The event-related potential called "Error Negativity" (Ne, ERN), which appears when subjects commit errors in choice reaction time tasks, is a marker of response monitoring. By introducing a response probability bias, we show that the Ne is sensitive to response expectancy. We further show that the small negativity evoked by correct responses (Ne-like, CRN) is also sensitive to response expectancy: On unexpected responses, the former decreases while the latter increases to such an extent that the amplitudes of the two components are in the same range of magnitude. Although the sensitivity of the Ne to response expectancy is compatible with the current models accounting for the Ne, the common sensitivity of the Ne and the Ne-like supports the idea that they reflect functionally similar monitoring processes.

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In a clinical perspective for the treatment of acute ischemic stroke, these data suggest that helium 1) should not be administered before or together with tissue plasminogen activator therapy due to the risk of inhibiting the benefit of tissue plasminogen activator-induced thrombolysis; and 2) could be an efficient neuroprotective agent if given after tissue plasminogen activator-induced reperfusion.

Nitrogen supersaturation and bubble formation can occur in the vascular system after diving, leading to death and nervous disorders from decompression sickness (DCS). Bubbles alter the vascular endothelium, activate platelets, and lead to focal ischemia with neurological damage mediated by the mechanosensitive TREK-1 neuronal potassium ion channel that sets pre- and postsynaptic resting membrane potentials. We report a neuroprotective effect associated with TREK-1. C57Bl6 mice were subjected to decompression from a simulated 90 msw dive. Of 143 mice that were wild type (WT) for TREK-1, 51.7% showed no DCS, 27.3% failed a grip test, and 21.0% died. Of 88 TREK-1 knockouts (KO), 26.1% showed no DCS, 42.0% failed a grip test, and 31.8% died. Mice that did not express TREK-1 had lower DCS resistance and were more likely to develop neurological symptoms. We conclude that the TREK-1 potassium channel was neuroprotective for DCS.