Dynamical Casimir effect for a massless scalar field between two concentric spherical shells

In this work we consider the dynamical Casimir effect for a massless scalar field -- under Dirichlet boundary conditions -- between two concentric spherical shells. We obtain a general expression for the average number of particle creation, for an arbitrary law of radial motion of the spherical shells, using two distinct methods: by computing the density operator of the system and by calculating the Bogoliubov coefficients. We apply our general expression to breathing modes: when only one of the shells oscillates and when both shells oscillate in or out of phase. We also analyze the number of particle production and compare it with the results for the case of plane geometry.Comment: Final version. To apear in Physical Review

Sonoluminescence and sonochemiluminescence from a microreactor

Micromachined pits on a substrate can be used to nucleate and stabilize microbubbles in a liquid exposed to an ultrasonic field. Under suitable conditions, the collapse of these bubbles can result in light emission (sonoluminescence, SL). Hydroxyl radicals (OH*) generated during bubble collapse can react with luminol to produce light (sonochemiluminescence, SCL). SL and SCL intensities were recorded for several regimes related to the pressure amplitude (low and high acoustic power levels) at a given ultrasonic frequency (200 kHz) for pure water, and aqueous luminol and propanol solutions. Various arrangements of pits were studied, with the number of pits ranging from no pits (comparable to a classic ultrasound reactor), to three-pits. Where there was more than one pit present, in the high pressure regime the ejected microbubbles combined into linear (two-pits) or triangular (three-pits) bubble clouds (streamers). In all situations where a pit was present on the substrate, the SL was intensified and increased with the number of pits at both low and high power levels. For imaging SL emitting regions, Argon (Ar) saturated water was used under similar conditions. SL emission from aqueous propanol solution (50 mM) provided evidence of transient bubble cavitation. Solutions containing 0.1 mM luminol were also used to demonstrate the radical production by attaining the SCL emission regions.Comment: http://www.sciencedirect.com/science/article/pii/S1350417712000855; ISSN 1350-417

Jean-Martin Charcot’s role in the 19th century study of music aphasia

Jean-Martin Charcot (1825–93) was a well-known French neurologist. Although he is widely recognized for his discovery of several neurological disorders and his research into aphasia, Charcot’s ideas about how the brain processes music are less well known. Charcot discussed the music abilities of several patients in the context of his ‘Friday Lessons’ on aphasia, which took place at the Salpêtrière Hospital in Paris in 1883–84. In his most comprehensive discussion about music, Charcot described a professional trombone player who developed difficulty copying music notation and playing his instrument, thereby identifying a new isolated syndrome of music agraphia without aphasia. Because the description of this case was published only in Italian by one of his students, Domenico Miliotti, there has been considerable confusion and under-acknowledgement of Charcot’s ideas about music and the brain. In this paper, we describe Charcot’s ideas regarding music and place them within the historical context of the growing interest in the neurological underpinnings of music abilities that took place in the 1880s

Target-dependence of sensory neurons: An ultrastructural comparison of axotomised dorsal root ganglion neurons with allowed or denied reinnervation of peripheral targets

Evidence is emerging for a role of rough endoplasmic reticulum (RER) in the form of stress granules, the unfolded protein response and protein bodies in the response of neurons to injury and in neurodegenerative diseases. Here, we have studied the role of the peripheral target in regulating the RER and polyribosomes of Nissl bodies in axotomised adult cat dorsal root ganglion (DRG) neurons where axonal regeneration and peripheral target reinnervation was either allowed or denied. Retrograde labelling with horseradish peroxidise was used as an independent marker to enable selection of only those DRG neuronal cell bodies with axons in the injured intercostal nerves. Indications of polyribosomal dispersal were seen by 6 h following axotomy, and by 24 h the normal orderly arrangement of lamellae of RER in Nissl bodies had become disorganised. These ultrastructural changes preceded light microscopical chromatolysis by 1–3 d. The retrograde response was maximal 8–32 d after axotomy. Clusters of debris-laden satellite cells/macrophages were present at this time but no ultrastructural evidence of neuronal apoptosis or necrosis was seen and there were no differences in the initial retrograde response according to the type of injury. By 64 d following axotomy with reinnervation, approximately half the labelled DRG neurons showed restoration of the orderly arrangement of RER and polyribosomes in their Nissl bodies. This was not seen after axotomy with reinnervation denied. We propose that the target-dependent changes in Nissl body ultrastructure described here are part of a continuum that can modify neuronal protein synthesis directed towards growth, maintenance or death of the neuron. This represents a possible structural basis for mediating the varied effects of neurotrophic interactions.I. P. Johnson and T. A. Sear

