On the generation of multipartite entangled states in Josephson architectures

We propose and analyze a scheme for the generation of multipartite entangled states in a system of inductively coupled Josephson flux qubits. The qubits have fixed eigenfrequencies during the whole process in order to minimize decoherence effects and their inductive coupling can be turned on and off at will by tuning an external control flux. Within this framework, we will show that a W state in a system of three or more qubits can be generated by exploiting the sequential one by one coupling of the qubits with one of them playing the role of an entanglement mediator.Comment: 10 pages, 3 figure

Premature changes in neuronal excitability account for hippocampal network impairment and autistic-like behavior in neonatal BTBR T+tf/J mice

Coherent network oscillations (GDPs), generated in the immature hippocampus by the synergistic action of GABA and glutamate, both depolarizing and excitatory, play a key role in the construction of neuronal circuits. In particular, GDPs-associated calcium transients act as coincident detectors for enhancing synaptic efficacy at emerging GABAergic and glutamatergic synapses. Here, we show that, immediately after birth, in the CA3 hippocampal region of the BTBR T+tf/J mouse, an animal model of idiopathic autism, GDPs are severely impaired. This effect was associated with an increased GABAergic neurotransmission and a reduced neuronal excitability. In spite its depolarizing action on CA3 pyramidal cells (in single channel experiments EGABA was positive to Em), GABA exerted at the network level an inhibitory effect as demonstrated by isoguvacine-induced reduction of neuronal firing. We implemented a computational model in which experimental findings could be interpreted as the result of two competing effects: a reduction of the intrinsic excitability of CA3 principal cells and a reduction of the shunting activity in GABAergic interneurons projecting to principal cells. It is therefore likely that premature changes in neuronal excitability within selective hippocampal circuits of BTBR mice lead to GDPs dysfunction and behavioral deficits reminiscent of those found in autistic patients

Association between the c. 2495 A>G ATP7B Polymorphism and Sporadic Alzheimer's Disease

Nonceruloplasmin-bound copper (“free”) is reported to be elevated in Alzheimer's disease (AD). In Wilson's disease (WD) Cu-ATPase 7B protein tightly controls free copper body levels. To explore whether the ATP7B gene harbours susceptibility loci for AD, we screened 180 AD chromosomes for sequence changes in exons 2, 5, 8, 10, 14, and 16, where most of the Mediterranean WD-causing mutations lie. No WD mutation, but sequence changes corresponding to c.1216 T>G Single-Nucleotide Polymorphism (SNP) and c.2495 A>G SNP were found. Thereafter, we genotyped 190 AD patients and 164 controls for these SNPs frequencies estimation. Logistic regression analyses revealed either a trend for the c.1216 SNP (P = .074) or a higher frequency for c.2495 SNP of the GG genotype in patients, increasing the probability of AD by 74% (P = .028). Presence of the GG genotype in ATP7B c.2495 could account for copper dysfunction in AD which has been shown to raise the probability of the disease

Different responses of mice and rats hippocampus CA1 pyramidal neurons to in vitro and in vivo-like inputs

The fundamental role of any neuron within a network is to transform complex spatiotemporal synaptic input patterns into individual output spikes. These spikes, in turn, act as inputs for other neurons in the network. Neurons must execute this function across a diverse range of physiological conditions, often based on species-specific traits. Therefore, it is crucial to determine the extent to which findings can be extrapolated between species and, ultimately, to humans. In this study, we employed a multidisciplinary approach to pinpoint the factors accounting for the observed electrophysiological differences between mice and rats, the two species most used in experimental and computational research. After analyzing the morphological properties of their hippocampal CA1 pyramidal cells, we conducted a statistical comparison of rat and mouse electrophysiological features in response to somatic current injections. This analysis aimed to uncover the parameters underlying these distinctions. Using a well-established computational workflow, we created ten distinct single-cell computational models of mouse CA1 pyramidal neurons, ready to be used in a full-scale hippocampal circuit. By comparing their responses to a variety of somatic and synaptic inputs with those of rat models, we generated experimentally testable hypotheses regarding species-specific differences in ion channel distribution, kinetics, and the electrophysiological mechanisms underlying their distinct responses to synaptic inputs during the behaviorally relevant Gamma and Sharp-Wave rhythms

Circadian Modulation of Neurons and Astrocytes Controls Synaptic Plasticity in Hippocampal Area CA1

