Human interaction with robotic systems: performance and workload evaluations.

We first tested the effect of differing tactile informational forms (i.e. directional cues vs. static cues vs. dynamic cues) on objective performance and perceived workload in a collaborative human-robot task. A second experiment evaluated the influence of task load and informational message type (i.e. single words vs. grouped phrases) on that same collaborative task. In both experiments, the relationship of personal characteristics (attentional control and spatial ability) to performance and workload was also measured. In addition to objective performance and self-report of cognitive load, we evaluated different physiological responses in each experiment. Results showed a performance-workload association for directional cues, message type and task load. EEG measures however, proved generally insensitive to such task load manipulations. Where significant EEG effects were observed, right hemisphere amplitude differences predominated, although unexpectedly these latter relationships were negative. Although EEG measures were partially associated with performance, they appear to possess limited utility as measures of workload in association with tactile displays. Practitioner Summary: As practitioners look to take advantage of innovative tactile displays in complex operational realms like human-robotic interaction, associated performance effects are mediated by cognitive workload. Despite some patterns of association, reliable reflections of operator state can be difficult to discern and employ as the number, complexity and sophistication of these respective measures themselves increase.

Mn-doped ZnO nanocrystals embedded in Al2O3: structural and electrical properties.

We report on the structural and electrical properties of Mn-doped ZnO/Al(2)O(3) nanostructures produced by the pulsed laser deposition technique. Grazing incidence small angle x-ray scattering (GISAXS) and Rutherford backscattering spectrometry revealed the multilayered structure in as-deposited samples. Annealing of the nanostructures was shown to promote the formation of nanocrystals embedded in the Al(2)O(3) matrix, as was evidenced by GISAXS and high resolution transmission microscopy. Particle-induced x-ray emission analysis showed a doping of 8 at.% Mn in ZnO. Grazing incidence x-ray diffraction and Raman spectroscopy demonstrated that the nanocrystals have the pure wurtzite ZnMnO crystalline phase. Resonant Raman scattering displayed an increase of intensity of the 1LO mode as well as broadening of the 2LO mode related to the size effect. Capacitance-voltage measurements showed carrier retention with a voltage shift higher than those reported for similar systems.

Investigation of surface plasmon resonance in gold/alumina composite films prepared by rf-sputtering.

Alumina films containing gold nanoparticles (NPs) were grown by magnetron radio frequency (rf) sputtering technique. They were investigated by transmission electron microscopy (TEM), X-ray diffraction (XRD) and optical absorption spectroscopy. It is suggested that the increase of the contrast of surface plasmon resonance band after annealing is connected with increasing of electron free mean path in Au NPs rather than with change in particle size distribution. The absorption spectra of the nanocomposites have been modelled taking into account a correction of the dielectric constant for electron mean free path limitation.

Extralunar dust in apollo cores?

Densities of nuclear tracks exceed 10(11) per square centimeter in several percent of the micrometer-size silicate grains from all depths in the 12-and 60-centimeter lunar cores. Either these grains were irradiated in space as extralunar dust or the ratio of iron to hydrogen in low-energy (about 1 million electron volts per nucleon) solar particles is orders of magnitude higher than in the photosphere.

Development of the cytosolic defence system against microsomal lipid peroxidation in rat liver.

Ascorbate-induced lipid peroxidation in rat liver microsomes reaches the adult level in 2-3 days. NADPH-induced peroxidation develops more gradually, in parallel with the activity of NADPH-cytochrome P-450 reductase, attaining adult levels by 10-12 days. The glutathione-dependent cytosolic enzyme activity which inhibits peroxidation is inhibited by bromosulphophthalein. The development of this system lags behind the development of microsomal lipid peroxidation between the ages of 2 and 20 days, allowing peroxidation to proceed.

Selective dopamine D-1 receptor agonists, SK&F 38393 and CY 208-243 reduce sucrose sham-feeding in the rat.