A spiral attractor network drives rhythmic locomotion

The joint activity of neural populations is high dimensional and complex. One strategy for reaching a tractable understanding of circuit function is to seek the simplest dynamical system that can account for the population activity. By imaging Aplysia’s pedal ganglion during fictive locomotion, here we show that its population wide activity arises from a low-dimensional spiral attractor. Evoking locomotion moved the population into a low-dimensional, periodic, decaying orbit - a spiral – in which it behaved as a true attractor, converging to the same orbit when evoked, and returning to that orbit after transient perturbation. We found the same attractor in every preparation, and could predict motor output directly from its orbit, yet individual neurons’ participation changed across consecutive locomotion bouts. From these results, we propose that only the low-dimensional dynamics for movement control, and not the high-dimensional population activity, are consistent within and between nervous systems

Malignant astrocyte swelling and impaired glutamate clearance drive the expansion of injurious spreading depolarization foci

Spreading depolarizations (SDs) indicate injury progression and predict worse clinical outcome in acute brain injury. We demonstrate in rodents that acute brain swelling upon cerebral ischemia impairs astroglial glutamate clearance and increases the tissue area invaded by SD. The cytotoxic extracellular glutamate accumulation (>15 mu M) predisposes an extensive bulk of tissue (4-5 mm(2)) for a yet undescribed simultaneous depolarization (SiD). We confirm in rat brain slices exposed to osmotic stress that SiD is the pathological expansion of prior punctual SD foci (0.5-1 mm(2)), is associated with astrocyte swelling, and triggers oncotic neuron death. The blockade of astrocytic aquaporin-4 channels and Na+/K+/Cl- co-transporters, or volume-regulated anion channels mitigated slice edema, extracellular glutamate accumulation (<10 mu M) and SiD occurrence. Reversal of slice swelling by hyperosmotic mannitol counteracted glutamate accumulation and prevented SiD. In contrast, inhibition of glial metabolism or inhibition of astrocyte glutamate transporters reproduced the SiD phenotype. Finally, we show in the rodent water intoxication model of cytotoxic edema that astrocyte swelling and altered astrocyte calcium waves are central in the evolution of SiD. We discuss our results in the light of evidence for SiD in the human cortex. Our results emphasize the need of preventive osmotherapy in acute brain injury

Toward a multiscale modeling framework for understanding serotonergic function

Despite its importance in regulating emotion and mental wellbeing, the complex structure and function of the serotonergic system present formidable challenges toward understanding its mechanisms. In this paper, we review studies investigating the interactions between serotonergic and related brain systems and their behavior at multiple scales, with a focus on biologically-based computational modeling. We first discuss serotonergic intracellular signaling and neuronal excitability, followed by neuronal circuit and systems levels. At each level of organization, we will discuss the experimental work accompanied by related computational modeling work. We then suggest that a multiscale modeling approach that integrates the various levels of neurobiological organization could potentially transform the way we understand the complex functions associated with serotonin

Conditional corticotropin-releasing hormone overexpression in the mouse forebrain enhances rapid eye movement sleep

Impaired sleep and enhanced stress hormone secretion are the hallmarks of stress-related disorders, including major depression. The central neuropeptide, corticotropin-releasing hormone (CRH), is a key hormone that regulates humoral and behavioral adaptation to stress. Its prolonged hypersecretion is believed to play a key role in the development and course of depressive symptoms, and is associated with sleep impairment. To investigate the specific effects of central CRH overexpression on sleep, we used conditional mouse mutants that overexpress CRH in the entire central nervous system (CRH-COE-Nes) or only in the forebrain, including limbic structures (CRH-COE-Cam). Compared with wild-type or control mice during baseline, both homozygous CRH-COE-Nes and -Cam mice showed constantly increased rapid eye movement (REM) sleep, whereas slightly suppressed non-REM sleep was detected only in CRH-COE-Nes mice during the light period. In response to 6-h sleep deprivation, elevated levels of REM sleep also became evident in heterozygous CRH-COE-Nes and -Cam mice during recovery, which was reversed by treatment with a CRH receptor type 1 (CRHR1) antagonist in heterozygous and homozygous CRH-COE-Nes mice. The peripheral stress hormone levels were not elevated at baseline, and even after sleep deprivation they were indistinguishable across genotypes. As the stress axis was not altered, sleep changes, in particular enhanced REM sleep, occurring in these models are most likely induced by the forebrain CRH through the activation of CRHR1. CRH hypersecretion in the forebrain seems to drive REM sleep, supporting the notion that enhanced REM sleep may serve as biomarker for clinical conditions associated with enhanced CRH secretion