Investigation on Nutrient Loads of Lake Taihu in China

Based on measured data and laboratory experiments, the spatial and temporal distribution of nutrient loads of Lake Taihu from the sources of river runoff, atmospheric bulk deposition and internal release was quantitatively analyzed. Results showed that: (1) In 2011, annual river inputs of total phosphorus (TP) and total nitrogen (TN) respectively were 2382.4 tons and 50245.0 tons, and annual river outputs of TP and TN respectively were 849.1 tons and 24236.7 tons, Huxi area was the major transverse source of nutrients as a large proportion of TP(71.6%) and TN(66.2%). (2) Annual nutrient loads of Lake Taihu were 3306.6 tons TP and 48007.0 tons TN, of which the contribution of river runoff, atmospheric bulk deposition and internal release to TP accounted for 46.3%, 38.3% and 15.4%, and that to TN accounted for 54.2%, 43.7% and 2.1%, respectively. (3) Inputs of nutrients to Lake Taihu were higher in summer (June to August), of which 983.9 tons TP and 8874.9 tons TN in June, 1420.9 tons TP and 7463.3 tons TN in July, 1347.1 tons TP and 7181.3 tons TN in August. The results have great significance for eutrophication control and water environment protection in Lake Taihu.

Na+-Ca2+ Exchanger Controls the Gain of the Ca2+ Amplifier in the Dendrites of Amacrine Cells

We have previously shown that disabling forward-mode Na+-Ca2+ exchange in amacrine cells greatly prolongs the depolarization-induced release of transmitter. To investigate the mechanism for this, we imaged [Ca2+]i in segments of dendrites during depolarization. Removal of [Na+]o produced no immediate effect on resting [Ca2+]i but did prolong [Ca2+]i transients induced by brief depolarization in both voltage-clamped and unclamped cells. In some cells, depolarization gave rise to stable patterns of higher and lower [Ca2+] over micrometer-length scales that collapsed once [Na+]o was restored. Prolongation of [Ca2+]i transients by removal of [Na+]o is not due to reverse mode operation of Na+-Ca2+ exchange but is instead a consequence of Ca2+ release from endoplasmic reticulum (ER) stores over which Na+-Ca2+exchange normally exercises control. Even in normal [Na+]o, hotspots for [Ca2+] could be seen following depolarization, that are attributable to local Ca2+-induced Ca2+ release. Hotspots were seen to be labile, probably reflecting the state of local stores or their Ca2+ release channels. When ER stores were emptied of Ca2+ by thapsigargin, [Ca2+] transients in dendrites were greatly reduced and unaffected by the removal of [Na+]o implying that even when Na+-Ca2+ exchange is working normally, the majority of the [Ca2+]i increase by depolarization is due to internal release rather than influx across the plasma membrane. Na+-Ca2+ exchange has an important role in controlling [Ca2+] dynamics in amacrine cell dendrites chiefly by moderating the positive feedback of the Ca2+ amplifier.