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BackgroundDepression is often comorbid with diabetes; however, undertreatment of depressive symptoms in people affected is common.ObjectiveWe studied preliminary acceptability and effectiveness of a fully automated, mobile phone, and web-based public health intervention, myCompass, for reducing depressive symptoms and improving mental health comorbidities in people with diabetes.MethodsIn this single-group feasibility study, 89 volunteers with type 1 (n=34) or type 2 (n=55) diabetes and at least mild depressive symptoms used myCompass for 7 weeks. Web-based measures of depressive and anxious symptoms, functional impairment, diabetes-specific variables, and user satisfaction were completed at baseline, postintervention, and 3-month follow-up.ResultsRetention rates were 54% (n=48) at postintervention and 36% (n=32) at follow-up. Depressive symptoms were significantly improved at postintervention (PConclusionsThe myCompass program shows promise as an acceptable and effective treatment for depression and comorbid mental health problems in people with diabetes. The program is broadly available, free to use, and may benefit patients with diabetes who do not access services and/or wish to manage their mental health themselves. Replication of these findings in a controlled study is warranted.

Seizure Termination by Acidosis Depends on ASIC1a. Ziemann AE, Schnizler MK, Albert GW, Severson MA, Howard MA 3rd, Welsh MJ, Wemmie JA. Nat Neurosci 2008;11(7):816–822. Most seizures stop spontaneously; however, the molecular mechanisms that terminate seizures remain unknown. Observations that seizures reduced brain pH and that acidosis inhibited seizures indicate that acidosis halts epileptic activity. Because acid-sensing ion channel 1a (ASIC1a) is exquisitely sensitive to extracellular pH and regulates neuron excitability, we hypothesized that acidosis might activate ASIC1a, which would terminate seizures. Disrupting mouse ASIC1a increased the severity of chemoconvulsant-induced seizures, whereas overexpressing ASIC1a had the opposite effect. ASIC1a did not affect seizure threshold or onset, but shortened seizure duration and prevented seizure progression. CO2 inhalation, long known to lower brain pH and inhibit seizures, required ASIC1a to interrupt tonic-clonic seizures. Acidosis activated inhibitory interneurons through ASIC1a, suggesting that ASIC1a might limit seizures by increasing inhibitory tone. Our results identify ASIC1a as an important element in seizure termination when brain pH falls and suggest both a molecular mechanism for how the brain stops seizures and new therapeutic strategies.