chloramine-t and tetrapentylammonium

chloramine-t has been researched along with tetrapentylammonium* in 1 studies

Other Studies

1 other study(ies) available for chloramine-t and tetrapentylammonium

Article	Year
Tetrapentylammonium block of chloramine-T and veratridine modified rat brain type IIA sodium channels. British journal of pharmacology, 2001, Volume: 132, Issue:8 Tetrapentylammonium (TPeA) block of rat brain type IIA sodium channel alpha subunit was studied using whole cell patch clamp. Results indicate that TPeA blocks the inactivating brain sodium channel in a potential and use-dependent manner similar to that of the cardiac sodium channel. Removal of inactivation using chloramine-T (CT) unmasks a time-dependent block by TPeA consistent with slow blocking kinetics. On the other hand, no time dependence is observed when inactivation is abolished by modification with veratridine. TPeA does not bind in a potential-dependent fashion to veratridine-modified channels and does not significantly affect gating of veratridine-modified channels suggesting that high affinity binding of TPeA to the brain sodium channel is lost after veratridine modification. Topics: Algorithms; Animals; Brain Chemistry; Cells, Cultured; Chloramines; Indicators and Reagents; Ion Channel Gating; Patch-Clamp Techniques; Quaternary Ammonium Compounds; Rats; Sodium Channel Blockers; Tosyl Compounds; Veratridine	2001

Article

Year

Tetrapentylammonium block of chloramine-T and veratridine modified rat brain type IIA sodium channels.

British journal of pharmacology, 2001, Volume: 132, Issue:8

Tetrapentylammonium (TPeA) block of rat brain type IIA sodium channel alpha subunit was studied using whole cell patch clamp. Results indicate that TPeA blocks the inactivating brain sodium channel in a potential and use-dependent manner similar to that of the cardiac sodium channel. Removal of inactivation using chloramine-T (CT) unmasks a time-dependent block by TPeA consistent with slow blocking kinetics. On the other hand, no time dependence is observed when inactivation is abolished by modification with veratridine. TPeA does not bind in a potential-dependent fashion to veratridine-modified channels and does not significantly affect gating of veratridine-modified channels suggesting that high affinity binding of TPeA to the brain sodium channel is lost after veratridine modification.

Topics: Algorithms; Animals; Brain Chemistry; Cells, Cultured; Chloramines; Indicators and Reagents; Ion Channel Gating; Patch-Clamp Techniques; Quaternary Ammonium Compounds; Rats; Sodium Channel Blockers; Tosyl Compounds; Veratridine

2001