Search

We investigate experimentally and theoretically the electron emission in collisions between He atoms and (q = 1, 2) projectiles at intermediate to high incident energies. We report on measured absolute values of double-differential cross-sections, as a function of the emitted electron energy and angle, at a collision energy of 440 keV u−1. The different contributions from target ionization, projectile ionization, and simultaneous target–projectile ionization are calculated with the quantum-mechanical continuum distorted wave and continuum distorted wave–eikonal initial state models, and with classical trajectory Monte Carlo simulations. There is an overall good agreement of the calculations with the experimental data for electron emission cross-sections. [ABSTRACT FROM AUTHOR]

We present data from a sample of 190 healthy adults including assessments of 4 cognitive factor scores, 12 cognitive tests, and 115 MRI-assessed neuroanatomical variables (cortical thicknesses, cortical and sub-cortical volumes, fractional anisotropy, and radial diffusivity). These data were used in estimating underlying sources of individual variation via independent component analysis (Watson et al., In press) [25].

Distorted wave models are employed to investigate the electron loss process induced by bare ions on biological targets. The two main reactions which contribute to this process, namely, the single electron ionization as well as the single electron capture are here studied. In order to further assess the validity of the theoretical descriptions used, the influence of particular mechanisms are studied, like dynamic screening for the case of electron ionization and energy deposition on the target by the impacting projectile for the electron capture one. Results are compared with existing experimental data., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Benzodiazepine (BZD) and non-BZD hypnotics improve sleep induction and sleep maintenance. BZD induces a further reduction of slow wave sleep (SWS) and rapid eye movement (REM) sleep, whereas SWS and REM values remain decreased during non-BZD administration. There is evidence indicating that the nonselective serotonin 5-HT(2A/2C) receptor antagonists, ritanserin, ketanserin, seganserin and ICI-169369, the selective 5-HT(2A) receptor antagonist eplivanserin and the 5-HT(2A) receptor inverse agonist pimavanserin, increase SWS in subjects with normal sleep. In addition, it has been shown that prior administration of ritanserin prevents the nitrazepam-induced suppression of SWS in normal subjects. Of note, ritanserin also induced an increase of SWS in poor sleepers, patients with chronic primary insomnia and psychiatric patients with a generalized anxiety disorder or a mood disorder. The 5-HT(2A) receptor inverse agonist APD-125 gave rise to a similar effect in patients with chronic primary insomnia. Thus, presently available evidence tends to indicate that the association of a 5-HT(2A) receptor antagonist or a 5-HT(2A) receptor inverse agonist with a BZD or a non-BZD hypnotic could be a valid alternative to normalize SWS in patients with primary or comorbid insomnia., (Copyright 2010 Prous Science, S.A.U. or its licensors. All rights reserved.)

Melatonin is synthesized and secreted during the dark period of the light-dark cycle. The rhythmic nocturnal melatonin secretion is directly generated by the circadian clock, located in mammals within the suprachiasmatic nucleus (SCN), and is entrained to a 24-hour period by the light-dark cycle. The periodic secretion of melatonin may be used as a circadian mediator to any system that can 'read' the message. In addition, direct effects of the hormone on the SCN could explain some of the melatonin effects on the circadian system. Duration of the melatonin nocturnal secretion is directly proportional to the length of the night and it has experimentally been demonstrated to be the critical parameter for photoperiod integration. The sites and mechanisms of action of melatonin for circadian and photoperiodic responses are far from being elucidated, but action through specific membrane receptor sites starts to emerge. A possible bicompartmental model of distribution for melatonin, the first compartment in plasma acting on peripheral organs and the second in the cerebrospinal fluid affecting neurally mediated functions at a much higher concentration, has recently been proposed. From earlier studies it was concluded that melatonin administration to humans reduces sleep latency and induces sleepiness and fatigue. More recently, the effect of lower pharmacologic or physiologic doses of melatonin was examined in different laboratories. These studies included young normal volunteers and patients with chronic insomnia, as well as dementia patients exhibiting sundowning syndrome. Irrespective of the method of assessment, melatonin showed effects in insomniac patients in most studies. With some exceptions, melatonin administration reduced sleep latency and/or increased total sleep time and sleep efficiency. Furthermore, melatonin was more effective when given to elderly insomniacs, or Alzheimer disease patients, although sleep improvement was not strictly correlated with prior levels of the hormone., (Copyright 2000 S. Karger AG, Basel)

