Rosanna Migliore
National Research Council
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Rosanna Migliore.
Journal of Physics A | 2008
M. Scala; Rosanna Migliore; A. Messina
We derive the master equation of a system of two coupled qubits by taking into account their interaction with two independent bosonic baths. Important features of the dynamics are brought to light, such as the structure of the stationary state at general temperatures and the behaviour of the entanglement at zero temperature, showing the phenomena of sudden death and sudden birth as well as the presence of stationary entanglement for long times. The model presented here is quite versatile and can be of interest in the study of both Josephson junction architectures and cavity-QED.
PLOS ONE | 2012
Michele Migliore; Rosanna Migliore
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.
Physical Review B | 2003
Rosanna Migliore; A. Messina
The dynamical behavior of a superconducting quantum interference device (an rf-SQUID) irradiated by a single-mode quantized electromagnetic field is theoretically investigated. Treating the SQUID as a flux qubit, we analyze the dynamics of the combined system within the low-lying energy Hilbert subspace both in the asymmetric and in the symmetric SQUID potential configurations. We show that the temporal evolution of the system is dominated by an oscillatory behavior characterized by more than one, generally speaking, incommensurable Rabi frequencies whose expressions are explicitly given. We find that the external parameters may be fixed in such a way to realize a control on the dynamical replay of the total system which, for instance, may be forced to exhibit a periodic evolution accompanied by the occurrence of an oscillatory disappearance of entanglement between the two subsystems. We demonstrate the possibility of generating quantum maximally entangled superpositions of the two macroscopically distinguishable states describing clockwise and counterclockwise supercurrents in the loop. The experimental feasibility of our proposal is briefly discussed.
European Physical Journal D | 2011
Matteo Scala; Rosanna Migliore; A. Messina; L. L. Sanchez-Soto
Abstract. The dissipative dynamics of two interacting qubits coupled to independent reservoirs at nonzero temperatures is investigated, paying special attention to the entanglement evolution. The counter-rotating terms in the qubit-qubit interaction give rise to stationary entanglement, traceable back to the ground state structure. The robustness of this entanglement against thermal noise is thoroughly analyzed, establishing that it can be detected at reasonable experimental temperatures. Some effects linked to a possible reservoir asymmetry are brought to light.
Physical Review B | 2006
Rosanna Migliore; Kazuya Yuasa; Hiromichi Nakazato; A. Messina
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
Scientific Reports | 2016
Giada Cellot; Laura Maggi; Maria Amalia Di Castro; Myriam Catalano; Rosanna Migliore; Michele Migliore; Maria Luisa Scattoni; Gemma Calamandrei; Enrico Cherubini
W
Biophysical Journal | 2015
Michele Migliore; Giada De Simone; Rosanna Migliore
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.
Neural Networks | 2011
Michele Migliore; Ignazio De Blasi; Domenico Tegolo; Rosanna Migliore
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.
Physical Review B | 2007
Rosanna Migliore; Kazuya Yuasa; Marina Guccione; Hiromichi Nakazato; A. Messina
Long-term potentiation (LTP) and long-term depression (LTD) are the two major forms of long-lasting synaptic plasticity in the mammalian neurons, and are directly related to higher brain functions such as learning and memory. Experimentally, they are characterized by a change in the strength of a synaptic connection induced by repetitive and properly patterned stimulation protocols. Although many important details of the molecular events leading to LTP and LTD are known, experimenters often report problems in using standard induction protocols to obtain consistent results, especially for LTD in vivo. We hypothesize that a possible source of confusion in interpreting the results, from any given experiment on synaptic plasticity, can be the intrinsic limitation of the experimental techniques, which cannot take into account the actual state and peak conductance of the synapses before the conditioning protocol. In this article, we investigate the possibility that the same experimental protocol may result in different consequences (e.g., LTD instead of LTP), according to the initial conditions of the stimulated synapses, and can generate confusing results. Using biophysical models of synaptic plasticity and hippocampal CA1 pyramidal neurons, we study how, why, and to what extent the phenomena observed at the soma after induction of LTP/LTD reflects the actual (local) synaptic state. The model and the results suggest a physiologically plausible explanation for why LTD induction is experimentally difficult to obtain. They also suggest experimentally testable predictions on the stimulation protocols that may be more effective.
Journal of Physics B | 2011
Rosanna Migliore; Matteo Scala; A. Napoli; Kazuya Yuasa; Hiromichi Nakazato; A. Messina
The neural mechanisms underlying schizophrenic behavior are unknown and very difficult to investigate experimentally, although a few experimental and modeling studies suggested possible causes for some of the typical psychotic symptoms related to this disease. The brain region most involved in these processes seems to be the hippocampus, because of its critical role in establishing memories for objects or events in the context in which they occur. In particular, a hypofunction of the N-methyl-D-aspartate (NMDA) component of the synaptic input on the distal dendrites of CA1 pyramidal neurons has been suggested to play an important role for the emergence of schizophrenic behavior. Modeling studies have investigated this issue at the network and cellular level. Here, starting from the experimentally supported assumption that hippocampal neurons are very specific, sparse, and invariant in their firing, we explore an experimentally testable prediction at the single neuron level. The model shows how and to what extent a pathological hypofunction of a context-dependent distal input on a CA1 neuron can generate hallucinations by altering the normal recall of objects on which the neuron has been previously tuned. The results suggest that a change in the context during the recall phase may cause an occasional but very significant change in the set of active dendrites used for feature recognition, leading to a distorted perception of objects.