Nasu T, Murase H, Shibata H.Gen Pharmacol. 1995 Mar;26(2):381-6. PMID: 7590091
Now that we do manganese-enhanced magnetic resonance imaging (MEMRI), we all know that manganese enters active cells during action potentials because it acts as a calcium surrogate and gets taken up by voltage-gated calcium channels. We also now know which type of channels are responsible for this, because this is the paper where the authors inhibited T-type and L-type cells to show that it's the L-type channels that allow manganese to enter the cell.In this paper, they clipped strips of ileal smooth muscle in to a strain gauge meter, and then washed the strips in a high-potassium solution to cause muscle contraction. They found that 5mM manganese was able to block contractions, seen by a decrease in muscle tension, presumably by occupying calcium binding sites but without being able to activate them as well as calcium can. They were also able to see that in calcium-free solutions, application of manganese could actually take the place of calcium and cause the contractions if the potassium solution was strong enough. This was able to be blocked by the L-type calcium blockers, nifedipine and D-600, while T-type calcium channel blockers were not able to do this. They were also able to show, using spectrophotometry, that tissue manganese content was significantly lower following L-type channel blockade, but not blockade of T-type channels.
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