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Strong-field ionization (SFI) is a key process for accessing real-time quantum dynamics of electrons on the attosecond timescale. The theoretical foundation of SFI was pioneered in the 1960s, and later refined by various analytical models. While asymptotic ionization rates predicted by these models have been tested to be in reasonable agreement for a wide range of laser parameters, predictions for SFI on the sub-laser-cycle timescale are either beyond the scope of the models or show strong qualitative deviations from full quantum-mechanical simulations. Here, using the unprecedented state specificity of attosecond transient absorption spectroscopy, we follow the real-time SFI process of the two valence spin-orbit states of xenon. The results reveal that the irreversible tunnelling contribution is accompanied by a reversible electronic population that exhibits an observable spin-orbit-dependent phase delay. A detailed theoretical analysis attributes this observation to transient ground-state polarization, an unexpected facet of SFI that cannot be captured by existing analytical models that focus exclusively on the production of asymptotic electron/ion yields.

We present attosecond transient-absorption experiments on xenon 4d-16p core-level states resonantly driven by intense (1.6×1014W/cm2) few-cycle near-infrared laser pulses. In this strongly driven regime, broad induced absorption features with half-cycle (1.3-fs) delay-dependent modulation are observed over the range of 58-65 eV, predicted as a signature of the breakdown of the rotating-wave approximation in strong-field driving of Autler-Townes splitting [A. N. Pfeiffer and S. R. Leone, Phys. Rev. A 85, 053422 (2012)PLRAAN1050-294710.1103/PhysRevA.85.053422]. Relevant atomic states are identified by a numerical model involving three electronic states, and the mechanism behind the broad induced absorption is discussed in the Floquet formalism. These results demonstrate that a near-infrared field well into the tunneling regime can still control the optical properties of an atomic system over a several-electron-volt spectral range and with attosecond precision.

Attosecond spectroscopy is a powerful technique for probing electron dynamics in fundamental systems. However, extending this method to cover a wide range of element-specific, core-hole transitions requires the availability of broadly tunable attosecond pulses. In this Letter, we present a new method for generating high-flux, high-contrast single attosecond pulses tunable across the range of 50-120 eV. The method is referred to as a Polarization ASSisted Amplitude GatE (PASSAGE) and uses a few-cycle driving pulse along with a partial polarization gate to extend the bandwidth of high harmonic emission in the temporally isolated, cut-off portion of the spectrum. The simplicity of this technique will help pave the way for implementing attosecond core-hole spectroscopy to probe more complex reactions and bring attosecond science into a multidisciplinary setting.

Attosecond transient absorption experiments are performed to study strong-field ionization dynamics in xenon and methyl bromide. Results in Xe depict half-cycle ionization steps that exhibit an apparent time delay between spin-orbit ionization channels.

Attosecond probing of core-level electronic transitions provides a sensitive tool for studying valence molecular dynamics with atomic, state, and charge specificity. In this report, we employ attosecond transient absorption spectroscopy to follow the valence dynamics of strong-field initiated processes in methyl bromide. By probing the 3d core-to-valence transition, we resolve the strong field excitation and ensuing fragmentation of the neutral σ* excited states of methyl bromide. The results provide a clear signature of the non-adiabatic passage of the excited state wavepacket through a conical intersection. We additionally observe competing, strong field initiated processes arising in both the ground state and ionized molecule corresponding to vibrational and spin-orbit motion, respectively. The demonstrated ability to resolve simultaneous dynamics with few-femtosecond resolution presents a clear path forward in the implementation of attosecond XUV spectroscopy as a general tool for probing competing and complex molecular phenomena with unmatched temporal resolution.