Gastric-fistulated rats were trained to sham-feed a 10% sucrose solution in a 60 min test. The selective dopamine D-1 receptor agonists, SK&F 38393 (3 and 10 mg/kg, s.c.) and CY 208-243 (1 and 3 mg/kg, s.c.) both produced dose-related reductions in sham-feeding. These effects were present in the first 5 min of the test period, and persisted throughout the remainder of the test. The data confirm and extend results for an anorectic effect of SK&F 38393 and demonstrate, for the first time, a similar anorectic effect of CY 208-243.

Effects of tifluadom on food consumption compared with chlordiazepoxide and kappa agonists in the rat.

Tifluadom (0.625-10.0 mg kg-1) was administered to non-deprived male rats which had been accustomed to eating a highly palatable diet in a 30 min test period. This compound, an opioid benzodiazepine, produced a significant increase in consumption of food when administered by the subcutaneous route, but not after intraperitoneal injection. Both chlordiazepoxide (1.25-20.0 mg kg-1) and the selective kappa opiate receptor agonist U-50,488 (0.3125-2.5 mg kg-1) also produced significant hyperphagic effects in the same feeding situation. In contrast, the two kappa opiate receptor agonists, ethylketocyclazocine (0.1-3.0 mg kg-1) and bremazocine (0.078-1.25 mg kg-1) brought about a dose-related suppression of food intake. Hence, the effects of kappa opiate receptor agonists in the feeding situation described here were not uniform. Furthermore, tifluadom could be likened either to a benzodiazepine or to a selective kappa receptor agonist. The hyperphagia induced by tifluadom was antagonized by naloxone, suggesting that the effect was mediated by an action at opiate receptors. It was not antagonized however by Ro15-1788 (10.0 and 20.0 mg kg-1), a selective benzodiazepine receptor antagonist, ruling out possible mediation by benzodiazepine receptors. The benzodiazepine receptor antagonist, CGS 8216, exhibited intrinsic activity when administered alone, and significantly reduced food consumption in tifluadom-treated and control animals.

Phencyclidine and corticosteroids induce apoptosis of a subpopulation of striatal neurons: a neural substrate for psychosis?

Phencyclidine, a non-competitive N-methyl-D-aspartate receptor antagonist and indirect dopamine agonist, has neuroprotective properties. Phencyclidine, however, can also exert toxic effects and causes degeneration of neurons in the retrosplenial cortex. In this paper we demonstrate that acute administration of a high dose of phencyclidine to rats, (80 mg/kg), also causes death of a subpopulation of striatal neurons. The dying cells exhibited many of the morphological and biochemical features of cells undergoing apoptosis as revealed by a silver methenamine stain, propidium iodide fluorescence histochemistry and a TUNEL procedure. The majority of the dying cells tended to be clustered within the dorsomedial aspect of the striatum. The type of striatal cell undergoing apoptosis was determined by stereotaxically injecting a colloidal gold retrograde anatomical tracer into the major areas of striatal termination prior to the administration of phencyclidine. This procedure demonstrated that phencyclidine induced striatal apoptosis is almost exclusively limited to striatopallidal neurons. A similar series of experiments was conducted to determine whether the synthetic corticosteroid, dexamethasone, also induces apoptosis of striatal neurons. Corticosteroids are known to be toxic to hippocampal neurons and interact with striatal dopamine transmission. Acute administration of dexamethasone, (20 mg/kg), induced apoptosis of a subpopulation of striatal cells. As was the case with phencyclidine, most of the dexamethasone-induced apoptotic striatal cells were striatopallidal neurons located within the dorsomedial striatum. The pathology during the early stages of Huntington's disease is restricted to an equivalent subpopulation of striatal neurons. Many Huntington's patients are extremely psychotic during this stage in the progression of the disease. Psychosis is also associated with the acute administration of both phencyclidine and dexamethasone to humans. We accordingly speculate that the selective loss of striatopallidal neurons in the dorsomedial striatum may represent the neural substrate of many forms of psychosis.

Dexamethasone induces limited apoptosis and extensive sublethal damage to specific subregions of the striatum and hippocampus: implications for mood disorders.

