433 research outputs found
The reconfigurable Josephson circulator/directional amplifier
Circulators and directional amplifiers are crucial non-reciprocal signal
routing and processing components involved in microwave readout chains for a
variety of applications. They are particularly important in the field of
superconducting quantum information, where the devices also need to have
minimal photon losses to preserve the quantum coherence of signals.
Conventional commercial implementations of each device suffer from losses and
are built from very different physical principles, which has led to separate
strategies for the construction of their quantum-limited versions. However, as
recently proposed theoretically, by establishing simultaneous pairwise
conversion and/or gain processes between three modes of a Josephson-junction
based superconducting microwave circuit, it is possible to endow the circuit
with the functions of either a phase-preserving directional amplifier or a
circulator. Here, we experimentally demonstrate these two modes of operation of
the same circuit. Furthermore, in the directional amplifier mode, we show that
the noise performance is comparable to standard non-directional superconducting
amplifiers, while in the circulator mode, we show that the sense of circulation
is fully reversible. Our device is far simpler in both modes of operation than
previous proposals and implementations, requiring only three microwave pumps.
It offers the advantage of flexibility, as it can dynamically switch between
modes of operation as its pump conditions are changed. Moreover, by
demonstrating that a single three-wave process yields non-reciprocal devices
with reconfigurable functions, our work breaks the ground for the development
of future, more-complex directional circuits, and has excellent prospects for
on-chip integration
Robust concurrent remote entanglement between two superconducting qubits
Entangling two remote quantum systems which never interact directly is an
essential primitive in quantum information science and forms the basis for the
modular architecture of quantum computing. When protocols to generate these
remote entangled pairs rely on using traveling single photon states as carriers
of quantum information, they can be made robust to photon losses, unlike
schemes that rely on continuous variable states. However, efficiently detecting
single photons is challenging in the domain of superconducting quantum circuits
because of the low energy of microwave quanta. Here, we report the realization
of a robust form of concurrent remote entanglement based on a novel microwave
photon detector implemented in the superconducting circuit quantum
electrodynamics (cQED) platform of quantum information. Remote entangled pairs
with a fidelity of are generated at Hz. Our experiment
opens the way for the implementation of the modular architecture of quantum
computation with superconducting qubits.Comment: Main paper: 7 pages, 4 figures; Appendices: 14 pages, 9 figure
Suppression of piriform cortex activity in rat by corticotropin-releasing factor 1 and serotonin 2A/C receptors
The piriform cortex (PC) is richly innervated by Corticotropin-releasing factor (CRF) and Serotonin (5-HT) containing axons arising from central amygdala and Raphe nucleus. CRFR1 and 5-HT2A/2CRs have been shown to interact in manner where CRFR activation subsequently potentiates the activity of 5-HT2A/2CRs. The purpose of this study was to determine how the activation of CRFR1 and/or 5-HT2Rs modulates PC activity at both the circuit and cellular level. Voltage sensitive dye imaging showed that CRF acting through CRFR1 dampened activation of the layer II of PC and interneurons of endopiriform nucleus. Application of the selective 5-HT2A/CR agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) following CRFR1 activation potentiated this effect. Blocking the interaction between CRFR1 and 5-HT2R with a Tat-CRFR1-CT peptide abolished this potentiation. Application of forskolin did not mimic CRFR1 activity but instead blocked it, while a protein kinase A antagonist had no effect. However, activation and antagonism of protein kinase C (PKC) either mimicked or blocked CRF modulation respectively. DOI had no effect when applied alone indicating that the prior activation of CRFR1 receptors was critical for DOI to show significant effects similar to CRF. Patch clamp recordings showed that both CRF and DOI reduced the synaptic responsiveness of layer II pyramidal neurons. CRF had highly variable effects on interneurons within layer III, both increasing and decreasing their excitability, but DOI had no effect on the excitability of this group of neurons. These data show that CRF and serotonin, acting through both CRFR1 and 5-HT2A/CRs, reduce the activation of the PC. This modulation may be an important blunting mechanism of stressor behaviours mediated through the olfactory cortex
CRF Mediates Stress-Induced Pathophysiological High-Frequency Oscillations in Traumatic Brain Injury
Copyright © 2019 Narla et al. It is not known why there is increased risk to have seizures with increased anxiety and stress after traumatic brain injury (TBI). Stressors cause the release of corticotropin-releasing factor (CRF) both from the hypothalamic pituitary adrenal (HPA) axis and from CNS neurons located in the central amygdala and GABAergic interneurons. We have previously shown that CRF signaling is plastic, becoming excitatory instead of inhibitory after the kindling model of epilepsy. Here, using Sprague Dawley rats we have found that CRF signaling increased excitability after TBI. Following TBI, CRF type 1 receptor (CRFR1)-mediated activity caused abnormally large electrical responses in the amygdala, including fast ripples, which are considered to be epileptogenic. After TBI, we also found the ripple (120-250 Hz) and fast ripple activity (\u3e250 Hz) was cross-frequency coupled with θ (3-8 Hz) oscillations. CRFR1 antagonists reduced the incidence of phase coupling between ripples and fast ripples. Our observations indicate that pathophysiological signaling of the CRFR1 increases the incidence of epileptiform activity after TBI. The use for CRFR1 antagonist may be useful to reduce the severity and frequency of TBI associated epileptic seizures
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