Fast optical source for quantum key distribution based on semiconductor optical amplifiers.

A novel integrated optical source capable of emitting faint pulses with different polarization states and with different intensity levels at 100 MHz has been developed. The source relies on a single laser diode followed by four semiconductor optical amplifiers and thin film polarizers, connected through a fiber network. The use of a single laser ensures high level of indistinguishability in time and spectrum of the pulses for the four different polarizations and three different levels of intensity. The applicability of the source is demonstrated in the lab through a free space quantum key distribution experiment which makes use of the decoy state BB84 protocol. We achieved a lower bound secure key rate of the order of 3.64 Mbps and a quantum bit error ratio as low as 1.14×10⁻² while the lower bound secure key rate became 187 bps for an equivalent attenuation of 35 dB. To our knowledge, this is the fastest polarization encoded QKD system which has been reported so far. The performance, reduced size, low power consumption and the fact that the components used can be space qualified make the source particularly suitable for secure satellite communication.

Increased extracellular 5-HT but no change in sleep after perfusion of a 5-HT1A antagonist into the dorsal raphe nucleus of rats.

AIM: The 5-HT(1A) receptor antagonist 4-Iodo-N-[2-[4-(methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinyl-benzamide hydrochloride (p-MPPI) (10 microM) was perfused into the dorsal raphe nucleus (DRN) to study simultaneously the effects of the drug on the DRN and frontal cortex extracellular serotonin (5-hydroxytryptamine, 5-HT) levels and concurring behavioural states. METHODS: Waking, slow wave sleep and rapid eye movement sleep were determined by polygraphic recordings during microdialysis perfusion and extracellular sample collection. The samples were analysed by microbore high-performance liquid chromatography coupled with electrochemical detection for analysis of 5-HT. RESULTS: p-MPPI perfusion into the DRN (n = 6) produced a sixfold 5-HT increase in the DRN during all behavioural states. The increased 5-HT level was most likely related to the blockage of 5-HT(1A) receptors in the DRN by p-MPPI. No significant effect was seen on sleep. CONCLUSION: Despite the dramatic increase in DRN extracellular 5-HT produced by p-MPPI, only a transient and nonsignificant effect on sleep was recorded. It is suggested that the usual coupling between 5-HT level and behavioural state may be lost when an excessive serotonergic output is pharmacologically achieved.

Experimental quantum coin tossing.

In this Letter we present the first implementation of a quantum coin-tossing protocol. This protocol belongs to a class of "two-party" cryptographic problems, where the communication partners distrust each other. As with a number of such two-party protocols, the best implementation of the quantum coin tossing requires qutrits, resulting in a higher security than using qubits. In this way, we have also performed the first complete quantum communication protocol with qutrits. In our experiment the two partners succeeded to remotely toss a row of coins using photons entangled in the orbital angular momentum. We also show the experimental bounds of a possible cheater and the ways of detecting him.

Distributing entanglement and single photons through an intra-city, free-space quantum channel.

We have distributed entangled photons directly through the atmosphere to a receiver station 7.8 km away over the city of Vienna, Austria at night. Detection of one photon from our entangled pairs constitutes a triggered single photon source from the sender. With no direct time-stable connection, the two stations found coincidence counts in the detection events by calculating the cross-correlation of locally-recorded time stamps shared over a public internet channel. For this experiment, our quantum channel was maintained for a total of 40 minutes during which time a coincidence lock found approximately 60000 coincident detection events. The polarization correlations in those events yielded a Bell parameter, S=2.27+/-0.019, which violates the CHSH-Bell inequality by 14 standard deviations. This result is promising for entanglement-based freespace quantum communication in high-density urban areas. It is also encouraging for optical quantum communication between ground stations and satellites since the length of our free-space link exceeds the atmospheric equivalent.

Practical quantum key distribution with polarization entangled photons.

We present an entangled-state quantum cryptography system that operated for the first time in a real-world application scenario. The full key generation protocol was performed in real-time between two distributed embedded hardware devices, which were connected by 1.45 km of optical fiber, installed for this experiment in the Vienna sewage system. The generated quantum key was immediately handed over and used by a secure communication application.

Effects of sleep deprivation on extracellular serotonin in hippocampus and frontal cortex of the rat.

