The Impact of Non-Equipartition on Cosmological Parameter Estimation from Sunyaev-Zel'dovich Surveys

The collisionless accretion shock at the outer boundary of a galaxy cluster should primarily heat the ions instead of electrons since they carry most of the kinetic energy of the infalling gas. Near the accretion shock, the density of the intracluster medium is very low and the Coulomb collisional timescale is longer than the accretion timescale. Electrons and ions may not achieve equipartition in these regions. Numerical simulations have shown that the Sunyaev-Zel'dovich observables (e.g., the integrated Comptonization parameter Y) for relaxed clusters can be biased by a few percent. The Y-mass relation can be biased if non-equipartition effects are not properly taken into account. Using a set of hydrodynamical simulations, we have calculated three potential systematic biases in the Y-mass relations introduced by non-equipartition effects during the cross-calibration or self-calibration when using the galaxy cluster abundance technique to constraint cosmological parameters. We then use a semi-analytic technique to estimate the non-equipartition effects on the distribution functions of Y (Y functions) determined from the extended Press-Schechter theory. Depending on the calibration method, we find that non-equipartition effects can induce systematic biases on the Y functions, and the values of the cosmological parameters Omega_8, sigma_8, and the dark energy equation of state parameter w can be biased by a few percent. In particular, non-equipartition effects can introduce an apparent evolution in w of a few percent in all of the systematic cases we considered. Techniques are suggested to take into account the non-equipartition effect empirically when using the cluster abundance technique to study precision cosmology. We conclude that systematic uncertainties in the Y-mass relation of even a few percent can introduce a comparable level of biases in cosmological parameter measurements.Comment: 10 pages, 3 figures, accepted for publication in the Astrophysical Journal, abstract abridged slightly. Typos corrected in version

Quantum Gravity Partition Functions in Three Dimensions

We consider pure three-dimensional quantum gravity with a negative cosmological constant. The sum of known contributions to the partition function from classical geometries can be computed exactly, including quantum corrections. However, the result is not physically sensible, and if the model does exist, there are some additional contributions. One possibility is that the theory may have long strings and a continuous spectrum. Another possibility is that complex geometries need to be included, possibly leading to a holomorphically factorized partition function. We analyze the subleading corrections to the Bekenstein-Hawking entropy and show that these can be correctly reproduced in such a holomorphically factorized theory. We also consider the Hawking-Page phase transition between a thermal gas and a black hole and show that it is a phase transition of Lee-Yang type, associated with a condensation of zeros in the complex temperature plane. Finally, we analyze pure three-dimensional supergravity, with similar results.Comment: 71 pages, 6 figure

An International Laboratory for Systems and Computational Neuroscience

The neural basis of decision-making has been elusive and involves the coordinated activity of multiple brain structures. This NeuroView, by the International Brain Laboratory (IBL), discusses their efforts to develop a standardized mouse decision-making behavior, to make coordinated measurements of neural activity across the mouse brain, and to use theory and analyses to uncover the neural computations that support decision-making. The neural basis of decision-making has been elusive and involves the coordinated activity of multiple brain structures. This NeuroView, by the International Brain Laboratory (IBL), discusses their efforts to develop a standardized mouse decision-making behavior, to make coordinated measurements of neural activity across the mouse brain, and to use theory and analyses to uncover the neural computations that support decision-making

Reducing bias in auditory duration reproduction by integrating the reproduced signal

Duration estimation is known to be far from veridical and to differ for sensory estimates and motor reproduction. To investigate how these differential estimates are integrated for estimating or reproducing a duration and to examine sensorimotor biases in duration comparison and reproduction tasks, we compared estimation biases and variances among three different duration estimation tasks: perceptual comparison, motor reproduction, and auditory reproduction (i.e. a combined perceptual-motor task). We found consistent overestimation in both motor and perceptual-motor auditory reproduction tasks, and the least overestimation in the comparison task. More interestingly, compared to pure motor reproduction, the overestimation bias was reduced in the auditory reproduction task, due to the additional reproduced auditory signal. We further manipulated the signal-to-noise ratio (SNR) in the feedback/comparison tones to examine the changes in estimation biases and variances. Considering perceptual and motor biases as two independent components, we applied the reliability-based model, which successfully predicted the biases in auditory reproduction. Our findings thus provide behavioral evidence of how the brain combines motor and perceptual information together to reduce duration estimation biases and improve estimation reliability