It has been shown previously that the synthetic corticosteroid dexamethasone induces apoptosis of granule cells in the dentate gyrus and striatopallidal neurons in the dorsomedial caudate-putamen. We investigated whether or not dexamethasone can induce damage to other neuronal populations. This issue was addressed using OX42 immunohistochemistry to visualise activated microglia and thereby gauge the extent of dexamethasone-induced neuronal death. A single dose of dexamethasone (20mg/kg, i.p.) administered to young male Sprague-Dawley rats induced a strong microglial reaction which was restricted to the striatum, the dentate gyrus and all of the CA subfields of the hippocampus. Some OX42-immunoreactive cells were also seen in the lateral septal nucleus. Subsequent quantitative analysis of silver/methenamine-stained sections confirmed that acute administration of dexamethasone induced apoptosis in the striatum and all regions of the hippocampus at doses as low as 0.7mg/kg. In contrast, dexamethasone failed to induce apoptosis in the lateral septal nucleus at doses up to 20mg/kg. The levels of dexamethasone-induced striatal and hippocampal apoptosis were attenuated by pretreatment with the corticosteroid receptor antagonist RU38486 (Mifepristone), which implies that the cell death was mediated by a corticosteroid receptor-dependent process. We further determined whether dexamethasone induced sublethal damage to neurons by quantifying reductions in the number of microtubule-associated protein-2-immunoreactive striatal and hippocampal cells following injection of the corticosteroid. Dexamethasone induced dramatic decreases in the striatum, with the dorsomedial caudate-putamen being particularly affected. Similar damage was seen in the hippocampus, with the dentate gyrus and CA1 and CA3 subfields being particularly vulnerable.Equivalent corticosteroid-induced neuronal damage may occur in mood disorders, where the levels of endogenous corticosteroids are often raised. Corticosteroid-induced damage of striatal and hippocampal neurons may also account for some of the cognitive deficits seen following administration of the drugs to healthy volunteers.

17 Beta-oestradiol attenuates dexamethasone-induced lethal and sublethal neuronal damage in the striatum and hippocampus.

Abnormal corticosteroid release is extensively associated with mood disorders. This association may result from the toxic actions of endogenous corticosteroids which can induce apoptosis of hippocampal neurons. Similarly, dexamethasone, a synthetic corticosteroid, can induce lethal and sublethal damage to rat hippocampal and striatal neurons and can result in steroid-induced psychoses in humans. The experiments reported here tested the hypothesis that pre-treatment with oestrogen would also attenuate dexamethasone-induced neuronal damage as oestrogens have neuroprotective actions against a variety of insults and falling levels of oestrogen are associated with increased vulnerability to mood disorders. Male Sprague-Dawley rats received three systemic injections which were a combination of vehicle, 17-beta-oestradiol (0.2 mg/kg, s.c.), the oestrogen receptor antagonist tamoxifen (10 mg/kg, s.c.) and dexamethasone (0.7 mg/kg, i.p.) and were killed 24 h after the final injection. Injections of dexamethasone (when preceded by vehicle injections) resulted in elevated levels of apoptosis and sub-lethal damage, as demonstrated by reduced levels of microtubule-associated protein-2-immunopositive neurons, in the striatum and hippocampus. This damage was regional with the dorsomedial caudate putamen and the dentate gyrus and CA1 and CA3 hippocampal sub-fields being particularly affected. Pretreatment with oestrogen substantially attenuated the dexamethasone-induced neuronal damage. This oestrogen-induced neuronal protection was in turn virtually eliminated by giving an initial injection of tamoxifen. These results suggest, therefore, that oestrogens can protect from corticosteroid-induced neuronal damage via an oestrogen receptor-mediated process.

Reversal of the anorectic effect of (+)-fenfluramine in the rat by the selective cholecystokinin receptor antagonist MK-329.