Sleep deprivation improves the mood of depressed patients, but the exact mechanism behind this effect is unclear. An enhancement of serotonergic neurotransmission has been suggested. In this study, we used in vivo microdialysis to monitor extracellular serotonin in the hippocampus and the frontal cortex of rats during an 8 h sleep deprivation period. These brain regions were selected since both have been implicated in depression. The behavioral state of the animal was continuously monitored by polygraphic recordings during the experiment. Sleep deprivation produced a gradual decline in extracellular serotonin levels, both in the hippocampus and in the frontal cortex. In order to investigate whether the reduction in serotonin was due to other factors than sleep deprivation, i.e. time of day effect, another experiment was performed. Here animals were allowed to sleep during most of the recording period. This experiment showed the expected changes in extracellular serotonin levels: consistently higher levels in the awake, non-sleep deprived animals compared to during sleep, but no time of day effect. The reduction in extracellular serotonin during sleep deprivation may suggest that serotonin does not play a major role in the mood-elevating effect of sleep deprivation. However, since 5-HT levels are strongly behavioral state dependent, by eliminating sleep, there may be a net increase in serotonergic neurotransmission during the sleep deprivation period.

Sleep and waking following microdialysis perfusion of the selective 5-HT1A receptor antagonist p-MPPI into the dorsal raphe nucleus in the freely moving rat.

The aim of this study was to examine the involvement of the dorsal raphe nucleus (DRN) presynaptic serotonergic 5-HT1A autoreceptors on sleep and waking parameters, in particular rapid eye movement (REM) sleep. In a previous study, the systemic administration of the selective 5-HT1A receptor antagonist p-MPPI reduced REM sleep in a dose-dependent manner suggesting a blockade of the 5-HT1A autoreceptors. In the present study, a blockade by microdialysis perfusion of 10 microM and 100 microM of p-MPPI for 7 h into the DRN in freely behaving rats influenced vigilance state only to a small extent. The administration of 10 microM of p-MPPI induced a reduction of total REM sleep mainly due to a suppression of REM sleep during the third 2 h period of the recording of sleep and waking. Perfusion of 100 microM of p-MPPI decreased total transition type sleep (TRANS) but the effect on REM sleep did not reach significance. There was no change in waking or slow wave sleep (SWS) following any of the doses. The data suggest that 5-HT1A receptor-mediated mechanisms in the DRN may be only moderately important in the serotonergic modulation of REM sleep.

[Sleep habits among adolescents]. / Søvnvaner hos ungdom.

BACKGROUND: Norwegian adolescents report very high-perceived morning sleepiness. Delayed sleep phase may be biologically linked to puberty; adolescents sleep less, but may need more sleep than prepubertal children. The study was designed to investigate sleep habits, circadian rhythm and subjective satisfaction with sleep. MATERIAL AND METHODS: Twenty-two high school students, age 17, and parents of 16 primary school pupils, age seven, answered a questionnaire on estimated sleep need, actual time in bed, sleep latency and adequacy of sleep. RESULTS: The average length of nocturnal sleep in the adolescents was 7.3 hrs on weekdays and 10.1 hrs on weekends. They went later to bed and rose earlier than the children, sleeping 1.7 hrs less before schooldays and 1.6 hrs more during the weekend than the 8.5 hrs which were their own sleep estimate. All the children were reported to satisfy their need for sleep, but none of the adolescents reported feeling content. The larger the difference between hours in bed on weekdays and hours in bed on weekends, the more dissatisfaction was observed. INTERPRETATION: The present data suggest that the adolescents were chronic partially sleep deprived and had a tendency toward delayed sleep phase. They did not satisfy their need for sleep as defined by themselves, due to late bedtime throughout the week. Also, the late bedtime and late rise time on weekends maintained or furthered the delayed sleep phase.

The selective 5-HT(1A) receptor antagonist p-MPPI antagonizes sleep--waking and behavioural effects of 8-OH-DPAT in rats.

