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 $0.57\pm0.01$ are generated at $200$ 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