Improvement of continuous-variable quantum key distribution systems by using optical preamplifiers

Continuous-variable quantum key distribution protocols, based on Gaussian modulation of the quadratures of coherent states, have been implemented in recent experiments. A present limitation of such systems is the finite efficiency of the detectors, which can in principle be compensated for by the use of classical optical preamplifiers. Here we study this possibility in detail, by deriving the modified secret key generation rates when an optical parametric amplifier is placed at the output of the quantum channel. After presenting a general set of security proofs, we show that the use of preamplifiers does compensate for all the imperfections of the detectors when the amplifier is optimal in terms of gain and noise. Imperfect amplifiers can also enhance the system performance, under conditions which are generally satisfied in practice.Comment: 11 pages, 7 figures, submitted to J. Phys. B (special issue on Few Atoms Optics

Field test of a continuous-variable quantum key distribution prototype

We have designed and realized a prototype that implements a continuous-variable quantum key distribution protocol based on coherent states and reverse reconciliation. The system uses time and polarization multiplexing for optimal transmission and detection of the signal and phase reference, and employs sophisticated error-correction codes for reconciliation. The security of the system is guaranteed against general coherent eavesdropping attacks. The performance of the prototype was tested over preinstalled optical fibres as part of a quantum cryptography network combining different quantum key distribution technologies. The stable and automatic operation of the prototype over 57 hours yielded an average secret key distribution rate of 8 kbit/s over a 3 dB loss optical fibre, including the key extraction process and all quantum and classical communication. This system is therefore ideal for securing communications in metropolitan size networks with high speed requirements.Comment: 15 pages, 6 figures, submitted to New Journal of Physics (Special issue on Quantum Cryptography

Feasibility of quantum key distribution through dense wavelength division multiplexing network

In this paper, we study the feasibility of conducting quantum key distribution (QKD) together with classical communication through the same optical fiber by employing dense-wavelength-division-multiplexing (DWDM) technology at telecom wavelength. The impact of the classical channels to the quantum channel has been investigated for both QKD based on single photon detection and QKD based on homodyne detection. Our studies show that the latter can tolerate a much higher level of contamination from the classical channels than the former. This is because the local oscillator used in the homodyne detector acts as a "mode selector" which can suppress noise photons effectively. We have performed simulations based on both the decoy BB84 QKD protocol and the Gaussian modulated coherent state (GMCS) QKD protocol. While the former cannot tolerate even one classical channel (with a power of 0dBm), the latter can be multiplexed with 38 classical channels (0dBm power each channel) and still has a secure distance around 10km. Preliminary experiment has been conducted based on a 100MHz bandwidth homodyne detector.Comment: 18 pages, 5 figure

Neurons Controlling Aplysia Feeding Inhibit Themselves by Continuous NO Production

Neural activity can be affected by nitric oxide (NO) produced by spiking neurons. Can neural activity also be affected by NO produced in neurons in the absence of spiking?Applying an NO scavenger to quiescent Aplysia buccal ganglia initiated fictive feeding, indicating that NO production at rest inhibits feeding. The inhibition is in part via effects on neurons B31/B32, neurons initiating food consumption. Applying NO scavengers or nitric oxide synthase (NOS) blockers to B31/B32 neurons cultured in isolation caused inactive neurons to depolarize and fire, indicating that B31/B32 produce NO tonically without action potentials, and tonic NO production contributes to the B31/B32 resting potentials. Guanylyl cyclase blockers also caused depolarization and firing, indicating that the cGMP second messenger cascade, presumably activated by the tonic presence of NO, contributes to the B31/B32 resting potential. Blocking NO while voltage-clamping revealed an inward leak current, indicating that NO prevents this current from depolarizing the neuron. Blocking nitrergic transmission had no effect on a number of other cultured, isolated neurons. However, treatment with NO blockers did excite cerebral ganglion neuron C-PR, a command-like neuron initiating food-finding behavior, both in situ, and when the neuron was cultured in isolation, indicating that this neuron also inhibits itself by producing NO at rest.Self-inhibitory, tonic NO production is a novel mechanism for the modulation of neural activity. Localization of this mechanism to critical neurons in different ganglia controlling different aspects of a behavior provides a mechanism by which a humeral signal affecting background NO production, such as the NO precursor L-arginine, could control multiple aspects of the behavior

Upregulation of α7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides

BACKGROUND: The alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR) is well known as a potent calcium ionophore that, in the brain, has been implicated in excitotoxicity and hence in the underlying mechanisms of neurodegenerative disorders such as Alzheimer's disease. Previous research implied that the activity of this receptor may be modified by exposure to a peptide fragment derived from the C-terminal region of the enzyme acetylcholinesterase. This investigation was undertaken to determine if the functional changes observed could be attributed to peptide binding interaction with the alpha7-nAChR, or peptide modulation of receptor expression. METHODOLOGY/PRINCIPAL FINDINGS: This study provides evidence that two peptides derived from the C-terminus of acetylcholinesterase, not only selectively displace specific bungarotoxin binding at the alpha7-nAChR, but also alter receptor binding properties for its familiar ligands, including the alternative endogenous agonist choline. Of more long-term significance, these peptides also induce upregulation of alpha7-nAChR mRNA and protein expression, as well as enhancing receptor trafficking to the plasma membrane. CONCLUSIONS/SIGNIFICANCE: The results reported here demonstrate a hitherto unknown relationship between the alpha7-nAChR and the non-enzymatic functions of acetylcholinesterase, mediated independently by its C-terminal domain. Such an interaction may prove valuable as a pharmacological tool, prompting new approaches for understanding, and combating, the process of neurodegeneration

Upregulation of α7 Nicotinic Receptors by Acetylcholinesterase C-Terminal Peptides

BACKGROUND: The alpha-7 nicotinic acetylcholine receptor (alpha7-nAChR) is well known as a potent calcium ionophore that, in the brain, has been implicated in excitotoxicity and hence in the underlying mechanisms of neurodegenerative disorders such as Alzheimer's disease. Previous research implied that the activity of this receptor may be modified by exposure to a peptide fragment derived from the C-terminal region of the enzyme acetylcholinesterase. This investigation was undertaken to determine if the functional changes observed could be attributed to peptide binding interaction with the alpha7-nAChR, or peptide modulation of receptor expression. METHODOLOGY/PRINCIPAL FINDINGS: This study provides evidence that two peptides derived from the C-terminus of acetylcholinesterase, not only selectively displace specific bungarotoxin binding at the alpha7-nAChR, but also alter receptor binding properties for its familiar ligands, including the alternative endogenous agonist choline. Of more long-term significance, these peptides also induce upregulation of alpha7-nAChR mRNA and protein expression, as well as enhancing receptor trafficking to the plasma membrane. CONCLUSIONS/SIGNIFICANCE: The results reported here demonstrate a hitherto unknown relationship between the alpha7-nAChR and the non-enzymatic functions of acetylcholinesterase, mediated independently by its C-terminal domain. Such an interaction may prove valuable as a pharmacological tool, prompting new approaches for understanding, and combating, the process of neurodegeneration