Mesolimbic fMRI activations during reward anticipation correlate with reward-related ventral striatal dopamine release

The dopaminergic mechanisms that control reward-motivated behavior are the subject of intense study, but it is yet unclear how, in humans, neural activity in mesolimbic reward-circuitry and its functional neuroimaging correlates are related to dopamine release. To address this question, we obtained functional magnetic resonance imaging (fMRI) measures of reward-related neural activity and [11C] raclopride positron emission tomography (PET) measures of dopamine release in the same human participants, while they performed a delayed monetary incentive task. Across the cohort, a positive correlation emerged between neural activity of the substantia nigra / ventral tegmental area (SN/VTA), the main origin of dopaminergic neurotransmission, during reward anticipation and reward-related [11C] raclopride displacement as an index of dopamine release in the ventral striatum, major target of SN/VTA dopamine neurons. Neural activity in the ventral striatum / nucleus accumbens itself also correlated with ventral striatal dopamine release.Additionally, high reward-related dopamine release was associated with increased activation of limbic structures, such as the amygdala and the hippocampus. The observed correlations of reward-related mesolimbic fMRI activation and dopamine release provide evidence that dopaminergic neurotransmission plays a quantitative role in human mesolimbic reward processing. Moreover, the combined neurochemical and hemodynamic imaging approach used here opens up new perspectives for the investigation of molecular mechanisms underlying human cognition

Sleep Deprivation Effects on Cognitive Performance

An experimental sleep deprivation study has been launched at the German Aerospace Center (DLR) in order to determine effects of varying degrees of sleepiness and alcohol on cognitive performance. A total of 48 subjects in cohorts of eight subjects each will stay for twelve consecutive days and nights in the AMSAN sleep laboratory in Cologne. During their stay in the laboratory, subjects are deprived of sleep in a successive manner totally and partially. In addition, on one day they are exposed to moderate alcohol levels. In between the interventions two recovery days are provided per design. A short test-battery of pilot’s and air traffic controller’s aptitudes is administered to the subjects including spatial orientation, perceptual speed and control of attention tests. In addition, self-concept of mental fitness is measured via a questionnaire prior to and after the cognitive tasks in order to examine whether potential performance decrements due to fatigue are recognized by the subjects. The study design and some preliminary data of the first two cohorts (N = 16) are presented in the paper

Effects of nocturnal aircraft noise on cognitive performance in the following morning: dose- response relationships in laboratory and field.

Objective: Nocturnal aircraft noise disturbs sleep and impairs recuperation. We investigated in laboratory and field studies whether noise-induced sleep fragmentation is associated with performance impairments in a psychomotor vigilance task (PVT) and a memory search task. Methods: In the laboratory, 112 participants were exposed to aircraft noise during 9 consecutive nights. In the field, 64 participants were examined during 9 consecutive nights in the vicinity of Cologne/Bonn airport. Reaction time, signal detection performance and subjective task load were recorded. Results: Dose–response relationships showed significant, linear impairments in reaction times. In the laboratory, reaction time in PVT increased with 0.13 ms/dB equivalent noise level (LAeq) plus 0.02 ms/noise event. In the field study, reaction time increased with 0.3 ms/dB LAeq. Participants worked significantly less accurate after nocturnal noise exposure. Conclusion Influences of LAeq and number of noise events on daytime performance were small but consistent and significant, stressing the potential public health impact of nocturnal noise exposure

Biodistribution and radiation dosimetry of the A1 adenosine receptor ligand 18F-CPFPX determined from human whole-body PET

(18)F-8-cyclopentyl-3-(3-fluoropropyl)-1-propylxanthine ((18)F-CPFPX) is a potent radioligand to study human cerebral A(1) adenosine receptors and their neuromodulatory and neuroprotective functions with positron emission tomography (PET). The purpose of this study was to determine the biodistribution and the radiation dose of (18)F-CPFPX by whole-body scans in humans.Six normal volunteers were examined with 12 whole-body PET scans from 1.5 min to 4.5 h after injection. Volumes of interest were defined over all visually identifiable organs, i.e. liver, gallbladder, kidneys, small intestines, heart, and brain to obtain the organs' volumes and time-activity curves (TACs). TACs were fitted with exponential functions, extrapolated, multiplied with the physical decay and normalized to injected activities so that the residence times could be computed as area under the curve. Radiation doses were calculated using the OLINDA/EXM software for internal dose assessment in nuclear medicine.The liver uptake shows peak values (decay-corrected) of up to 35% of the injected radioactivity. About 30% is eliminated by bladder voiding. The highest radiation dose is received by the gallbladder (136.2 +/- 66.1 muSv/MBq), followed by the liver (84.4 +/- 10.6 muSv/MBq) and the urinary bladder (78.3 +/- 7.1 muSv/MBq). The effective dose was 17.6 +/- 0.5 muSv/MBq.With 300 MBq of injected (18)F-CPFPX a subject receives an effective dose (ICRP 60) of 5.3 mSv. Thus the effective dose of an (18)F-CPFPX study is comparable to that of other (18)F-labelled neuroreceptor ligands