Systemic administration of the selective 5-HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin HBr (8-OH-DPAT) increases waking and reduces slow wave sleep (SWS) and rapid eye movement (REM) sleep in the freely moving rat. The selective 5-HT(1A) antagonist 4-(2'-methoxy-phenyl)-1-[2'-(n-2"-pyridinyl)-p-iodobenzamido]-ethyl-piperazine (p-MPPI) induces a dose-related decrease in REM sleep. The present study examined p-MPPI's potential as an antagonist of the sleep and waking responses elicited by 8-OH-DPAT. Also, the experiments explored the ability of p-MPPI to block behavioural reactions of the 5-HT syndrome induced by 8-OH-DPAT, and whether p-MPPI induced any behavioural effects of its own. This study demonstrated that pre-treatment with p-MPPI (5 mg/kg intraperitoneal (i.p.)) 30 min before 8-OH-DPAT (0.375 mg/kg subcutaneously (s.c.)) reduced the effect of 8-OH-DPAT on waking and REM sleep. Also, p-MPPI (5 and 10 mg/kg i.p.) reduced the effect of 8-OH-DPAT on locomotion and partially or completely antagonized hindlimb abduction and flat body posture. No overt behavioural change was produced by p-MPPI alone. Thus, p-MPPI behaved as a true 5-HT(1A) antagonist.

Sleep-wake effects following the selective 5-HT(1A) receptor antagonist p-MPPI in the freely moving rat.

The 5-HT(1A) receptors appear to play an important role in the serotonergic modulation of sleep and waking. Both presynaptic somatodendritic 5-HT(1A) autoreceptors and postsynaptic 5-HT(1A) heteroreceptors may be involved. The present study addressed the question of whether the selective 5-HT(1A) receptor antagonist 4-(2'-methoxy-phenyl)-1-[2'-(n-2"-pyridinyl)-p-iodobenzamido]-ethy l-p iperazine (p-MPPI) affected sleep and waking and whether such an effect would be dose-related. Polygraphic recording of sleep and waking in freely moving rats was employed following control injection and three doses of p-MPPI (1, 5 and 10 mg/kg i.p. in a balanced order design. Waking was increased and deep slow wave sleep decreased, while rapid eye movement (REM) sleep was suppressed over the first 6 h following injection, compared to after control injection. REM sleep was also suppressed following 10 mg/kg i.p. of p-MPPI as compared to following 1 mg/kg i.p. of p-MPPI. The interpretation of the effects is complex and the effects are not easily compatible with a simple model for serotonergic sleep-waking modulation. However, the REM sleep reduction probably reflects p-MPPIs ability to block the presynaptic 5-HT(1A) autoreceptors, increasing the firing activity in the serotonergic neurones and possibly inhibiting serotonin sensitive REM sleep active neurones.

Serotonin and the sleep/wake cycle: special emphasis on microdialysis studies.

Several areas in the brainstem and forebrain are important for the modulation and expression of the sleep/wake cycle. Even if the first observations of biochemical events in relation to sleep were made only 40 years ago, it is now well established that several neurotransmitters, neuropeptides, and neurohormones are involved in the modulation of the sleep/wake cycle. Serotonin has been known for many years to play a role in the modulation of sleep, however, it is still very controversial how and where serotonin may operate this modulation. Early studies suggested that serotonin is necessary to obtain and maintain behavioral sleep (permissive role on sleep). However, more recent microdialysis experiments provide evidence that the level of serotonin during W is higher in most cortical and subcortical areas receiving serotonergic projections. In this view the level of extracellular serotonin would be consistent with the pattern of discharge of the DRN serotonergic neurons which show the highest firing rate during W, followed by a decrease in slow wave sleep and by virtual electrical silence during REM sleep. This suggests that during waking serotonin may complement the action of noradrenaline and acetylcholine in promoting cortical responsiveness and participate to the inhibition of REM-sleep effector neurons in the brainstem (inhibitory role on REM sleep). The apparent inconsistency between an inhibitory and a facilitatory role played by serotonin on sleep has at least two possible explanations. On the one hand serotonergic modulation on the sleep/wake cycle takes place through a multitude of post-synaptic receptors which mediate different or even opposite responses; on the other hand the achievement of a behavioral state depends on the complex interaction between the serotonergic and other neurotransmitter systems. The main aim of this commentary is to review the role of brain serotonin in relation to the sleep/wake cycle. In particular we highlight the importance of microdialysis for on-line monitoring of the level of serotonin in different areas of the brain across the sleep/wake cycle.