The effect of flesinoxan, a selective 5-HT1A receptor agonist, WAY 100635, a selective 5-HT1A receptor antagonist, and (+/-)pindolol, a mixed beta-adrenoceptor and 5-HT1A/B receptor antagonist, on spontaneous sleep was studied in adult rats implanted for chronic sleep recordings. Drugs were infused directly into the dorsal raphe nucleus (DRN). Direct application of flesinoxan (25.0 and/or 50.0 ng) into the DRN induced a significant increment of REM sleep (REMS) during the second and third 2 h period of recording. On the other hand, microinjection into the DRN of (+/-)pindolol (100.0 and/or 200.0 ng), and WAY 100635 (12.5, 25.0 and 50.0 ng) significantly reduced REMS during the first and/or second 2 h recording period. Our findings support previous studies indicating that microdialysis perfusion of the 5-HT1A receptor agonist 8-OHDPAT into the DRN increases REMS. In addition, they favor the proposal that microinjection of 5-HT1A receptor antagonists into the DRN would suppress 5-HT inhibition and reduce REMS.

The effects of the benzodiazepine1 (BZ1) receptor agonist SX-3228 were studied in rats (N = 12) implanted for chronic sleep procedures. Administration of 0.5, 1.0 and 2.5 mg/kg SX-3228, sc, to rats 1 h after the beginning of the light phase of the light-dark cycle induced a significant reduction of rapid-eye-movement sleep (REMS) during the third recording hour. Moreover, slow wave sleep (SWS) was increased during the fourth recording hour after the two largest doses of the compound. Administration of 0.5, 1.0 and 2.5 mg/kg SX-3228 one hour after the beginning of the dark period of the light-dark cycle caused a significant and maintained (6-h recording period) reduction of waking (W), whereas SWS and light sleep (LS) were increased. REMS values tended to increase during the entire recording period; however, the increase was statistically significant only for the 1.0 mg/kg dose during the first recording hour. In addition, a significant and dose-related increase of power density in the delta and the theta regions was found during nonREM sleep (LS and SWS) in the dark period. Our results indicate that SX-3228 is a potent hypnotic when given to the rat during the dark period of the light-dark cycle. Moreover, the sleep induced by SX-3228 during the dark phase closely resembles the physiological sleep of the rat.

Effects of the 5-HT3 receptor agonist, m-chlorophenylbiguanide (10.0-40.0 microg), on sleep and waking were studied in control, vehicle-treated and 6-hydroxydopamine-injected rats. Bilateral injections of m-chlorophenylbiguanide into the nucleus accumbens of the control and the vehicle-infused animals significantly increased waking and reduced slow wave sleep. Rapid eye movement sleep (REM sleep) remained unchanged. Pretreatment with the selective 5-HT3 receptor antagonist, MDL 72222 (1aH,3a,5a, H-tropan-3-yl-3,5-dichloro-benzoate) (0.5 mg/kg, s.c.), reversed the effects of m-chlorophenylbiguanide (10.0-20.0 microg) on sleep and waking in the control group. Administration of the 5-HT3 receptor agonist to the 6-hydroxydopamine-treated animals modified only slightly the time spent in wakefulness and slow wave sleep, while REM sleep was significantly and dose dependently reduced. Our findings further support the proposal that increase of wakefulness and reduction of slow wave sleep after activation of 5-HT3 receptors, is partly related to the release of endogenous dopamine.

The present study evaluated the effects of histamine H3 receptor agonist BP 2.94 or H3 receptor antagonist carboperamide (MR 16155) given by oral route on sleep and waking in rats surgically prepared for long-term recordings. BP 2.94 produced a significant increase of slow-wave sleep (SWS) that was related to slight decreases of waking, light sleep, and REM sleep. Carboperamide significantly increased waking and decreased SWS and REM sleep. Pretreatment with carboperamide prevented the effect of BP 2.94 on SWS. It is suggested that the effects of BP 2.94 or carboperamide on sleep and waking could depend on changes in the availability of histamine at the postsynaptic H1 receptor. Alternatively, activation or blockade of the H3 heteroreceptors found in the central catecholamine, indolamine, and acetylcholine nerve endings could inhibit or increase the release of noradrenaline, serotonin, dopamine, and acetylcholine. This would secondarily result in changes of sleep variables.

