Moving in response to an unseen visual stimulus.

OBJECTIVE: Whether consciousness has a causal role in voluntary movements is not clear. Backward masking blocks a stimulus from becoming conscious, but it can trigger movement in a reaction time paradigm. We hypothesize that if backward masking is used in a choice reaction time paradigm, when the visible stimulus (S2) differs from the masked stimulus (S1), the movement will often differ from conscious intent. We did such a study employing electroencephalography (EEG) to explore the brain activity associated with this effect. METHODS: Twenty healthy adults participated in a choice reaction time task with a backwardly masked stimulus and EEG. They moved right or left hand in response to the direction of an arrow. S2 was congruent or incongruent with S1. When incongruent, responses were frequently concordant with S1, with faster reaction time than when responding to S2 and thought to be a mistake. RESULTS: We show that it is possible to trigger movements from the unperceived stimuli indicating consciousness is not causal since the movement was not in accord with intent. EEG showed information flow from occipital cortex to motor cortex. CONCLUSIONS: Occipital activity was the same despite response, but the parietal and frontal EEG differed. When responding to S1, the motor cortex responded as soon as information arrived, and when responding to S2, the motor cortex responded with a delay allowing for other brain processing prior to movement initiation. While the exact time of conscious recognition of S2 is not clear, when there is a response to S1, the frontal cortex signals an "error", but this is apparently too late to veto the movement. SIGNIFICANCE: While consciousness does not initiate the movement, it monitors the concordance of intent and result.

Cerebral preparation of spontaneous movements: An EEG study.

OBJECTIVE: The current study sought to determine whether there is a Bereitschaftspotential (BP) before uninstructed, spontaneous movements. METHODS: 14 participants were seated on a comfortable armchair for one hour without any instruction except not to fall asleep and to keep their eyes open. Electroencephalography (EEG) and electromyography (EMG) activity were recorded during the whole session. EEG activity was analyzed before spontaneous movements and compared with EEG activity before repetitive, instructed movements in a separate session. RESULTS: BPs were identified in most participants with the spontaneous movements. The BPs with spontaneous movements were mostly localized in the medial frontocentral regions. The BPs with the instructed movements were localized primarily in the central regions and had larger amplitude. CONCLUSION: Presence of a BP before movement does not depend on instruction and may be independent of conscious volition. The amplitude of the BP may depend on the amount of attention. SIGNIFICANCE: This study shows that the presence of a BP before movement is not an "artifact" of the experimental instructions.

Altered Redox State Modulates Endothelial KCa2.3 and KCa3.1 Levels in Normal Pregnancy and Preeclampsia.

AIMS: Altered redox state has been related to the development of normal pregnancy (NP) and preeclampsia (PE). Endothelial KCa2.3 and KCa3.1 (KCas) play an important role in vasodilation, and KCas levels are affected by oxidative stress. We investigated the mechanisms of oxidative stress-mediated KCas expression modulation during NP and PE. RESULTS: Human uterine microvascular endothelial cells were incubated in serum from normal nonpregnant women (n = 13) and women with NP (n = 24) or PE (n = 15), or in vascular endothelial growth factor (VEGF), oxidized low-density lipoprotein (ox-LDL), progesterone, or estradiol-17ß (E2)-containing medium for 24 h. NP serum elevated H2O2 levels via reducing catalase and glutathione peroxidase 1 levels, thereby enhancing KCas levels via a H2O2/fyn/extracellular signal-regulated kinase (ERK)-mediated pathway. VEGF enhanced H2O2 and KCas levels and KCa3.1 currents. KCas were upregulated and KCas activation-induced endothelium-dependent relaxation (EDR) was augmented in vessels from pregnant mice and rats. Whereas PE serum, ox-LDL, progesterone, or soluble fms-like tyrosine kinase 1 (sFlt-1) elevated superoxide levels via elevating NADPH oxidase 2 (NOX2) and NOX4 levels and reducing superoxide dismutase (SOD) 1 levels, thereby downregulating KCas. sFlt-1 inhibited EDR. PE serum- or progesterone-induced alterations in levels of KCas were reversed by polyethylene glycol-SOD, NOX inhibition, or E2. Innovation and Conclusions: This is the first study of how endothelial KCas levels are modulated during NP and PE. KCas were upregulated by soluble serum factors such as VEGF via H2O2 generation in NP, and were downregulated by serum factors such as progesterone and ox-LDL via superoxide generation in PE, which may contribute to hemodynamic adaptations in NP or to the development of PE.

Hydration status affects osteopontin expression in the rat kidney.

Osteopontin (OPN) is a secretory protein that plays an important role in urinary stone formation. Hydration status is associated with the development of urolithiasis. This study was conducted to examine the effects of dehydration and hydration on OPN expression in the rat kidney. Animals were divided into three groups, control, dehydrated, and hydrated. Kidney tissues were processed for light and electron microscope immunocytochemistry, in situhybridization, and immunoblot analysis. Dehydration induced a significant increase in OPN protein expression, whereas increased fluid intake induced a decrease in protein expression. Under control conditions, OPN protein and mRNA expression were only detected in the descending thin limb (DTL). Dehydration induced increased expression in the DTL and the development of detectable expression in the thick ascending limb (TAL). In contrast, OPN expression levels declined to less than the controls in the DTL after hydration, while no expression of either protein or mRNA was detectable in the TAL. Immunoelectron microscopy demonstrated that hydration status altered tubular ultrastructure and intracellular OPN expression in the Golgi apparatus and secretory cytoplasmic vesicles. These data confirm that changes in oral fluid intake can regulate renal tubular epithelial cell OPN expression.