TRP, inositol 1,4,5-trisphosphate receptors, and capacitative calcium entry

106

Recently, we described a novel 3-pSstores in permeabilized human platelets resulted in the release of endogenous factor, which activated 3-pS channels in isolated inside-out membrane patches excised from SMC and exposed to permeabilized platelets. The same 3-pS channels in excised membrane patches were also activated by acid extracts of CIF derived from human platelets with depleted Ca 2؉ stores, which also stimulated Ca 2؉ influx upon injection into Xenopus oocytes. Specific high pressure liquid chromatography fractions of platelet extracts were found to have CIF activity when injected into oocytes and activate 3-pS channels in excised membrane patches. These data show for the first time that CIF produced by mammalian cells and yeast with depleted Ca 2؉ stores directly activates native 3-pS cation channels, which in intact SMC are activated by Ca 2؉ store depletion.

Section: Discussionmentioning

confidence: 99%

Calcium Influx Factor Directly Activates Store-operated Cation Channels in Vascular Smooth Muscle Cells

Trepakova¹,

Csutora²,

Hunton³

et al. 2000

106

“…Until recently the best candidates for I CRAC have been proteins of the TRP family (21,22). Members in TRPC subfamily had been shown to gate in response to the state of Ca 2ϩ stores (22)(23)(24)(25); however, in each case complete recapitulation of classical I CRAC was lacking (26). Two newer members of the TRPV group (27), ECaC1 and CaT1, have been described with characteristics similar to endogenous I CRAC (28 -30).…”

Section: Capacitative Calcium Entry (Cce)mentioning

confidence: 99%

CaT1 Contributes to the Stores-operated Calcium Current in Jurkat T-lymphocytes

Cui¹,

Bian

Kagan

et al. 2002

“…Because the inward current activated by ACh is a specific Na ϩ current, we termed it I Na-ACh . Mechanisms of Activation of I Na-ACh -As in other cells (37,38), lowering the Ca 2ϩ content of the endoplasmic reticulum in ␤-cells activates conductances for Ca 2ϩ and perhaps other ionic species including Na ϩ (25,39). Even if such a mechanism slightly contributes to the current, it is not responsible for I Na-ACh , because ACh still activated the inward current after emptying of the endoplasmic reticulum Ca 2ϩ stores by thapsigargin.…”

Section: Muscarinic Activation Of Namentioning

confidence: 99%

G Protein-independent Activation of an Inward Na+Current by Muscarinic Receptors in Mouse Pancreatic β-Cells

Rolland¹,

Henquin²,

Gilon³

2002

Depolarization of pancreatic ␤-cells is critical for stimulation of insulin secretion by acetylcholine but remains unexplained. Using voltage-clamped ␤-cells, we identified a small inward current produced by acetylcholine, which was suppressed by atropine or external Na ؉ omission, but was not mimicked by nicotine, and was insensitive to nicotinic antagonists, tetrodotoxin, 4,4-diisothiocyanostilbene-2,2-disulfonic acid (DiDS), thapsigargin pretreatment, and external Ca 2؉ and K ؉ removal. This suggests that muscarinic receptor stimulation activates voltage-insensitive Na ؉ channels distinct from store-operated channels. No outward Na ؉ current was produced by acetylcholine when the electrochemical Na ؉ gradient was reversed, indicating that the channels are inward rectifiers. No outward K ؉ current occurred either, and the reversal potential of the current activated by acetylcholine in the presence of Na ؉ and K ؉ was close to that expected for a Na ؉ -selective membrane, suggesting that the channels opened by acetylcholine are specific for Na ؉ . Overnight pretreatment with pertussis toxin or the addition of guanosine 5-O-(3-thiotriphosphate) (GTP-␥-S) or guanosine-5-O-(2-thiodiphosphate) (GDP-␤-S) instead of GTP to the pipette solution did not alter this current, excluding involvement of G proteins. Injection of a current of a similar amplitude to that induced by acetylcholine elicited electrical activity in ␤-cells perifused with a subthreshold glucose concentration. These results demonstrate that muscarinic receptor activation in pancreatic ␤-cells triggers, by a G protein-independent mechanism, a selective Na ؉ current that explains the plasma membrane depolarization.