The effects of partial 5-HT1A receptor agonists buspirone (0.010-4.0 mg/kg), ipsapirone (0.010-6.0 mg/kg), and gepirone (0.025-4.0 mg/kg) on sleep and waking were studied in vehicle-treated and 5,7-dihydroxytryptamine (5,7-DHT)-injected rats. 5,7-DHT-treated animals showed a marked and significant serotonin and 5-HIAA depletion in the raphe regions of the pons and upper brain stem, cerebral cortex, hippocampus, and striatum. Subcutaneous administration of the partial agonists to both the vehicle-infused and the 5,7-DHT-treated animals significantly increased waking (W) and reduced light sleep (LS), slow-wave sleep (SWS), and REM sleep (REMS). Pretreatment with (-)pindolol (2.0 mg/kg) reversed the effects of buspirone and gepirone on W and non-REM sleep (LS + SWS) whereas REMS remained suppressed. (-)-Pindolol failed to reverse the effects of ipsapirone on sleep and W. The present results tend to indicate that increased W after acute administration of buspirone, ipsapirone, or gepirone depends upon the activation of postsynaptic 5-HT1A receptors. The well-known anxiolytic action observed after chronic administration of the azapirones seems to be related to mechanisms other that these involved in their stimulant effect.

The effects of the selective histamine H1-receptor agonist, 2-(3-trifluoromethylphenyl)histamine, were studied in rats implanted with electrodes for chronic sleep recordings. 2-(3-Trifluoromethylphenyl)histamine (80-120 micrograms) injected into the left lateral ventricle increased wakefulness, whereas slow wave sleep was reduced. Pretreatment with pyrilamine (2.0 mg/kg) prevented the effects of the H1-receptor agonist on wakefulness and slow wave sleep. Our results further support the involvement of histamine in the modulation of the waking state.

The effect of 5-HT1A receptor agonist 8-OH-DPAT on sleep and wakefulness was studied in rats with selective serotonin depletion after ICV administration of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT). Injection of 8-OH-DPAT to vehicle-treated animals induced biphasic effects, such that low doses (0.010 mg/kg) which act perferentially on the somatodendritic autoreceptor decreased wakefulness (W) and increased slow wave sleep (SWS), while higher doses (0.375 mg/kg) which stimulate postsynaptic receptors caused opposite effects. REM sleep was suppressed irrespective of the dosage given. Injection of the 0.010 mg/kg dose in the 5,7-DHT-treated rats did not result in significant changes in sleep or W. On the other hand, the 0.375 mg/kg dose produced changes in sleep variables which were similar to those described in the vehicle-treated animals. Our findings tend to indicate that increased SWS after low doses of 8-OH-DPAT depends upon the activation of inhibitory somatodendritic 5-HT1A receptors, while increased W after higher doses of the compound is related to stimulation of postsynaptic receptors.

A trial was carried out to determine the effect of ritanserin or a placebo on sleep and mood in two groups of abstinent alcoholic patients. Their condition was characterized by both alcohol dependence and dysthymia, associated with a personality disorder. They were included in the study after 30 days of sobriety. Ritanserin was given at a daily dose of 10 mg for 28 days and was preceded (10 days) and followed (2 days) by a placebo. Plasma ritanserin concentration after administration of the 28th dose was higher than after the first dose. Peak levels of ritanserin from the first to the 28th dose increased approximately three-fold. In the ritanserin group there was a reduction of total waking time. Total sleep time increase was associated with significantly larger amounts of nonrapid eye movement sleep. Slow wave sleep and rapid eye movement sleep (in minutes or as a percent of total sleep time) were not significantly modified. Patients on ritanserin achieved a progressive improvement of their dysthymia. As compared to the placebo group, a statistically significant decrease of the Hamilton Rating Scale for Depression and Hamilton Rating Scale for Anxiety was found in the ritanserin group after 1 week of treatment. The absence of an effect in the placebo-treated group suggests that the clinical response and sleep improvement were mainly related to ritanserin administration.

