RESUMO
The tunnelling of a particle through a potential barrier is a key feature of quantum mechanics that goes to the core of wave-particle duality. The phenomenon has no counterpart in classical physics, and there are no well constructed dynamical observables that could be used to determine 'tunnelling times'. The resulting debate1-5 about whether a tunnelling quantum particle spends a finite and measurable time under a potential barrier was reignited in recent years by the advent of ultrafast lasers and attosecond metrology6. Particularly important is the attosecond angular streaking ('attoclock') technique7, which can time the release of electrons in strong-field ionization with a precision of a few attoseconds. Initial measurements7-10 confirmed the prevailing view that tunnelling is instantaneous, but later studies11,12 involving multi-electron atoms-which cannot be accurately modelled, complicating interpretation of the ionization dynamics-claimed evidence for finite tunnelling times. By contrast, the simplicity of the hydrogen atom enables precise experimental measurements and calculations13-15 and makes it a convenient benchmark. Here we report attoclock and momentum-space imaging16 experiments on atomic hydrogen and compare these results with accurate simulations based on the three-dimensional time-dependent Schrödinger equation and our experimental laser pulse parameters. We find excellent agreement between measured and simulated data, confirming the conclusions of an earlier theoretical study17 of the attoclock technique in atomic hydrogen that presented a compelling argument for instantaneous tunnelling. In addition, we identify the Coulomb potential as the sole cause of the measured angle between the directions of electron emission and peak electric field: this angle had been attributed11,12 to finite tunnelling times. We put an upper limit of 1.8 attoseconds on any tunnelling delay, in agreement with recent theoretical findings18 and ruling out the interpretation of all commonly used 'tunnelling times'19 as 'time spent by an electron under the potential barrier'20.
RESUMO
In this Letter, the statement 'I.I. and A.B. performed computations at the NCI Australia' was missing from the Acknowledgements section. This has been corrected online.
RESUMO
Reports of an inverse relationship between nicotine intake, due to cigarette smoking, and the incidence of Alzheimer's disease (AD) prompted us to investigate the effects of nicotine on amyloid beta-protein precursor (AbetaPP) processing in rat. Over-production and/or altered metabolism of AbetaPP, resulting in increased amyloid beta-peptide (Abeta), appear pivotal in the pathogenesis of AD. Abeta is generated proteolytically from betaPP by a group of secretases. AbetaPP cleavage by gamma-secretase results in the secretion of a truncated soluble betaPP (sAPPgamma) that contains intact Abeta. Nicotine, 1 and 8 mg/kg/day, doses commensurate with cigarette smoking and a higher but well tolerated dose, respectively, was administered over 14 days and Western blot analysis was performed on sAPP fragments. Both doses significantly reduced sAPPgamma. These actions were blocked by nicotinic receptor antagonism. Whereas nicotinic antagonists alone had no effect on either total sAPP or sAPPgammalevels in CSF, muscarinic antagonism significantly elevated them; suggesting that muscarinic rather than nicotinic receptor silence alters processing of AbetaPP to favor a potentially amyloidogenic route. Combined nicotine and muscarinic antagonism attenuated the action of the latter to elevate sAPPgamma, indicating that nicotine modifies AbetaPP processing away from potentially amyloidogenic products. These results suggest that within the brain, levels of total sAPP, sAPPgamma and, accordingly, Abeta are subject to cholinergic manipulation, offering therapeutic potential at the level of AbetaPP processing to decrease Abetadeposition.