Differential lifetime success and performance of native and non-native Atlantic salmon examined under communal natural conditions.

The lifetime success and performance characteristics of communally reared offspring of wild native Burrishoole (native), ranched native (ranched) and non-native (non-native) Atlantic salmon Salmo salar from the adjacent Owenmore River were compared. Non-native year parr showed a substantial downstream migration, which was not shown by native and ranched parr. This appears to have been an active migration rather than competitive displacement and may reflect an adaptation to environmental or physiographic conditions within the Owenmore River catchment where the main nursery habitat is downstream of the spawning area. There were no differences between native and ranched in smolt output or adult return. Both of these measures, however, were significantly lower for the non-native group. A greater proportion of the non-native Atlantic salmon was taken in the coastal drift nets compared to the return to the Burrishoole system, probably as a result of the greater size of the non-native fish. The overall lifetime success of the non-native group, from fertilized egg to returning adult, was some 35% of native and ranched. The ranched group showed a significantly greater male parr maturity, a greater proportion of 1+ year smolts, and differences in sex ratio and timing of freshwater entry of returning adults compared to native, which may have fitness implications under specific conditions.

Ca2+- and volume-sensitive chloride currents are differentially regulated by agonists and store-operated Ca2+ entry.

Using patch-clamp and calcium imaging techniques, we characterized the effects of ATP and histamine on human keratinocytes. In the HaCaT cell line, both receptor agonists induced a transient elevation of [Ca2+]i in a Ca2+-free medium followed by a secondary [Ca2+]i rise upon Ca2+ readmission due to store-operated calcium entry (SOCE). In voltage-clamped cells, agonists activated two kinetically distinct currents, which showed differing voltage dependences and were identified as Ca2+-activated (ICl(Ca)) and volume-regulated (ICl, swell) chloride currents. NPPB and DIDS more efficiently inhibited ICl(Ca) and ICl, swell, respectively. Cell swelling caused by hypotonic solution invariably activated ICl, swell while regulatory volume decrease occurred in intact cells, as was found in flow cytometry experiments. The PLC inhibitor U-73122 blocked both agonist- and cell swelling–induced ICl, swell, while its inactive analogue U-73343 had no effect. ICl(Ca) could be activated by cytoplasmic calcium increase due to thapsigargin (TG)-induced SOCE as well as by buffering [Ca2+]i in the pipette solution at 500 nM. In contrast, ICl, swell could be directly activated by 1-oleoyl-2-acetyl-sn-glycerol (OAG), a cell-permeable DAG analogue, but neither by InsP3 infusion nor by the cytoplasmic calcium increase. PKC also had no role in its regulation. Agonists, OAG, and cell swelling induced ICl, swell in a nonadditive manner, suggesting their convergence on a common pathway. ICl, swell and ICl(Ca) showed only a limited overlap (i.e., simultaneous activation), although various maneuvers were able to induce these currents sequentially in the same cell. TG-induced SOCE strongly potentiated ICl(Ca), but abolished ICl, swell, thereby providing a clue for this paradox. Thus, we have established for the first time using a keratinocyte model that ICl, swell can be physiologically activated under isotonic conditions by receptors coupled to the phosphoinositide pathway. These results also suggest a novel function for SOCE, which can operate as a "selection" switch between closely localized channels.