TABLE 1.
The triggering mechanisms of TRP and TRPL channels
| Supporting evidence | Difficulties | |
|---|---|---|
| Excitation by lipids | Inhibition of DAG kinase enhances channel activity in vivo (123, 124, 126) | Application of DAG has no effect on channel excitation in vivo (S. Frechter and B. Minke, unpublished data) |
| The LIC of a PLC mutant with a very small residual response to light was partially rescued in the double mutant PLC/DAG kinase (123, 124) | Removal of a putative DAG lipase does not block channel opening (138) | |
| PUFAs open the channels both in vivo and in heterologous expression systems (124, 125) | The PUFAs’ effect in heterologous expression systems is blocked upon inhibition of PLC (110)
PUFAs’ activation kinetics in vivo is slower by 2–3 orders of magnitude relative to the activation by light (123, 125) |
|
| Ca2+ is necessary but not sufficient for excitation | 10 mM BAPTA but not 10 mM EGTA blocks channel activation by light and metabolic inhibition. In Ca2+ deprived cells application of Ca2+ combined with the metabolic inhibition mimics the response to light in the dark (kinetics and amplitude) (101) | Photorelease of caged Ca2+ in blind mutants does not open the channels (103) |
| Embryonic Drosophila photoreceptors are incapable of responding to light unless first provided with Ca2+ via the whole-cell pipette (98) | Genetic elimination of the single known InsP3R in Drosophila has no effect on excitation (128) | |
| Application of the InsP3R antagonist 2APB reversibly blocks the light response (129) | 2APB is known to have nonspecific effects (129) |