Performance impairment during four days partial sleep deprivation compared with the acute effects of alcohol and hypoxia

Objective: Subjects were exposed to cumulated partial sleep deprivation (psd), alcohol intake and hypoxia in a sequential design to examine the impact on neurobehavioral performance. Methods: Sixteen healthy male volunteers were enrolled in this study and were exposed in turn, after adaptation and baseline measurements, to one day of periods of hypoxia, one day of alcohol intake and one day for recovering (with 8h time in bed TIB). Subsequently the exposition of those conditions is that the subjects spent 5h night restriction daily for four consecutive days, followed by two recovery days. Performance was tested five (or six) times per day with reaction time task (SRT) and unstable tracking task (UTT). Results: The performance impairment showed to be cumulative in both tests over the four sleep deprivation days and differed significantly from baseline. Corresponding performance deficits under the influence of the stressors were for SRT: four days psd, 13% O2 concentration and a blood alcohol concentration (BAC) of around 0.4–0.6‰ for UTT: four days psd, 13% O2 concentration and a BAC of around 0.6‰. One night of 8h sleep restored performance nearly to baseline level. Conclusions: A sleeping time of 5h per night for four consecutive days impairs performance in such a way that traffic safety may be compromised

Schlaf und kognitive Leistung: Wirkung von Kaffee auf Koffein-sensitive Personen

Fragestellung: Wegen seiner förderlichen Wirkung auf Leistung und Wachheit ist Kaffee ein beliebtes Getränk. Sein Konsum kann jedoch den Tiefschlaf vermindern. Wir untersuchten, welche Wirkung Kaffee bei chronischer Schlafrestriktion auf den Tiefschlaf und die kognitive Leistung zeigt. Patienten und Methoden: Probanden im Alter von 20 bis 40 Jahren wurden in 4 Gruppen über 9 Tage hinweg im Schlaflabor untersucht. Die Kontrollgruppe (N=15) hatte immer eine Bettzeit (time in bed, TIB) von 8 Stunden. Die übrigen 3 Gruppen (Restriktionsgruppe, Koffeingruppe, Decaff-Gruppe) hatten in den ersten drei Nächten eine TIB von 8 Stunden, danach wurde die TIB für 5 Nächte auf 5 Stunden verkürzt, dann folgte zur Erholung eine Nacht mit 8 Stunden TIB. Die Restriktionsgruppe (N=20) erhielt keine weitere Intervention. Die Koffeingruppe (N=17) konsumierte täglich 300 g Kaffee (300 mg Koffein) während der Schlafrestriktionsphase, die Decaff-Gruppe (N=17) trank die gleiche Menge entkoffeinierten Kaffees. Für diese beiden Gruppen wurden bevorzugt Koffein-sensitive Träger des C/C-Allels des Adenosin-A2A-Rezeptors (ADORA c.1976) selektiert. Der Schlaf wurde mit einer Polysomnographie aufgezeichnet. Die Tagesleistung wurde mit einem Psychomotorischen Vigilanztest gemessen. Gruppenunterschiede in der Tiefschlafdauer (N3) und der Reaktionsgeschwindigkeit (1/Reaktionszeit) wurden mit einer gemischten ANOVA mit Bonferroni-Korrektur (α<0,016) analysiert. Ergebnisse: In der Restriktionsgruppe und der Decaff-Gruppe war N3 nur in der ersten verkürzten Nacht vermindert (p<0,01). Die Koffeingruppe zeigte einen Trend zu weniger N3 in den verkürzten Nächten 1 bis 4, sodass sie ein kumulatives N3-Defizit über die Restriktionsnächte (-31 min, n.s.) aufbaute. Die Reaktionsgeschwindigkeit der Koffeingruppe war schneller als die der Restriktionsgruppe an den ersten beiden Tagen nach Schlafrestriktion (p<0,002) und auch schneller als die der Decaff-Gruppe (p=0,014) am ersten Tag nach Schlafrestriktion. Im Unterschied zur Restriktionsgruppe und Decaff-Gruppe verbesserte sich die Reaktionsgeschwindigkeit jedoch nicht nach der Erholungsnacht. Schlussfolgerung: Die Reaktionsgeschwindigkeit blieb bei Koffein-sensitiven Personen, die während der Schlafrestriktion ∼300 mg Koffein tranken, für zwei Tage auf einem ausgeschlafenen Niveau. Der dann folgende Leistungseinbruch blieb im Gegensatz zu den anderen Schlafentzugsgruppen auch nach der Erholung bestehen. Dies scheint ein stärkerer N3-Verlust zu bewirken