The effects of the histamine H3 receptor agonist, (R)-alpha-methylhistamine were compared with those of the histamine H3 antagonist, thioperamide, in rats implanted with electrodes for chronic sleep recordings. (R)-alpha-Methylhistamine (1.0-4.0 micrograms) injected bilaterally into the premammillary area where histamine immunoreactive neurons have been detected increased slow wave sleep, whereas wakefulness and REM sleep were decreased. No significant effects were observed when (R)-alpha-methylhistamine (1.0-8.0 mg/kg) was administered i.p. Thioperamide (1.0-4.0 mg/kg i.p.) increased wakefulness and decreased slow wave sleep and REM sleep. Pretreatment with thioperamide (4.0 mg/kg) prevented the effects of (R)-alpha-methylhistamine (2.0 micrograms) on slow wave sleep and wakefulness. Our results further support an active role for histamine in the control of the waking state.

The effect of moclobemide, a short-acting, reversible, preferential type-A MAO inhibitor (300 mg daily in three divided doses), on the sleep of eight depressed patients was assessed by polysomnographic recordings in a 4-week therapeutic trial. Six patients showed an improvement greater than 50% on the Hamilton Depression Rating Scale. Compared to placebo, patients receiving moclobemide showed improved sleep continuity as judged by the decrease in wake time after sleep onset and total wake time, particularly during the intermediate and late stages of drug administration. Total sleep time increase was comprised of larger amounts of stage 2 NREM sleep. REM sleep latency was significantly increased and REM sleep % decreased during the drug administration period. However, in contrast to the older, non-selective and selective MAOIs, moclobemide had a mild REM sleep suppressant effect.

The effects of the H1-receptor antagonist diphenhydramine and the brain-penetrating H2-receptor antagonist zolantidine were studied in rats implanted for chronic sleep recordings. Diphenhydramine (1.0-4.0 mg/kg) significantly increased slow wave sleep and decreased wakefulness. Zolantidine (0.25-8.0 mg/kg) had no significant effects on any of the sleep parameters examined. One possibility is that zolantidine did not enter the brain in sufficient concentration to produce significant changes on sleep and wakefulness. Another possibility is that blockade of H2-receptor involved parts of the brain other than those implicated in the sleep-wake cycle. The feasibility remains that H2-receptors are not involved in sleep regulation. The absence of selective, brain-penetrating H2-receptor agonists precludes a more detailed analysis of the role of this subtype of receptor in the control of sleep and wakefulness.

The effect of the D1 dopamine (DA) receptor agonist SKF 38393 was compared with that produced by the D1-receptor antagonist, SCH 23390, in rats implanted with electrodes for chronic sleep recordings. SKF 38393 (0.1 to 4.0 mg/kg) significantly suppressed rapid-eye-movement sleep (REMS) after the highest dose. SCH 23390 (0.1 to 2.0 mg/kg) increased slow-wave sleep (SWS), whereas wakefulness (W) and REMS were decreased. Pretreatment with SKF 38393 (0.5 mg/kg) prevented the effects of SCH 23390 (0.25 mg/kg) on W and SWS. However, REM sleep showed a further depression. Pretreatment with SKF 38393 (2.0 mg/kg) or SCH 23390 (0.25 mg/kg) failed to modify the increase of SWS and decrease of W induced by D2 receptor agonist bromocriptine (0.5 mg/kg) in a dose that selectively stimulates DA autoreceptors. On the other hand, SCH 23390 (0.25 mg/kg) failed to prevent REMS depression induced by bromocriptine (6.0 mg/kg) in a dose that preferentially acts at postsynaptic sites. Pretreatment with SCH 23390 (0.25 mg/kg) prevented the increase of W and decrease of SWS induced by the 5-HT2 receptor agonist DOI (0.25 mg/kg). Given the "fragility" of REMS in the rat, nonspecific factors could be contributing to its depression after SKF 38389 or SCH 23390 administration. Inhibition of D1 receptors could be responsible for SCH 23390-induced increase of SWS and decrease of W. However, a blockade of 5-HT2 receptors could be partly involved in these effects. Neither SKF 38393 nor SCH 23390 exerted activity on the sleep-wake cycle, which could be considered to reflect effects at DA autoreceptors.

