Entanglement in Finitely Correlated Spin States

We derive bounds for the entanglement of a spin with an (adjacent and non-adjacent) interval of spins in an arbitrary pure finitely correlated state (FCS) on a chain of spins of any magnitude. Finitely correlated states are otherwise known as matrix product states or generalized valence-bond states. The bounds become exact in the limit of the entanglement of a single spin and the half-infinite chain to the right (or the left) of it. Our bounds provide a proof of the recent conjecture by Benatti, Hiesmayr, and Narnhofer that their necessary condition for non-vanishing entanglement in terms of a single spin and the ``memory'' of the FCS, is also sufficient . Our result also generalizes the study of entanglement in the ground state of the AKLT model by Fan, Korepin, and Roychowdhury. Our result permits one to calculate more efficiently, numerically and in some cases even analytically, the entanglement of arbitrary finitely correlated quantum spin chains.Comment: PACS 03.67.Mn, 05.50.+q. Minor typos in v1 corrected. In v2: expanded Introduction and Discussion. Simplified proof of the main resul

Area law for fixed points of rapidly mixing dissipative quantum systems

We prove an area law with a logarithmic correction for the mutual information for fixed points of local dissipative quantum system satisfying a rapid mixing condition, under either of the following assumptions: the fixed point is pure, or the system is frustration free.Comment: 17 pages, 1 figure. Final versio

Stability of Local Quantum Dissipative Systems

This is the author accepted manuscript. The final version is available from Springer at http://link.springer.com/article/10.1007%2Fs00220-015-2355-3.Open quantum systems weakly coupled to the environment are modeled by completely positive, trace preserving semigroups of linear maps. The generators of such evolutions are called Lindbladians. In the setting of quantum many-body systems on a lattice it is natural to consider Lindbladians that decompose into a sum of local interactions with decreasing strength with respect to the size of their support. For both practical and theoretical reasons, it is crucial to estimate the impact that perturbations in the generating Lindbladian, arising as noise or errors, can have on the evolution. These local perturbations are potentially unbounded, but constrained to respect the underlying lattice structure. We show that even for polynomially decaying errors in the Lindbladian, local observables and correlation functions are stable if the unperturbed Lindbladian has a unique fixed point and a mixing time which scales logarithmically with the system size. The proof relies on Lieb-Robinson bounds, which describe a finite group velocity for propagation of information in local systems. As a main example, we prove that classical Glauber dynamics is stable under local perturbations, including perturbations in the transition rates which may not preserve detailed balance

Rapid mixing and stability of quantum dissipative systems

This is the author accepted manuscript. The final version is available from APS at http://journals.aps.org/pra/abstract/10.1103/PhysRevA.91.040302.The physics of many materials is modeled by quantum many-body systems with local interactions. If the model of the system is sensitive to noise from the environment, or small perturbations to the original interactions, it will not model properly the robustness of the real physical system it aims to describe, or be useful when engineering novel systems for quantum information processing. We show that local observables and correlation functions of local Liouvillians are stable to local perturbations if the dynamics is rapidly mixing and has a unique xed point. No other condition is required.T. S. C. is supported by the Royal Society, and was pre- viously supported by the Juan de la Cierva program of the Spanish MICIM. A. L. and D. P.-G. acknowledge support from MINECO (grant MTM2011-26912), Comunidad de Madrid (grant QUITEMAD+-CM, ref. S2013/ICE-2801) and the European CHIST-ERA project CQC (funded partially by MINECO grant PRI-PIMCHI-2011-1071). A. L. is supported by MINECO FPI fellowship BES-2012- 052404. S. M. acknowledges funding provided by IQIM, an NSF Physics Frontiers Center with support of the Gordon and Betty Moore Foundation through Grant #GBMF1250, and AFOSR Grant #FA8750-12-2-0308. The authors would like to thank the hospitality of the Centro de Ciencias Pedro Pascual in Benasque, where part of this work was carried out

Large Bottleneck Size in Cauliflower Mosaic Virus Populations during Host Plant Colonization

The effective size of populations (Ne) determines whether selection or genetic drift is the predominant force shaping their genetic structure and evolution. Despite their high mutation rate and rapid evolution, this parameter is poorly documented experimentally in viruses, particularly plant viruses. All available studies, however, have demonstrated the existence of huge within-host demographic fluctuations, drastically reducing Ne upon systemic invasion of different organs and tissues. Notably, extreme bottlenecks have been detected at the stage of systemic leaf colonization in all plant viral species investigated so far, sustaining the general idea that some unknown obstacle(s) imposes a barrier on the development of all plant viruses. This idea has important implications, as it appoints genetic drift as a constant major force in plant virus evolution. By co-inoculating several genetic variants of Cauliflower mosaic virus into a large number of replicate host plants, and by monitoring their relative frequency within the viral population over the course of the host systemic infection, only minute stochastic variations were detected. This allowed the estimation of the CaMV Ne during colonization of successive leaves at several hundreds of viral genomes, a value about 100-fold higher than that reported for any other plant virus investigated so far, and indicated the very limited role played by genetic drift during plant systemic infection by this virus. These results suggest that the barriers that generate bottlenecks in some plant virus species might well not exist, or can be surmounted by other viruses, implying that severe bottlenecks during host colonization do not necessarily apply to all plant-infecting viruses

Morpho-Rheological Fingerprinting of Rod Photoreceptors Using Real-Time Deformability Cytometry

