IndraLab

Statements


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"Fluoxetine, a commonly used antidepressant, was reported to block the currents of several potassium channels, which are mediated by Kv1.1, Kv1.3, Kv1.4, Kv1.5, Kv3.1, Kv4.3, hERG and TREK-1 XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"TREK-1 may modulate potassium current of glomus cells and/or afferent nerve endings in the rat carotid body."

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"Ln et al. (2011) demonstrated that TREK-1 mRNA expression was significantly reduced in the left ventricular infarct region after MI, resulting in decreased potassium efflux, prolonged repolarization time, and prolonged APD."

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"Stretch-activated potassium currents are primarily driven by TREK channels, which play an important role in cardiac mechano-electrical feedback, both at the cellular level (e.g., presence in principal cells such as pacemakers and cardiomyocytes) and at the system level through their involvement in the regulation of heartbeat force and rate (6, 19, 82)."

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"There is enough evidence supporting the hypothesis that potassium outward currents driven by TREK channels play an important role not only in the normal functioning of the cardiovascular system, where its mechanical sensitivity plays a central aspect, but also in some relevant pathologies such as AF and other cardiac conditions."

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"The decreased excitability of CA2 PNs apparently results from an upregulated leak potassium current mediated by TREK channels , leading to a more hyperpolarized resting membrane potential."

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"Similarly, thermal pain sensitivity was alleviated in the ipsilateral hindpaws on the fifth day after siRNA‐Sort1 injection as compared to that after siRNA‐sham injection (Figure 8F).2.7 Decreased Potassium Current Mediated by TREK1 and TREK2 in Prediabetic DRG Neurons."

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"38 In order to understand the changes in potassium currents mediated by TREK1 and TREK2 channels (I ) under painful prediabetic conditions, further investigation is necessary."

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"Based on previous and current studies, astrocytic TWIK-1 and TREK-1 increased by AEG-1 potentially contribute to the protection of excitatory neuronal death by absorbing extracellular potassium ions secreted from activated neurons under pathological conditions."

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"l-Lactate-induced TREK1 upregulation is a novel finding of physiological significance as TREK1 channels contribute to neuroprotection by enhancing potassium buffering and glutamate clearance capacity of astrocytes."

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"Initially the inhibition of the TREK 1 channel causes dissociation of the C-terminal domain from the cell membrane and prevents the passage of potassium ions."