endogenous ET-1may ... influencesynaptic transmission in the NTS
the potentialto strongly influenceafferent synaptic transmission
Here we have explored the ability of endogenous dopamine , present in slices containing the prefrontal cortexto influenceexcitatory synaptic transmission
SHANK3 deficiency is knownto causeimpairments in synaptic transmission
drug actionsinfluencingGABAergic synaptic transmission
AD - related presenilin mutation ( 3(passive) caused byexcitatory synaptic transmission
exocytosis of the acidic contents of synaptic vesicles(passive) is caused byexcitatory synaptic transmission
gene mutation or environmental toxicantinfluencessynaptic transmission at all
the loss of proteins at excitatory synaptic inputs(passive) caused byglutamatergic synaptic transmission
disruptions in a specific synaptic proteinmight influenceaberrant synaptic transmission
Altered ubiquitination of these substrates when Nedd4 - 2 ’s function is compromisedcould contributeto aberrant synaptic transmission
The delayed and deficient maturation of astrocytes might , in parallel , lead to disruption of glutamatergic , potassium , and neuromodulatory homoeostasisresultingin dysregulated synaptic transmission
the APP cleavage product Aβinfluencessynaptic transmission at the postsynapse
the NIS applicants(passive) discovered recently byglutamatergic synaptic transmission
As a result , the decreased synaptic strength due to TRIAD3A knockdown in neurons could not be rescued by the TRIAD3A missense variantsthereby causingaberrant synaptic transmission
The ACSF included picrotoxin ( 50 μm ) during all recordingsto preventinhibitory synaptic transmission
1994 ; Benson and Cohen , 1996 ) , has been shown to result in complete suppression of action potentials ( Craig et al . , 1994thereby preventingevoked synaptic transmission
several factorsinfluencingGABAergic synaptic transmission
these eventsmight contributeto evoked synaptic transmission
CACNA1A ( XP 176influencesglutamatergic synaptic transmission
View at PubMedView at PublisherSeverely impairedcausesneuromuscular synaptic transmission
more inhibition to the second pyramidal cellcausesmore inhibition to the second pyramidal cell
to human ASDs and that the R451C knockin mice may be a useful model for studying autism - related behaviors.[less ] PMID : 17823315 Mesh Headingsmay contributeto human ASDs and that the R451C knockin mice may be a useful model for studying autism - related behaviors.[less ] PMID : 17823315 Mesh Headings
from fast - spiking but not from somatostatin - positive interneurons — University of Texas Southwestern Medical Center Jay R. Gibson , Kimberly M. Huberoriginatingfrom fast - spiking but not from somatostatin - positive interneurons — University of Texas Southwestern Medical Center Jay R. Gibson , Kimberly M. Huber
in LTP.[7would resultin LTP.[7
from fast - spiking but not from somatostatin - positive interneuron 'soriginatingfrom fast - spiking but not from somatostatin - positive interneuron 's
in LTP.[8 ... Timeline of consolidation[editwould resultin LTP.[8 ... Timeline of consolidation[edit
the disordered , synchronous firing of neurons that underlies a seizurecan triggerthe disordered , synchronous firing of neurons that underlies a seizure
long - term potentiation ( LTP ) at C - fiber synapses and hyperalgesia [ 45triggeringlong - term potentiation ( LTP ) at C - fiber synapses and hyperalgesia [ 45
the sensitivity of postsynaptic kainate receptorsinfluencingthe sensitivity of postsynaptic kainate receptors
cellular events over a wide rangeto influencecellular events over a wide range
to increased nociceptive output by facilitating the input of primary binary options on autopilot neurons onto nociceptive otions in the dorsal horn , or between dorsal horn neurons themselvesleadsto increased nociceptive output by facilitating the input of primary binary options on autopilot neurons onto nociceptive otions in the dorsal horn , or between dorsal horn neurons themselves
to an increase in the postsynaptic Ca(2 + ) concentration that is believed to activate the signaling pathways that shifts the rhythmic expression of circadian clock genesleadsto an increase in the postsynaptic Ca(2 + ) concentration that is believed to activate the signaling pathways that shifts the rhythmic expression of circadian clock genes
to an increase in the postsynaptic Ca2 + concentration that is believed to activate the signaling pathways that shifts the rhythmic expression of circadian clock genesleadsto an increase in the postsynaptic Ca2 + concentration that is believed to activate the signaling pathways that shifts the rhythmic expression of circadian clock genes
cortical signalmay influencecortical signal
neuronal output(passive) caused byneuronal output
to excessive neuronal synchronization in the epileptogenic zone ( EZ ) of the braincan leadto excessive neuronal synchronization in the epileptogenic zone ( EZ ) of the brain
File Select item 192891371.Excitatory and(passive) is ... influencedFile Select item 192891371.Excitatory and
Related citations Select item 1928913719.Excitatory and(passive) is ... influencedRelated citations Select item 1928913719.Excitatory and
to these processescan contributeto these processes
to the propagation of the high [ Ca2+]i region ... see Discussioncontributedto the propagation of the high [ Ca2+]i region ... see Discussion
to seizure activitycontributedto seizure activity
four decades agowas discoveredfour decades ago
in increased dopamine releasewill resultin increased dopamine release
to excitotoxicity " Type 2 : Associated with procaine penicillin , sulfonamides , fluoroquinolones , and macrolidesStarts within days of the first antibiotic dose and resolves within a few daysFrequentlyleadingto excitotoxicity " Type 2 : Associated with procaine penicillin , sulfonamides , fluoroquinolones , and macrolidesStarts within days of the first antibiotic dose and resolves within a few daysFrequently
in the development of an ataxic phenotype in mice [ 48resultingin the development of an ataxic phenotype in mice [ 48
to diminished inhibition ( ∼50 % ) in neuronal circuitsleadingto diminished inhibition ( ∼50 % ) in neuronal circuits
in SAresultsin SA
to autonomic failureleadingto autonomic failure
from 7-day corticosterone treatmentresultingfrom 7-day corticosterone treatment
the flow of information through the neural networkinfluencesthe flow of information through the neural network
to granule cell hyperexcitability in slice culturesmay contributeto granule cell hyperexcitability in slice cultures
from electrical stimulation of presumed GP efferentsresultingfrom electrical stimulation of presumed GP efferents
the “ virtual ” absence of activation when it is measured extracraniallymay causethe “ virtual ” absence of activation when it is measured extracranially