Distinct cell-types within the retina are mainly specified by morphological and molecular parameters, however, physical properties are increasingly recognized as a valuable tool to characterize and distinguish cells in diverse tissues. High-throughput analysis of morpho-rheological features has recently been introduced using real-time deformability cytometry (RT-DC) providing new insights into the properties of different cell-types. Rod photoreceptors represent the main light sensing cells in the mouse retina that during development forms apically the densely packed outer nuclear layer. Currently, enrichment and isolation of photoreceptors from retinal primary tissue or pluripotent stem cell-derived organoids for analysis, molecular profiling, or transplantation is achieved using flow cytometry or magnetic activated cell sorting approaches. However, such purification methods require genetic modification or identification of cell surface binding antibody panels. Using primary retina and embryonic stem cell-derived retinal organoids, we characterized the inherent morpho-mechanical properties of mouse rod photoreceptors during development based on RT-DC. We demonstrate that rods become smaller and more compliant throughout development and that these features are suitable to distinguish rods within heterogenous retinal tissues. Hence, physical properties should be considered as additional factors that might affect photoreceptor differentiation and retinal development besides representing potential parameters for label-free sorting of photoreceptors

Altered synaptic plasticity and behavioral abnormalities in CNGA3-deficient mice

The role of the cyclic nucleotide-gated (CNG) channel CNGA3 is well established in cone photoreceptors and guanylyl cyclase-D-expressing olfactory neurons. To assess a potential function of CNGA3 in the mouse amygdala and hippocampus, we examined synaptic plasticity and performed a comparative analysis of spatial learning, fear conditioning and step-down avoidance in wild-type mice and CNGA3 null mutants (CNGA3(-/-) ). CNGA3(-/-) mice showed normal basal synaptic transmission in the amygdala and the hippocampus. However, cornu Ammonis (CA1) hippocampal long-term potentiation (LTP) induced by a strong tetanus was significantly enhanced in CNGA3(-/-) mice as compared with their wild-type littermates. Unlike in the hippocampus, LTP was not significantly altered in the amygdala of CNGA3(-/-) mice. Enhanced hippocampal LTP did not coincide with changes in hippocampus-dependent learning, as both wild-type and mutant mice showed a similar performance in water maze tasks and contextual fear conditioning, except for a trend toward higher step-down latencies in a passive avoidance task. In contrast, CNGA3(-/-) mice showed markedly reduced freezing to the conditioned tone in the amygdala-dependent cued fear conditioning task. In conclusion, our study adds a new entry on the list of physiological functions of the CNGA3 channel. Despite the dissociation between physiological and behavioral parameters, our data describe a so far unrecognized role of CNGA3 in modulation of hippocampal plasticity and amygdala-dependent fear memory

Metabolic analysis of vitreous/lens and retina in wild type and retinal degeneration mice

Photoreceptors are the light-sensing cells of the retina and the major cell type affected in most inherited retinal degenerations. Different metabolic pathways sustain their high energetic demand in physiological conditions, particularly aerobic glycolysis. The principal metabolome of the mature retina has been studied, but only limited information is available on metabolic adaptations in response to key developmental events, such as eye opening. Moreover, dynamic metabolic changes due to retinal degeneration are not well understood. Here, we aimed to explore and map the ocular metabolic dynamics induced by eye opening in healthy (wild type) or Pde6b-mutant (retinal degeneration 1, Rd1) mice, in which photoreceptors degenerate shortly after eye opening. To unravel metabolic differences emerging before and after eye opening under physiological and pathophysiological conditions, we performed nuclear magnetic resonance (NMR) spectrosco-py-based metabolome analysis of wild type and Rd1 retina and vitreous/lens. We show that eye opening is accompanied by changes in the concentration of selected metabolites in the retina and by alterations in the vitreous/lens composition only in the retinal degeneration context. As such, we identify N-Acetylaspartate as a potential novel vitreous/lens marker reflecting progressive retinal degeneration. Thus, our data can help elucidating mechanisms underlying key events in retinal physiology and reveal changes occurring in pathology, while highlighting the importance of the vitreous/lens in the characterization of retinal diseases.Proteomic

Remote and reversible inhibition of neurons and circuits by small molecule induced potassium channel stabilization

Manipulating the function of neurons and circuits that translate electrical and chemical signals into behavior represents a major challenges in neuroscience. In addition to optogenetic methods using light-activatable channels, pharmacogenetic methods with ligand induced modulation of cell signaling and excitability have been developed. However, they are largely based on ectopic expression of exogenous or chimera proteins. Now, we describe the remote and reversible expression of a Kir2.1 type potassium channel using the chemogenetic technique of small molecule induced protein stabilization. Based on shield1-mediated shedding of a destabilizing domain fused to a protein of interest and inhibition of protein degradation, this principle has been adopted for biomedicine, but not in neuroscience so far. Here, we apply this chemogenetic approach in brain research for the first time in order to control a potassium channel in a remote and reversible manner. We could show that shield1-mediated ectopic Kir2.1 stabilization induces neuronal silencing in vitro and in vivo in the mouse brain. We also validated this novel pharmacogenetic method in different neurobehavioral paradigms. The DD-Kir2.1 may complement the existing portfolio of pharmaco- and optogenetic techniques for specific neuron manipulation, but it may also provide an example for future applications of this principle in neuroscience research