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the deletion of pex14resultedin cytoplasmic redistribution of TmpL - GFP and DsRed - AbHex1 fluorescence signals
two distinct ionic conductancescausedepolarization and developmentally precede GABA and l - glutamate signaling
a slow neuromodulatory pathwayleadsto increased AT1 and glutamate receptor - dependent signaling in the PVN
The data suggest that uptake of glutamate , which is predominately carriedout by glial cellscan preventspill - over of glutamate and activation of metabotropic glutamate receptors
pathwaysleadingto increased AT1 and glutamate receptor - dependent signaling in the PVN
molecular crowding in the post - synaptic densitycausesanomalous diffusion of glutamate receptors
2 ) elevation of neurotoxic Hcy and homocysteic acidcausingactivation of NMDA and glutamate receptors
inflammatory pro- cessescan contributeto ictogenesis ... power enhance signaling via glutamate receptors and ebb GABAergic signaling
loss of presynaptic presenilin ... sufficientto causeimpaired glutamate neurotransmitter release and LTP
the accumulation of glutamatewould ... resultin overstimulation of glutamate receptors and glutamate excitotoxicity
Algernon ’s lead compound ... the NMDA receptor glutamatepreventssignaling by the neurotransmitter glutamate
the excitatory transmission between neuronsinfluencethe excitatory transmission between neurons
in calcium signaling , a major form of glial excitabilitycan resultin calcium signaling , a major form of glial excitability
rapid dopaminergic activity and thus the communication of behaviorally relevant information from ventral tegmental area dopamine cells to forebrain areasinfluencerapid dopaminergic activity and thus the communication of behaviorally relevant information from ventral tegmental area dopamine cells to forebrain areas
local MMP-9 release ... leading to MMP - mediated synaptic plasticity events [ 104–106 ... presumably via extracellular proteins , such as integrins , laminins , cadherins , β - dystroglycan , brevican , and tenascin - R , which have all been implicated in hippocampal LTP [ 57 , 58 , 67causeslocal MMP-9 release ... leading to MMP - mediated synaptic plasticity events [ 104–106 ... presumably via extracellular proteins , such as integrins , laminins , cadherins , β - dystroglycan , brevican , and tenascin - R , which have all been implicated in hippocampal LTP [ 57 , 58 , 67
This learning benefit(passive) is caused byThis learning benefit
alsocan causealso
to depolarisation.93 Excessive or uncontrolled depolarisation of neuronsleadsto depolarisation.93 Excessive or uncontrolled depolarisation of neurons
in exaggerated long - term depressionresultsin exaggerated long - term depression
kar activation(passive) is influenced bykar activation
in increased motivation and energy levelsresultin increased motivation and energy levels