Background: Lead neurotoxicity is a major health problem known as a risk factor for neurodegenerative diseases, including the manifestation of parkinsonism-like disorder. While lead is known to preferentially accumulate in basal ganglia, the mechanisms underlying behavioral disorders remain unknown. Here, we investigated the neurophysiological and biochemical correlates of motor deficits induced by sub-chronic injections of lead. Methods: Sprague Dawely rats were exposed to sub-chronic injections of lead (10 mg/kg, i.p.) or to a single i.p. injection of 50 mg/kg N -(2-chloroethyl)- N -ethyl-2-bromobenzylamine hydrochloride (DSP-4), a drug known to induce selective depletion of noradrenaline. Rats were submitted to a battery of behavioral tests, including the open field for locomotor activity and rotarod for motor coordination. Electrophysiological recordings were carried out in three major basal ganglia nuclei, the subthalamic nucleus (STN), globus pallidus (GP), and substantia nigra pars reticulata (SNr). At the end of experiments, post-mortem tissue level of the three monoamines (dopamine, noradrenaline, and serotonin) and their metabolites has been determined using HPLC. Results: Lead intoxication significantly impaired exploratory and locomotor activity as well as motor coordination. It resulted in a significant reduction in the level of noradrenaline in the cortex and dopamine and its metabolites, DOPAC, and HVA, in the striatum. The tissue level of serotonin and its metabolite 5-HIAA was not affected in the two structures. Similarly, DSP-4, which induced a selective depletion of noradrenaline, significantly decreased exploratory, and locomotor activity as well as motor coordination. L-DOPA treatment did not improve motor deficits induced by lead and DSP-4 in the two animal groups. Electrophysiological recordings showed that both lead and DSP-4 did not change the firing rate but resulted in a switch from the regular normal firing to irregular and bursty discharge patterns of STN neurons. Neither lead nor DSP-4 treatments changed the firing rate and the pattern of GP and SNr neurons. Conclusions: Our findings provide evidence that lead represents a risk factor for inducing parkinsonism-like deficits. As the motor deficits induced by lead were not improved by L-DOPA, we suggest that the deficits may be due to the depletion of noradrenaline and the parallel disorganization of STN neuronal activity.

Lead exposure has been reported to produce many clinical features, including parkinsonism. However, its consequences on the circadian rhythms are still unknown. Here we aimed to examine the circadian rhythms of locomotor activity following lead intoxication and investigate the mechanisms by which lead may induce alterations of circadian rhythms in rats. Male Wistar rats were injected with lead or sodium acetate (10 mg/kg/day, i.p.) during 4 weeks. Both groups were tested in the "open field" to quantify the exploratory activity and in the rotarod to evaluate motor coordination. Then, animals were submitted to continuous 24 h recordings of locomotor activity under 14/10 Light/dark (14/10 LD) cycle and in complete darkness (DD). At the end of experiments, the clock proteins BMAL1, PER1-2, and CRY1-2 were assayed in the suprachiasmatic nucleus (SCN) using immunohistochemistry. We showed that lead significantly reduced the number of crossing in the open field, impaired motor coordination and altered the daily locomotor activity rhythm. When the LD cycle was advanced by 6 h, both groups adjusted their daily locomotor activity to the new LD cycle with high onset variability in lead-intoxicated rats compared to controls. Lead also led to a decrease in the number of immunoreactive cells (ir-) of BMAL1, PER1, and PER2 without affecting the number of ir-CRY1 and ir-CRY2 cells in the SCN. Our data provide strong evidence that lead intoxication disturbs the rhythm of locomotor activity and alters clock proteins expression in the SCN. They contribute to the understanding of the mechanism by which lead induce circadian rhythms disturbances.

Synapses are essential components of neurons and allow information to travel coordinately throughout the nervous system to adjust behavior to environmental stimuli and to control body functions, memories, and emotions. Thus, optimal synaptic communication is required for proper brain physiology, and slight perturbations of synapse function can lead to brain disorders. In fact, increasing evidence has demonstrated the relevance of synapse dysfunction as a major determinant of many neurological diseases. This notion has led to the concept of synaptopathies as brain diseases with synapse defects as shared pathogenic features. In this review, which was initiated at the 13th International Society for Neurochemistry Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental disorders (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer and Parkinson disease). We finally discuss the appropriateness and potential implications of gathering synapse diseases under a single term. Understanding common causes and intrinsic differences in disease-associated synaptic dysfunction could offer novel clues toward synapse-based therapeutic intervention for neurological and neuropsychiatric disorders. In this Review, which was initiated at the 13th International Society for Neurochemistry (ISN) Advanced School, we discuss basic concepts of synapse structure and function, and provide a critical view of how aberrant synapse physiology may contribute to neurodevelopmental (autism, Down syndrome, startle disease, and epilepsy) as well as neurodegenerative disorders (Alzheimer's and Parkinson's diseases), gathered together under the term of synaptopathies. Read the Editorial Highlight for this article on page 783., (© 2016 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry.)

