Hyporheic Source and Sink of Nitrous Oxide

Nitrous oxide (N2O) is a potent greenhouse gas with an estimated 10% of anthropogenic N2O coming from the hyporheic zone of streams and rivers. However, difficulty in making accurate fine-scale field measurements has prevented detailed understanding of the processes of N2O production and emission at the bedform and flowline scales. Using large-scale, replicated flume experiments that employed high-density chemical concentration measurements, we have been able to refine the current conceptualization of N2O production, consumption, and emission from the hyporheic zone. We present a predictive model based on a Damköhler-type transformation (τ̃) in which the hyporheic residence times (τ) along the flowlines are multiplied by the dissolved oxygen consumption rate constants for those flowlines. This model can identify which bedforms have the potential to produce and emit N2O, as well as the portion and location from which those emissions may occur. Our results indicate that flowlines with τ̃up (τ̃ as the flowline returns to the surface flow) values between 0.54 and 4.4 are likely to produce and emit N2O. Flowlineswith τ̃up values of less than 0.54 will have the same N2O as the surface water and those with values greater than 4.4 will likely sink N2O (reference conditions: 17C, surface dissolved oxygen 8.5 mg/L). N2O production peaks approximately at τ̃ = 1.8. A cumulative density function of τ̃up values for all flowlines in a bedform (or multiple bedforms) can be used to estimate the portion of flowlines, and in turn the portion of the streambed, with the potential to emit N2O

Compensatory changes in the hippocampus of somatostatin knockout mice: upregulation of somatostatin receptor 2 and its function in the control of bursting activity and synaptic transmission

Somatostatin-14 (SRIF) co-localizes with c-aminobutyric acid (GABA) in the hippocampus and regulates neuronal excitability. A role of SRIF in the control of seizures has been proposed, although its exact contribution requires some clarification. In particular, SRIF knockout (KO) mice do not exhibit spontaneous seizures, indicating that compensatory changes may occur in KO. In the KO hippocampus, we examined whether specific SRIF receptors and ⁄ or the cognate peptide cortistatin-14 (CST) compensate for the absence of SRIF. We found increased levels of both sst2 receptors (sst2) and CST, and we explored the functional consequences of sst2 compensation on bursting activity and synaptic responses in hippocampal slices. Bursting was decreased by SRIF in wild-type (WT) mice, but it was not affected by either CST or sst2 agonist and antagonist. sst4 agonist increased bursting frequency in either WT or KO. In WT, but not in KO, its effects were blocked by agonizing or antagonizing sst2, suggesting that sst2 and sst4 are functionally coupled in the WT hippocampus. Bursting was reduced in KO as compared with WT and was increased upon application of sst2 antagonist, while SRIF, CST and sst2 agonist had no effect. At the synaptic level, we observed that in WT, SRIF decreased excitatory postsynaptic potentials which were, in contrast, increased by sst2 antagonist in KO. We conclude that sst2 compensates for SRIF absence and that its upregulation is responsible for reduced bursting and decreased excitatory transmission in KO mice. We suggest that a critical density of sst2 is needed to control hippocampal activity