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We previously demonstrated a role for BK channels in generating the day-night difference in frequency [14].
Experimental [13], [30] and theoretical [25] studies, have proposed a role for voltage-gated calcium channels in generating directional responses in the SBACs.
Our results rule out the hypothesis of a role of BK channels in generating the pause, as we found the pause to be longer in BK−/− than in WT PCs, and unchanged following paxilline microinjection.
To investigate the role of chloride channels in generating cornea wound electric current via active chloride flux, we measured wound electric current with a vibrating probe [7], [37] in the presence of 200 µM broad-spectrum chloride channel blocker DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulfonic 4,4'-diisothiocyanatostilbene-2,2'-disulfonic 4,4'-diisothiocyanatostilbene-2,2'-disulfonic 4,4'-diisothiocyanatostilbene-2,2'-disulfonic
The contribution of these channels in generating the Bk effects remains to be established.
These results underscore the central role of T-type Ca2+ channels in generating the normal thalamocortical oscillations that become impaired during absence seizures.
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It has been reported that some electrocyte-specific ion channels involved in generating the electric discharge appear to be evolving at a higher than expected rate in electric fishes (see [ 23, 24] for a discussion of the NaV1.4a sodium channels in electrocytes).
However, the role of CNG channels and Ca2+ stores in generating transient and sustained signals downstream from the cone OS is unclear.
The data also reveals a structural basis for the model of auditory chordotonal transduction in which the TRPN and TRPV channels play sequential roles in generating and amplifying the receptor potential, but have opposing roles in regulating active ciliary motility.
The strongest argument that V1-bypassing subcortical channels must be involved in generating the observed V2, V3 activity is provided by multi-unit receptive field maps recorded inside the V2 LPZ (Figure 8).
Mechanosensitive calcium channels were strongly implicated in generating Ca 2+ responses to mechanical stimulations in previous studies and were confirmed to provide a critical contribution to both local and global Ca 2+ responses in our study.
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