On-line detection of extracellular levels of serotonin in dorsal raphe nucleus and frontal cortex over the sleep/wake cycle in the freely moving rat.

We used in vivo microdialysis coupled with polygraphic recording to monitor 5-hydroxytryptamine levels in the dorsal raphe nucleus and frontal cortex across waking, slow-wave sleep and rapid eye-movement sleep. Male Sprague-Dawley rats were prepared with electroencephalogram and electromyogram electrodes. Microdialysis probes were placed in dorsal raphe nucleus and/or frontal cortex. Dialysate samples were manually collected during polygraphically-defined behavioural states and the level of serotonin was assayed by means of microbore high-performance liquid chromatography separation and electrochemical detection. Samples from microdialysis probes histologically localized to the dorsal raphe nucleus and frontal cortex showed different levels of extracellular 5-hydroxytryptamine in waking, slow-wave sleep and rapid eye-movement sleep. In dorsal raphe nucleus the extracellular level of serotonin was highest in waking, decreased in slow-wave sleep to 69% and in rapid eye-movement sleep to 39% of waking mean level (waking 3.2 +/- 0.9; slow-wave sleep 2.2 +/- 0.8; rapid eye-movement sleep 1.3 +/- 0.4 fmol/sample). Mean extracellular levels of serotonin in frontal cortex displayed a similar pattern (waking 1.7 +/- 0.4; slow-wave sleep 1.0 +/- 0.3; rapid eye-movement 0.5 +/- 0.05 fmol/sample). In frontal cortex, rapid eye-movement sleep samples were only obtained in three animals. Our findings are consistent with previous results in cats, and suggest that in rats also, extracellular 5-hydroxytryptamine levels in dorsal raphe nucleus and frontal cortex across the sleep/wake cycle might reflect serotonergic neuronal activity. The findings stress the importance of controlling for behavioural state when investigating neurochemical correlates of serotonergic function.

EEG power densities (0.5-20 Hz) in different sleep-wake stages in rats.

Frontofrontal and frontoparietal EEG power densities (0.5-20 Hz) in waking, light and deep slow-wave sleep, transition-type sleep, and rapid-eye-movement (REM) sleep were investigated for 8 h during the light period in 16 male Wistar rats. The data indicate that as delta activity (0.5-4.5 Hz) increased from light to deep slow-wave sleep, the number of epochs per scoring epoch with high sigma activity (11-16 Hz) as well as power densities in the rest of the spectrum (5-20 Hz) including sigma frequencies also increased. This is in parallel with other rat studies but contrasts findings in humans, where EEG sigma activity is reported to decrease as sleep deepens. During the 8-h recording period, delta activity decreased whereas sigma activity increased.

Changes in sleep and wakefulness following 5-HT1A ligands given systemically and locally in different brain regions.

Serotonin (5-HT) has been implicated in the regulation of vigilance, but whether 5-HT is important for sleep or waking processes remains controversial. This review addresses the role of 5-HT1A receptors in sleep and wakefulness. Systemic administration of 5-HT1A agonists consistently increases wakefulness, whereas slow wave sleep (SWS) and REM (rapid-eye movement) sleep are reduced. However, systemic 5-HT1A agonists also produce a delayed increase in deep slow wave sleep, or an increase in slow wave activity. Intrathecal administration of a selective 5-HT1A agonist produces an increase in SWS, whereas wakefulness is reduced, presumably by stimulating 5-HT1A receptors located presynaptically on primary afferents in the spinal cord. Microinjection of serotonin into the region of the cholinergic basalis neurons produces an increase in slow wave activity, presumably by stimulating 5-HT1A receptors. Microdialysis perfusion of a selective 5-HT1A agonist into the dorsal Raphe nucleus causes an increase in REM sleep, whereas the other sleep/wake stages are unaltered. The REM sleep increase is likely due to a decrease in 5-HT neuronal activity, and thereby reduced 5-HT neurotransmission in projection areas, e.g. the laterodorsal and pedunculopontine tegmental nuclei. Direct injection of a selective 5-HT1A agonist into the pedunculopontine tegmental nuclei reduces REM sleep, consistent with such a hypothesis. These complex sleep/wake data of 5-HT1A ligands suggest that 5-HT1A receptor activation may increase waking, increase slow wave sleep or increase REM sleep depending on where the 5-HT1A receptors are located within the central nervous system.

