The readiness potential (RP), a slow buildup of electrical potential recorded at the scalp using electroencephalography, has been associated with neural activity involved in movement preparation. It became famous thanks to Benjamin Libet (Brain 1983;106:623-642), who used the time difference between the RP and self-reported time of conscious intention to move to argue that we lack free will. The RP's informativeness about self-generated action and derivatively about free will has prompted continued research on this neural phenomenon. Here, we argue that recent advances in our understanding of the RP, including computational modeling of the phenomenon, call for a reassessment of its relevance for understanding volition and the philosophical problem of free will. The Readiness PotentialThe readiness potential (RP) (see Glossary) or Bereitschaftspotential (BP) is a brain signal linked to voluntary movement. Its existence has been used to argue against the possibility of free will. Originally identified by Kornhuber and Deeke [1], the RP emerges from the analysis of electroencephalogram (EEG) data recorded during experimental tasks involving spontaneous or self-paced movements. When EEG traces, recorded during such a task, are time-locked to movement onset and averaged together, a slow negative-going electrical potential is evident leading up to movement onset (Box 1). The RP is prominent at central electrode sites located above mesial motor cortical areas and peaks contralateral to the moving limb. In experiments that average data from multiple subjects making self-paced movements, the RP is highly replicable. The RP has traditionally been interpreted as a sign of planning and preparation for movement and it is well-established as a reliable signal that precedes self-initiated movement in the group average. However, recent literature raises questions about the RP's ontological status as a real signal in the brain, its relation to action, its significance for arguments about volition, and its implications for free will. We review this recent literature and offer a reinterpretation of the nature of the signal that undermines its relevance for classic arguments against free will.

Plasma membrane monoamine transporter (PMAT) is a newly discovered monoamine transporter belonging to the equilibrative nucleoside transporter family. Highly expressed in the brain, PMAT represents a major uptake2 transporter that may play a role in monoamine clearance. Although human PMAT has been functionally characterized at the molecular level, rodent models are often used to evaluate PMAT function in ex vivo and in vivo studies. The aim of this study was to examine if there is potential species difference in the functional characteristics of PMAT between human, rat and mouse. A set of transfected cells stably expressing human PMAT (MDCK/hPMAT), rat Pmat (MDCK/rPmat) and mouse Pmat (Flp293/mPmat) were constructed. In MDCK/hPMAT, MDCK/rPmat and Flp293/mPmat cells, cellular localization analyses revealed that hPMAT, rPmat and mPmat are expressed and mainly localized to the plasma membranes of cells. The uptake of MPP+, serotonin and dopamine by MDCK/hPMAT, MDCK/rPmat and Flp293/mPmat cells was significantly increased compared with those by the mock transfection control. In contrast, two nucleosides, uridine and adenosine, minimally interacted with PMAT/Pmat in all species. The hPMAT-, rPmat- and mPmat-mediated uptakes of MPP+, serotonin and dopamine were saturable, with Km values of 33.7 µM, 70.2 µM and 49.5 µM (MPP+),116 µM, 82.9 µM and 231 µM (serotonin), and 201 µM, 271 µM and 466 µM (dopamine), respectively, suggesting similar substrate affinities between human and rodent PMAT/Pmat. The prototypical inhibitors, decynium 22 and GBR12935, also showed similar inhibition potencies between species. In conclusion, the present study demonstrated interspecies similarities in the functional characteristics of human and rodent PMAT/Pmat, which indicate a practical utility of rat and mouse animal models for further investigating and extrapolating the in vivo function of PMAT in humans.

Vancomycin is the drug of choice for methicillin-resistant Staphylococcus aureus keratitis and other ocular infections. Vancomycin ophthalmic drops are not commercially available and require compounding. The present study was designed to investigate the stability of vancomycin ophthalmic drops in normal saline, phosphate-buffered saline (PBS), and balanced salt solution (BSS) while stored at room temperature or under refrigeration. Vancomycin ophthalmic drops (50 mg/mL) were aseptically prepared from commercially available intravenous powder using PBS, BSS, and saline. Solutions were stored at room temperature and in a refrigerator for 28 days. The vancomycin stability was tested by a microbiology assay and high-performance liquid chromatography HPLC analysis immediately after formulation and at days 7, 14, and 28 after storage at room temperature or under refrigeration. The pH, turbidity was also tested. Vancomycin formulations in PBS, BSS and normal saline had initial pH of 5; 5.5; 3 respectively. The formulation in PBS developed turbidity and a slight decrease in pH upon storage. Microbiological assay did not show any change in zone of inhibition with any of the formulation upon storage either at room temperature or under refrigeration. HPLC analysis did not detect any decrease in vancomycin concentration or the accumulation of degraded products in any of the formulations upon storage either at room temperature or under refrigeration. Vancomycin ophthalmic drops prepared using PBS, BSS, and normal saline were stable up to the tested time point of 28 days, irrespective of their storage temperature.