Resolving photon number states in a superconducting circuit

Electromagnetic signals are always composed of photons, although in the circuit domain those signals are carried as voltages and currents on wires, and the discreteness of the photon's energy is usually not evident. However, by coupling a superconducting quantum bit (qubit) to signals on a microwave transmission line, it is possible to construct an integrated circuit in which the presence or absence of even a single photon can have a dramatic effect. Such a system can be described by circuit quantum electrodynamics (QED)-the circuit equivalent of cavity QED, where photons interact with atoms or quantum dots. Previously, circuit QED devices were shown to reach the resonant strong coupling regime, where a single qubit could absorb and re-emit a single photon many times. Here we report a circuit QED experiment in the strong dispersive limit, a new regime where a single photon has a large effect on the qubit without ever being absorbed. The hallmark of this strong dispersive regime is that the qubit transition energy can be resolved into a separate spectral line for each photon number state of the microwave field. The strength of each line is a measure of the probability of finding the corresponding photon number in the cavity. This effect is used to distinguish between coherent and thermal fields, and could be used to create a photon statistics analyser. As no photons are absorbed by this process, it should be possible to generate non-classical states of light by measurement and perform qubit-photon conditional logic, the basis of a logic bus for a quantum computer.     

Habenular α5 nicotinic receptor subunit signalling controls nicotine intake

Genetic variation in CHRNA5, the gene encoding the α5 nicotinic acetylcholine receptor subunit, increases vulnerability to tobacco addiction and lung cancer, but the underlying mechanisms are unknown. Here we report markedly increased nicotine intake in mice with a null mutation in Chrna5. This effect was 'rescued' in knockout mice by re-expressing α5 subunits in the medial habenula (MHb), and recapitulated in rats through α5 subunit knockdown in MHb. Remarkably, α5 subunit knockdown in MHb did not alter the rewarding effects of nicotine but abolished the inhibitory effects of higher nicotine doses on brain reward systems. The MHb extends projections almost exclusively to the interpeduncular nucleus (IPN). We found diminished IPN activation in response to nicotine in α5 knockout mice. Further, disruption of IPN signalling increased nicotine intake in rats. Our findings indicate that nicotine activates the habenulo-interpeduncular pathway through α5-containing nAChRs, triggering an inhibitory motivational signal that acts to limit nicotine intake.