Sleep-wake and eeg effects following adenosine a1 agonism and antagonism: similarities and interactions with sleep-wake and eeg effects following a serotonin reuptake inhibitor in rats.

Adenosine is currently being investigated as a possible mediator of a homeostatic sleep need. Reports from different laboratories suggest that both adenosine A1 agonists and selective serotonin reuptake inhibitors (SSRI) increase deep slow wave sleep (SWS-2) after an interval. In this study, the sleep-wake effects of the adenosine A1 agonist N6-cyclopentyladenosine (CPA) and the SSRI zimeldine are directly compared in the same animals. Since the SWS-2 increase following SSRIs may be secondary to increased adenosine levels during the initially increased waking, it was also investigated whether the adenosine A1 antagonist 8-cyclopentyltheofylline (CPT) would inhibit the SWS-2 increase following the serotonin reuptake inhibitor. Both the adenosine A1 agonist CPA and the SSRI zimeldine increased SWS-2 after an interval. Both drugs increased slow wave activity and decreased 9-20 Hz activity during SWS-2. Both the adenosine A1 antagonist CPT, zimeldine and the two drugs combined initially increased waking and subsequently increased SWS-2 after 2 or 4 h. All treatments increased 2-6 Hz activity in SWS-2 after 2h. Thus, CPT did not antagonize the SWS-2 increase of zimeldine. Based on the sleep and power spectral effects it is suggested that the adenosine A1 antagonist potentiated the zimeldine effect, possibly due to antagonism of adenosine A1 inhibition of serotonin release. The data indicate that the delayed SWS-2 and slow wave activity increases following zimeldine are not due to increased stimulation of adenosine A1 receptors following the initial sleep loss.

Sleep/waking effects of a selective 5-HT1A receptor agonist given systemically as well as perfused in the dorsal raphe nucleus in rats.

Sleep/waking stages and behavior were studied following the selective 5-HT1A agonist 8-OH-DPAT given subcutaneously (s.c.) (0.010-0.375 mg/kg) as well as perfused continuously (10 microM) for 6 h into the dorsal raphe nucleus (DRN) using microdialysis. Given systemically, 8-OH-DPAT at 0.375 mg/kg s.c. induced 5-HT behavioral syndrome, increased waking to 149% and reduced slow wave sleep (SWS) to 86%, transition to 76% and rapid eye movement (REM) sleep to 73%. The effect on deep SWS (SWS-2) was biphasic, with an increase after 2 h. 8-OH-DPAT at 0.010 mg/kg did not have any vigilance effects. 8-OH-DPAT perfusion in DRN produced a fourfold increase in REM sleep compared to perfusion of artificial cerebrospinal fluid. This is consistent with the hypothesis that reduced 5-HT neurotransmission following 5-HT1A autoreceptor stimulation will disinhibit cholinergic REM-promoting mesopontine neurons and thereby lead to a REM sleep increase. The other sleep/waking stages were not significantly affected by 8-OH-DPAT perfusion in DRN.

Hypothermia and the 5-HT syndrome induced by CGS 12066B independently of 5-HT(1B) receptor activation.

The effects of CGS 12066B (3-14mg/kg), a putative 5-HT(1B) agonist, on 5-HT behavioral syndrome, motor activity and body temperature, were investigated in rats. The animals were well adapted to the experimental conditions before testing, and data sampling started at the same hour for each rat. The highest dose of CGS 12066B clearly reduced body temperature and induced flat body posture and hindlimb abduction. No significant change was seen in motor activity. The CGS 12066B-induced changes were not antagonized by 5-HT(1B) receptor antagonists, or antagonists at other 5-HT receptor. In fact, the 5-HT(1A) antagonist NAN-190 and especially the non-selective 5-HT antagonist methiothepin, with definite 5-HT(1B) receptor blocking properties, both potentiated the decrease in body temperature. The findings suggest that the behavioral and body temperature effects of CGS 12066B are not easily explained by 5-HT(1B) receptor stimulation, but may be mediated by activation of non-serotonergic mechanisms. Similar conclusions in studies with other 5-HT(1B) agonists suggest a common problem with such drugs.

Citalopram: differential sleep/wake and EEG power spectrum effects after single dose and chronic administration.

