Results for synaptic translation from English to Maltese

activation of ampa receptors by glutamate is thought to be responsible for most fast excitatory synaptic transmission in the brain.
l-attivazzjoni ta’ riċetturi ampa minn glutamate hi maħsuba li hi responsabbli għall-iktar trasmissjoni sinattika eċċitatorja veloċi fil-moħħ.

this binding site is the synaptic vesicle protein 2a, believed to be involved in vesicle fusion and neurotransmitter exocytosis.
dan il-post fejn jeħel huwa l-proteina tal-bużżieqa tas-sinapsi 2a , li hu magħruf li hu involut fil-fużjoni tal-bużżieqa u exositożi ta’ neurotransmitter.

amifampridine blocks voltage-dependent potassium channels, thereby prolonging pre-synaptic cell membrane depolarisation.
amifampridine jimblokka l-kanali tal-potassju dipendenti fuq il-vultaġġ, u b’hekk itawwal id- depolarizzazzjoni presinaptika tal-membrana taċ-ċelluli.

this finding suggests that the interaction between levetiracetam and the synaptic vesicle protein 2a seems to contribute to the antiepileptic mechanism of action of the medicinal product.
dan it-tagħrif jissuġġerixxi li l-interazzjoni bejn levtiracetam u l-proteina tal- bużżieqa tas-sinapsi 2a donnhom jikkontribwixxu għall-mekkaniżmu t’azzjoni kontra l-epilessija tal- prodott mediċinali.

preclinical research suggests guanfacine modulates signalling in the prefrontal cortex and basal ganglia through direct modification of synaptic noradrenalin transmission at the alpha 2- adrenergic receptors.
riċerka preklinika tissuġġerixxi li guanfacine jimmodula s-senjalazzjoni fil-kortiċi prefrontali u l-gangliji bażali permezz ta’ modifikazzjoni diretta tat-trasmissjoni sinattika ta’ noradrenalin fir-riċetturi alpha adrenerġiċi.

the exact way in which levetiracetam works is still unclear but it attaches to a protein called synaptic vesicle protein 2a, which is involved in the release of chemical messengers from nerve cells.
il-mod preċiż kif jaħdem levetiracetam għadu mhux ċar iżda jidher li dan jaqbad ma’ proteina msejħa proteina sinaptika vexxili 2a, li għandha sehem fir- rilaxx ta’ messaġġiera kimiċi miċ-ċelloli tan-nervituri.

levetiracetam and related analogs show a rank order of affinity for binding to the synaptic vesicle protein 2a which correlates with the potency of their anti-seizure protection in the mouse audiogenic model of epilepsy.
levetiracetam u sustanzi relatati oħra juru affinita` li jeħlu mal-proteina tal-bużżieqa tas-sinapsi 2a b’rata li tikkorralata mal-qawwa tal-protezzjoni li jagħtu kontra l-aċċessjonijiet fil-mudell ta’ l-epilessija awdjoġeniku fil-ġurdien.

brivaracetam displays a high and selective affinity for synaptic vesicle protein 2a (sv2a), a transmembrane glycoprotein found at presynaptic level in neurons and in endocrine cells.
brivaracetam juri affinita` għolja u selettiva għal synaptic vesicle protein 2a (sv2a), transmembrane glycoprotein li jinstgħab fill-livell ta’ presynaptic f’neurons u f’ celloli endrokriniċi.

afoxolaner acts at ligand-gated chloride channels, in particular those gated by the neurotransmitter gamma-aminobutyric acid (gaba), thereby blocking pre- and post-synaptic transfer of chloride ions across cell membranes.
afoxolaner jaġixxi fil-kanali ta’ ligand-gated chloride, b’mod partikulari dawk gated min-newrotrażmettitur gamma- aminobutyric acid (gaba) b’hekk jiġi mblukkat it-trasferiment tal-joni tal-chloride tul il-membrani taċ-ċelluli qabel u wara t-trasferiment sinattiku.