced receptor internalization and resensitization
neuronal hyperexcitability and development of seizurescausesneuronal hyperexcitability and development of seizures
to enhanced accumulation ofleadsto enhanced accumulation of
to the pathobiology of NMOcould contribute indirectlyto the pathobiology of NMO
to FM1 - 43 destainingledto FM1 - 43 destaining
to increased intracellular levels of Ca2leadsto increased intracellular levels of Ca2
to excitotoxic neuronal injury ( Sattler et al . , 2001leadto excitotoxic neuronal injury ( Sattler et al . , 2001
to STAT activationleadingto STAT activation
to the induction and regulation of synaptic plasticity - including long term potentiation ( LTP ) and long term depression ( LTDcontributeto the induction and regulation of synaptic plasticity - including long term potentiation ( LTP ) and long term depression ( LTD
a reduction in F - actinalso causeda reduction in F - actin
to a cascade of events that culminate in excitotoxic cell death ( for review , see refs , 70 and 71leadsto a cascade of events that culminate in excitotoxic cell death ( for review , see refs , 70 and 71
in contact - depending killing of targets and cytokine productionresultin contact - depending killing of targets and cytokine production
in apoptosis of cancer cells ( 43resultsin apoptosis of cancer cells ( 43
alsocontributesalso
to opposing influences on cAMP responseleadingto opposing influences on cAMP response
apoptosis in autismmay causeapoptosis in autism
excitement in the braincan ... causeexcitement in the brain
to opposing influences on cAMP response element - binding proteinleadingto opposing influences on cAMP response element - binding protein
to Ca2 + overload , the latter via phospholipase C and Ins(1,4,5contributeto Ca2 + overload , the latter via phospholipase C and Ins(1,4,5
alsocan causealso
in exaggerated long - term depressionresultsin exaggerated long - term depression
from too little glutamate presentmay resultfrom too little glutamate present
increases in electrical excitement in neuronscausesincreases in electrical excitement in neurons
a reduction in F - actincauseda reduction in F - actin
to enhanced cognitive function such as increased learning and memoryleadingto enhanced cognitive function such as increased learning and memory
to excitotoxicity andcan contributeto excitotoxicity and
to OFFcenter and ON - center bipolar cell responsesleadto OFFcenter and ON - center bipolar cell responses
in impaired spatial learningresultingin impaired spatial learning
in neuronal deathcan resultin neuronal death
from the ... Analysisoriginatingfrom the ... Analysis
significantlyDo ... contributesignificantly
in synaptic dysfunction and lossultimately resultingin synaptic dysfunction and loss
from the surface layeroriginatingfrom the surface layer
to subsequent excitotoxicityleadsto subsequent excitotoxicity
to GABA synthesis and inhibitory synaptic strengthcontributesto GABA synthesis and inhibitory synaptic strength