Despite the documented post-infectious neurological complications of a central nervous system (CNS) Mycoplasma infection in humans, very few studies have investigated the acute inflammatory responses and sickness behaviours induced by CNS Mycoplasma infections. We therefore determined the effect of acute central administration of fibroblast-stimulating lipopeptide-1 (FSL-1), derived from Mycoplasma salivarium, and FAM-20 from a more pathogenic species, namely Mycoplasma pneumoniae, on behavioural and inflammatory responses in rats. Male Sprague-Dawley rats had radiotransmitters implanted, intra-abdominally, to measure body temperature and cage activity continuously. After recovery from surgery, rats were conditioned in a fear conditioning task and then immediately received an intra-cisterna magna (i.c.m.) injection of either: (1) FSL-1 (10 or 100μg/5μl) or its vehicle (phosphate-buffered saline, 5μl), or (2) FAM-20 (10 or 100μg/5μl) or its vehicle (dimethyl sulfoxide, 5μl). Body mass and food intake were measured daily. Memory was assessed seven days after injection using fear conditioning tests. A single, i.c.m. injection of either FSL-1 or FAM-20 induced profound, dose-dependent fever, anorexia, lethargy and body mass stunting in rats. Moreover, rats that received an i.c.m. injection of 100μg/5μl FAM-20 had a significant increase in the concentration of IL-1β in both the hypothalamus and the hippocampus for ~27h after injection. Seven days after FSL-1 or FAM-20 injection, when body mass of rats still was stunted, they maintained their memory for fear of the context and for fear of the tone, despite the increase in hippocampal IL-1β concentration after FAM-20 administration. Thus, acute simulated CNS Mycoplasma infections caused pronounced sickness responses and brain inflammation in rats, but spared fear memory., (Copyright © 2016 Elsevier Inc. All rights reserved.)

The phase and period responses to short light pulses were studied in the jerboa, a seasonal, hibernating, nocturnal rodent from the Atlas region in Morocco. The jerboa, which is a saltatory species, showed precise activity onsets and offsets under a light-dark (LD) cycle using infrared captors to record locomotor activity. When released into constant darkness (DD), the majority of animals showed a circadian period (tau) < 24 h (mean tau = 23.89 +/- 0.13 h) and a lengthening of the activity span, alpha. Animals were subsequently exposed to up to eight 15-min light pulses, each separated by at least 2 wks, for up to 160 days in DD. During this span, most individuals maintained robust circadian rhythmicity, with clearly defined activity onsets and offsets, similar levels of total activity, duration of alpha, and percent activity occurring during the subjective night. The phase response curve (PRC) is typical of other nocturnal rodents, with light eliciting delays during late subjective day and early subjective night (CT8-CT19) and advances during late subjective night to early subjective day (CT19-CT2). A dead zone, when light had no effect on phase, is observed during mid-subjective day (CT3-CT8). A few individuals showed large (> 9 h) Type 0 phase resetting near the singularity region (CT19) that resulted in a complete phase reversal, but otherwise displayed normal phase-shifting responses at other CT times. The tau response curve showed a decrease in period from early to late subjective night with increases at other times, but these changes were small (maximum < 9 min) and highly variable. There was a distinct tendency for animals that had an initial short tau in DD to conserve a short tau during the series of light pulses and, inversely, for animals with long tau to conserve a long tau. This suggests possible constraints on the plasticity of variation of tau in relation to the endogenous period of the animal.