The H1-receptor agonist 2-thiazolylethylamine (2-TEA) given by i.c.v. route dose-dependently increased wakefulness (W) and decreased NREM sleep (NREMS) and REM sleep (REMS) in rats prepared for chronic sleep recordings. The H1-receptor antagonists pyrilamine and diphenhydramine given by i.p. route decreased W and increased NREMS. Pyrilamine prevented the increase of W and decrease of NREMS produced by 2-TEA. However, REMS reduction was not antagonized, what tends to suggest that two different mechanisms could be involved in the 2-TEA-induced effects on NREMS and REMS. Cimetidine which blocks H2-receptors, when given by i.p. route showed no significant effects on sleep and W. Administration of the H2-receptor agonist dimaprit and the H2-receptor antagonists cimetidine, metiamide and ranitidine by i.c.v. route induced the appearance of high voltage spikes at cortical leads, thus leaving inconclusive the matter of their effects on sleep and wakefulness. Our results tend to support the proposal that the H1-receptor intervenes in sleep-wakefulness regulation. Limitations in the available H2-receptor agonists and antagonists presently preclude a more detailed analysis of the role of H2-receptors on sleep and W.

The effects of the dopamine D-2 receptor agonist, quinpirole, were compared with those produced by dopamine D-2 antagonist, YM-09151-2, in rats implanted with electrodes for chronic sleep recordings. Quinpirole (0.015-1.0 mg/kg) induced biphasic effects such that low doses decreased wakefulness and increased sleep, while higher doses induced the opposite effects. At 0.015 mg/kg, YM-09151-2 slightly augmented wakefulness, while at 1.0-2.0 mg/kg it significantly increased light sleep but depressed REM sleep. Pretreatment with YM-09151-2 in a dose which preferentially acts at presynaptic sites reversed the suppressant effects of a low dose of quinpirole on wakefulness and slow wave sleep. In contrast, the administration of YM-09151-2 in a dose which blocks postsynaptic D-2 receptors prevented the effect of a high dose of quinpirole on wakefulness and slow wave sleep; the depression of REM sleep was not affected. The opposite effects observed on the waking EEG after activation of either dopamine autoreceptors or postsynaptic D-2 receptors with adequate doses of quinpirole tend to indicate an active role for DA in the control of the waking state.

DSP-4, a neurotoxin which produces a marked and long-lasting depletion of norepinephrine (NE) in the central nervous system, was given in a dose of 50 mg/kg by i.p. route to rats prepared for chronic sleep recordings. Light sleep was significantly increased and REM sleep decreased during the first 2 days following DSP-4. Thereafter, REM sleep showed a consistent increase which attained significance on days 5 and 6 postinjection, thus indicating a permissive role for NE on this behavioral state. We examined also whether pretreatment with DSP-4 would modify the effects of clonidine, yohimbine, methoxamine, or clenbuterol on sleep and wakefulness. The sensitivity to alpha 2-agents, methoxamine, and clenbuterol was respectively slightly increased or unchanged, decreased, and clearly increased after DSP-4.

Mean heart rates and their variability indices during REM sleep and the frequency of cardiac arrhythmias during the sleep-awake cycle were determined in a group of coronary patients with disturbances of cardiac rhythm. In some patients there was a temporal relationship of atrial and ventricular premature contractions with slow-wave sleep, REM sleep or wakefulness. However, when they were considered as a group, no significant correlation could be observed. Furthermore, the sinus arrhythmia characteristic of REM sleep was not found to be exaggerated in those patients.

The effects of clozapine on the spontaneous firing rate of noradrenergic (NE, locus coeruleus), dopaminergic (DA, zona compacta, ventral tegmental area) and non-dopaminergic (zona reticulata) neurons was studied in chloral hydrate anesthetized rats. Clozapine administered intraperitoneally significantly increased the spontaneous activity of NE and DA neurons. After a cumulative dose of 8 mg/kg clozapine, the increase of mean firing rate per min of zona compacta and ventral tegmental area neurons attained almost similar values. Amphetamine reversed the clozapine-induced stimulation of NE and DA neurons. Zona reticulata neurons were depressed by clozapine. Neither amphetamine nor physostigmine were effective in antagonizing the inhibition. Our results suggest that clozapine blocks central NE and DA receptors. Furthermore, they fail to reveal a smaller sensitivity of the striatum as compared to the limbic system to the effects of clozapine.