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Here, we have been able to directly demonstrate that β-III spectrin and ankyrin R positively modulate neuronal sodium currents.
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Here, we show for the first time that ankyrin R, in association with β-III spectrin, has a critical role in modulating neuronal sodium channel activity and hence neuron excitability.
We further examined the potency of these two compounds to inhibit neuronal sodium currents recorded from cultured hippocampal neurons.
Furthermore, TET1 can negatively modulate neuronal differentiation independent of its catalytic activity and through srGAP3.
This suggests an attempt to modulate neuronal hyperexcitability in migraine patients.
The application of UCNPs has recently been extended to optogenetically modulate neuronal activity using near-infrared light.
In real cortical tissues there are an abundance of metabolic processes whose combined effect is to modulate neuronal response.
It is reported that in central nervous system, glial cells release MVs, which modulate neuronal function in normal condition.
Cytokines, including interleukin-6 (IL-6), modulate neuronal plasticity and stress coping.
This clearly demonstrates that these compounds functionally antagonize native neuronal sodium channel currents.
Neurosteroids, i.e., allopregnanolone (AP), epiallopregnanolone (EP), dehydroepiandrosterone (DHEA) and deydroepiandrosterone sulfate (DHEAS), rapidly modulate neuronal firing rate and might be involved in the pathogenesis of migraine [1].
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