Most animal species operate according to a 24-h period set by the suprachiasmatic nucleus (SCN) of the hypothalamus. The rhythmic activity of the SCN modulates hippocampal-dependent memory, but the molecular and cellular mechanisms that account for this effect remain largely unknown. Here, we identify cell-type-specific structural and functional changes that occur with circadian rhythmicity in neurons and astrocytes in hippocampal area CA1. Pyramidal neurons change the surface expression of NMDA receptors. Astrocytes change their proximity to synapses. Together, these phenomena alter glutamate clearance, receptor activation, and integration of temporally clustered excitatory synaptic inputs, ultimately shaping hippocampal-dependent learning in vivo. We identify corticosterone as a key contributor to changes in synaptic strength. These findings highlight important mechanisms through which neurons and astrocytes modify the molecular composition and structure of the synaptic environment, contribute to the local storage of information in the hippocampus, and alter the temporal dynamics of cognitive processing

Know Your Current Ih: Interaction with a Shunting Current Explains the Puzzling Effects of Its Pharmacological or Pathological Modulations

The non-specific, hyperpolarization activated, Ih current is particularly involved in epilepsy and it exhibits an excitatory or inhibitory action on synaptic integration in an apparently inconsistent way. It has been suggested that most of the inconsistencies could be reconciled invoking an indirect interaction with the M-type K+ current, another current involved in epilepsy. However, here we show that the original experiments, and the simplified model used to explain and support them, cannot explain in a conclusive way the puzzling Ih actions observed in different experimental preparations. Using a realistic model, we show instead how and why a shunting current, such as that carried by TASK-like channels, and dependent on Ih channel is able to explain virtually all experimental findings on Ih up- or down-regulation by modulators or pathological conditions. The model results suggest several experimentally testable predictions to characterize in more details this elusive and peculiar interaction, which may be of fundamental importance in the development of new treatments for all those pathological and cognitive dysfunctions caused, mediated, or affected by Ih

26th Annual Computational Neuroscience Meeting (CNS*2017): Part 3 - Meeting Abstracts - Antwerp, Belgium. 15–20 July 2017

This work was produced as part of the activities of FAPESP Research,\ud Disseminations and Innovation Center for Neuromathematics (grant\ud 2013/07699-0, S. Paulo Research Foundation). NLK is supported by a\ud FAPESP postdoctoral fellowship (grant 2016/03855-5). ACR is partially\ud supported by a CNPq fellowship (grant 306251/2014-0)

Typical experimental and model findings on <i>I_h</i>.

<p><b>a</b>) simulation of ZD7288 application during a 0.33 nA somatic current injection: at <i>t</i> = 500 the <i>I_h</i> was blocked by resetting the peak conductance to 0; <b>b</b>) (<i>top</i>) increase in the dendritic firing rate after <i>I_h</i> upregulation following febrile seizures induction (adapted from Fig. 2A of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0036867#pone.0036867-DyhrfjeldJohnsen2" target="_blank">[3]</a>); (<i>bottom</i>) simulation of <i>I_h</i> upregulation in febrile seizures; traces are dendritic recordings during a 500 ms current injection (0.4 nA at ∼280 µm), using a 3× increase in <i>g_{h_pk}</i> (from 0.01 mS/cm²) to obtain about the same depolarization (∼3 mV) and the same increase (∼3×) in the number of APs observed in the experiments; <b>c</b>) (<i>top</i>) experimental recordings demonstrating an increase in temporal summation at the soma during distal dendritic EPSPs after ZD2288 application (taken and redrawn from Fig. 1b of <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0036867#pone.0036867-Magee1" target="_blank">[22]</a>, with permission by Macmillan Publishers Ltd, copyright (1999)); simulation of EPSPs temporal summation during a 50 Hz train of 5 dendritic EPSPs activated under different conditions; the bars above the plots represent the timing of <i>I_h</i> block (modeling ZD7288 application), and a somatic current injection (0.11 nA) modeling the experimental protocol to restore the original membrane resting potential after ZD7288 <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0036867#pone.0036867-Magee1" target="_blank">[22]</a>; traces are somatic recordings during proximal (24 µm) or distal (500 µm) stimulation of the main trunk; peak synaptic conductances (1.7 and 5 nS for proximal and distal stimulations, respectively) were adjusted to obtain the same peak somatic depolarization during the first EPSP under control conditions; <i>g_{h_pk}</i> = 0.01 mS/cm².</p

Parameter values best fitting the experimental traces in Fig. 1a.

<p>Parameter values best fitting the experimental traces in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0036867#pone-0036867-g001" target="_blank">Fig. 1a</a>.</p