The threshold for the McGurk effect in audio-visual noise decreases with development

Across development, vision increasingly infuences audio-visual perception. This is evidenced in illusions such as the McGurk efect, in which a seen mouth movement changes the perceived sound. The current paper assessed the efects of manipulating the clarity of the heard and seen signal upon the McGurk efect in children aged 3–6 (n=29), 7–9 (n=32) and 10–12 (n=29) years, and adults aged 20–35 years (n=32). Auditory noise increased, and visual blur decreased, the likelihood of vision changing auditory perception. Based upon a proposed developmental shift from auditory to visual dominance we predicted that younger children would be less susceptible to McGurk responses, and that adults would continue to be infuenced by vision in higher levels of visual noise and with less auditory noise. Susceptibility to the McGurk efect was higher in adults compared with 3–6-year-olds and 7–9-yearolds but not 10–12-year-olds. Younger children required more auditory noise, and less visual noise, than adults to induce McGurk responses (i.e. adults and older children were more easily infuenced by vision). Reduced susceptibility in childhood supports the theory that sensory dominance shifts across development and reaches adult-like levels by 10 years of age

Fold change and p-value cutoffs significantly alter microarray interpretations

<p>Abstract</p> <p>Background</p> <p>As context is important to gene expression, so is the preprocessing of microarray to transcriptomics. Microarray data suffers from several normalization and significance problems. Arbitrary fold change (FC) cut-offs of >2 and significance p-values of <0.02 lead data collection to look only at genes which vary wildly amongst other genes. Therefore, questions arise as to whether the biology or the statistical cutoff are more important within the interpretation. In this paper, we reanalyzed a zebrafish (<it>D. rerio</it>) microarray data set using GeneSpring and different differential gene expression cut-offs and found the data interpretation was drastically different. Furthermore, despite the advances in microarray technology, the array captures a large portion of genes known but yet still leaving large voids in the number of genes assayed, such as leptin a pleiotropic hormone directly related to hypoxia-induced angiogenesis.</p> <p>Results</p> <p>The data strongly suggests that the number of differentially expressed genes is more up-regulated than down-regulated, with many genes indicating conserved signalling to previously known functions. Recapitulated data from Marques et al. (2008) was similar but surprisingly different with some genes showing unexpected signalling which may be a product of tissue (heart) or that the intended response was transient.</p> <p>Conclusions</p> <p>Our analyses suggest that based on the chosen statistical or fold change cut-off; microarray analysis can provide essentially more than one answer, implying data interpretation as more of an art than a science, with follow up gene expression studies a must. Furthermore, gene chip annotation and development needs to maintain pace with not only new genomes being sequenced but also novel genes that are crucial to the overall gene chips interpretation.</p

Dopamine neurons modulate neural encoding and expression of depression-related behaviour

Major depression is characterized by diverse debilitating symptoms that include hopelessness and anhedonia1. Dopamine neurons involved in reward and motivation are among many neural populations that have been hypothesized to be relevant, and certain antidepressant treatments, including medications and brain stimulation therapies, can influence the complex dopamine system. Until now it has not been possible to test this hypothesis directly, even in animal models, as existing therapeutic interventions are unable to specifically target dopamine neurons. Here we investigated directly the causal contributions of defined dopamine neurons to multidimensional depression-like phenotypes induced by chronic mild stress, by integrating behavioural, pharmacological, optogenetic and electrophysiological methods in freely moving rodents. We found that bidirectional control (inhibition or excitation) of specified midbrain dopamine neurons immediately and bidirectionally modulates (induces or relieves) multiple independent depression symptoms caused by chronic stress. By probing the circuit implementation of these effects, we observed that optogenetic recruitment of these dopamine neurons potently alters the neural encoding of depression-related behaviours in the downstream nucleus accumbens of freely moving rodents, suggesting that processes affecting depression symptoms may involve alterations in the neural encoding of action in limbic circuitry