The sleep/wake effects of the selective serotonin re-uptake inhibitor citalopram were studied in both a single-dose study with three dose levels (0.5, 2.0 and 5.0 mg/kg), and a 5-week chronic administration study (15 mg/kg/24 h). Single doses of citalopram resulted in a dose-dependent inhibition of rapid eye movement (REM) sleep. After chronic citalopram treatment there was a sustained REM sleep inhibition. Single doses of citalopram resulted in only minor changes in non-REM (NREM) sleep as well as in NREM EEG power spectral density. Chronic administration resulted in a major shift from SWS-2 to SWS-1. The observed corresponding changes in EEG power density were regional. A 30 to 40 percent reduction of power density in the 0.5-15 Hz range in the fronto-parietal EEG derivation was seen for the whole 8-h registration period. In the fronto-frontal EEG derivation only minor changes were seen. A decreasing trend in NREM sleep power density between 0.5 and 7 Hz, usually seen during the course of the light period, was not observed in the chronic condition, but was seen in control and single-dose condition, suggesting altered diurnal distribution of slow wave activity in the chronic condition. The data indicate that acute and chronic administration of citalopram shows clear differences in sleep effect, which may be caused by alteration of serotonergic transmission, and may be related to the antidepressant effect.

Sleep and EEG power spectrum effects of the 5-HT1A antagonist NAN-190 alone and in combination with citalopram.

The sleep and waking and EEG power spectrum effects of the putative 5-HT1A antagonist NAN-190 (0.5 mg/kg, i.p.) were studied alone and in co-administration with the selective serotonin re-uptake inhibitor citalopram (5.0 mg/kg, i.p.) in the rat. Citalopram, as in a prior dose-response study, reduced REM sleep. In addition, a slight increase in NREM sleep was observed. Citalopram reduced NREM fronto-parietal (FP) EEG power density in the 5-20 Hz range. When administered alone, NAN-190 suppressed REM sleep in the first 2 h, and reduced SWS-2 in the first 4 after administration. NAN-190 also suppressed selectively NREM sleep slow-wave activity in both fronto-frontal (FF) and FP EEG power spectrum. When administered in combination with citalopram, an attenuation of the power density reduction in the 7-15 Hz range in the FF EEG of citalopram alone, was observed. However, the EEG power spectral density and REM sleep suppressive effects of NAN-190 were both augmented. The results are compatible with the notion that serotonin is involved in the modulation of the slow wave activity in the EEG during NREM sleep. The results are cordant with other data suggesting that postsynaptic 5-HT1A stimulation might increase slow wave activity in the NREM EEG, and that serotonergic stimulation of other receptor subtypes (possibly 5-HT2) may decrease slow wave activity in the NREM EEG.

Sleep/waking effects following intrathecal administration of the 5-HT(1A) Agonist 8-OH-DPAT alone and in combination with the putative 5-HT(1A) antagonist NAN-190 in rats.

Sleep, waking, and EEG power spectra were investigated in rats after intrathecal (IT) administration of a 5-HT(1A) agonist and a 5-HT(1A) antagonist. Total slow wave sleep (TSWS) was increased and waking was decreased over the 8-h recording period after the 5-HT(1A) agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (38 nmol). Within TSWS, SWS1 was unchanged while SWS-2 tended to be increased. The 5-HT(1A) antagonist 1-[2-Methoxyphenyl)-4-(4-(2-phthalimido)-butyl]piperazine hydrobromide (NAN-190) did not change any sleep/waking stages. Combined treatment with 8-OH-DPAT and NAN-190 increased variance. Following the combination, sleep and waking were not significantly different from control. SWS-2 tended to be reduced compared to the effect of 8-OH-DPAT alone. There were no systematic changes in neither waking nor TSWS fronto-frontal or fronto-parietal EEG power spectrum after any of the treatments, indicating that sleep quality was not changed. The results confirm earlier data suggesting that in the spinal cord, stimulation of 5-HT(1A) receptors have a dampening effect on transmission of sensory information, leading to deactivation and thereby increased sleep tendency. The reason why the 8-OH-DPAT effect was not clearly antagonized by the putative 5-HT1A antagonist NAN-190, may be due to the generally weak antagonistic and also partial agonistic effect of NAN-190 as reported in the literature.