Input-specific control of reward and aversion in the ventral tegmental area

Ventral tegmental area (VTA) dopamine neurons have important roles in adaptive and pathological brain functions related to reward and motivation. However, it is unknown whether subpopulations of VTA dopamine neurons participate in distinct circuits that encode different motivational signatures, and whether inputs to the VTA differentially modulate such circuits. Here we show that, because of differences in synaptic connectivity, activation of inputs to the VTA from the laterodorsal tegmentum and the lateral habenula elicit reward and aversion in mice, respectively. Laterodorsal tegmentum neurons preferentially synapse on dopamine neurons projecting to the nucleus accumbens lateral shell, whereas lateral habenula neurons synapse primarily on dopamine neurons projecting to the medial prefrontal cortex as well as on GABAergic (γ-aminobutyric-acid-containing) neurons in the rostromedial tegmental nucleus. These results establish that distinct VTA circuits generate reward and aversion, and thereby provide a new framework for understanding the circuit basis of adaptive and pathological motivated behaviours.National Institutes of Health (U.S.) (Grant NIH NS069375)JPB FoundationNational Institute of Mental Health (U.S.

Cholinergic Interneurons Mediate Fast VGluT3-Dependent Glutamatergic Transmission in the Striatum

The neurotransmitter glutamate is released by excitatory projection neurons throughout the brain. However, non-glutamatergic cells, including cholinergic and monoaminergic neurons, express markers that suggest that they are also capable of vesicular glutamate release. Striatal cholinergic interneurons (CINs) express the Type-3 vesicular glutamate transporter (VGluT3), although whether they form functional glutamatergic synapses is unclear. To examine this possibility, we utilized mice expressing Cre-recombinase under control of the endogenous choline acetyltransferase locus and conditionally expressed light-activated Channelrhodopsin2 in CINs. Optical stimulation evoked action potentials in CINs and produced postsynaptic responses in medium spiny neurons that were blocked by glutamate receptor antagonists. CIN-mediated glutamatergic responses exhibited a large contribution of NMDA-type glutamate receptors, distinguishing them from corticostriatal inputs. CIN-mediated glutamatergic responses were insensitive to antagonists of acetylcholine receptors and were not seen in mice lacking VGluT3. Our results indicate that CINs are capable of mediating fast glutamatergic transmission, suggesting a new role for these cells in regulating striatal activity

Designer receptors show role for ventral pallidum input to ventral tegmental area in cocaine seeking.

The ventral pallidum is centrally positioned within mesocorticolimbic reward circuits, and its dense projection to the ventral tegmental area (VTA) regulates neuronal activity there. However, the ventral pallidum is a heterogeneous structure, and how this complexity affects its role within wider reward circuits is unclear. We found that projections to VTA from the rostral ventral pallidum (RVP), but not the caudal ventral pallidum (CVP), were robustly Fos activated during cue-induced reinstatement of cocaine seeking--a rat model of relapse in addiction. Moreover, designer receptor-mediated transient inactivation of RVP neurons, their terminals in VTA or functional connectivity between RVP and VTA dopamine neurons blocked the ability of drug-associated cues (but not a cocaine prime) to reinstate cocaine seeking. In contrast, CVP neuronal inhibition blocked cocaine-primed, but not cue-induced, reinstatement. This double dissociation in ventral pallidum subregional roles in drug seeking is likely to be important for understanding the mesocorticolimbic circuits underlying reward seeking and addiction