1. Experiments were conducted to determine whether or not the effect of (+)-fenfluramine (3.0 mg kg-1, i.p.) on food intake can be antagonized by the selective cholecystokinin receptor antagonist MK-239 (formerly L364,718; (3S(-)-N-(2,3-dihydro-1-methyl-2-oxo-5-phenyl-1-H-1,4-benzodiazepin++ +-3-yl)-1H- indole-2-carboxamide). Two feeding paradigms were employed. In the first, non-deprived rats were familiarized with eating a highly palatable, sweetened mash in a 30 min test. In the second, freely-feeding rats were trained to consume powdered chow in their home-cages, and their intake was monitored over the first 6 h of the night-period. 2. In doses of 30.0 and 100.0 micrograms kg-1, s.c., MK-329 almost completely blocked the anorectic effect of (+)-fenfluramine in the palatable food intake test. These doses of MK-329 have previously been reported to antagonize the anorectic effect produced by exogenous cholecystokinin-octapeptide (CCK8) in rats. Both doses of MK-329 were also effective in significantly attenuating the anorectic effect of (+)-fenfluramine in nocturnal free-feeding animals over a 6 h-period. 3. MK-329 (10.0-100.0 micrograms kg-1, s.c.) failed to antagonize the anorectic effect of either the specific dopamine D2-receptor agonist quinpirole (0.3 mg kg-1, s.c.) or the beta-carboline FG 7142 (10.0 mg kg-1, i.p.) in the palatable food intake test. 4. MK-329 (10.0-300.Opgkg-1, s.c.) had no effect, when administered alone, on the level of palatable food intake in non-deprived rats, even when substantial satiation was produced by a pre-feeding procedure. Furthermore, MK-329 had no effect, when administered alone, on nocturnal food intake in freelyfeeding rats. 5. In conclusion, not only was MK-329 a potent antagonist of the effect of CCK8 on food intake, it also blocked the effect of (+)-fenfluramine to a significant degree. The effect of MK-329 was selective in that the anorectic effects of either quinpirole or FG 7142 remained unaffected. Administered alone, MK-329 did not affect food intake, indicating that its reversal of (+ -fenfluramine-induced anorexia was not secondary to an intrinsic hyperphagic effect. The results provide some evidence that the depressant effect of (+ )-fenfluramine on food intake depends on the activity of endogenous CCK.

Antagonism of the discriminative stimulus effects of cocaine at two training doses by dopamine D2-like receptor antagonists.

RATIONALE: The relative contributions of different dopamine receptor subtypes to the discriminative stimulus effects of cocaine may be influenced by the training dose of cocaine. Substitution tests with dopamine receptor agonists have suggested that the role of dopamine D2-like receptors is diminished relative to that of D1-like receptors at a training dose of 3 mg/kg cocaine compared with a training dose of 10 mg/kg. OBJECTIVES: To test whether dopamine D2-like receptor antagonists were differentially effective at attenuating cocaine's discriminative stimulus effects at different training doses, and to test for the first time an antagonist that is selective for the dopamine D2 receptor within the D2-like receptor subfamily. METHODS: Rats were trained to press one lever after receiving cocaine and another after receiving saline (maintaining >95% drug-appropriate responding). Three dopamine D2-like receptor antagonists (haloperidol, raclopride and L-741,626) were tested in rats trained at 3 mg/kg or 10 mg/kg cocaine. At the lower training dose, the D1-like receptor antagonist SCH 39166 was also tested. RESULTS: The antagonists were not differentially effective between training groups: they all produced parallel, rightward shifts in cocaine's dose-effect function, indicating surmountable antagonism. CONCLUSIONS: The results demonstrate that D2-like receptor antagonists with different affinities for the various D2-like receptors can antagonise the discriminative stimulus effects of cocaine at two training doses. Importantly, antagonism by L-741,626 implies that stimulation of D2 receptors alone (not D3 or D4 receptors) is sufficient to mediate cocaine's discriminative stimulus effects. Finally, the claim that D1-like receptors are preferentially involved at low training doses of cocaine is only consistent with the current findings if indirect stimulation of D2 receptors by low doses of cocaine remains necessary for the expression of the D1-like receptor-mediated effect.

Benzodiazepine receptor ligands and the consumption of a highly palatable diet in non-deprived male rats.

Non-deprived rats were familiarized with a highly palatable diet until baseline consumption in a 60-min daily access period had stabilised. The benzodiazepine receptor agonist midazolam (1.25-10.0 mg/kg, IP) produced a large, dose-related increase in food consumption during the first 30 min of access. It also produced significant, short-term hyperphagia in animals which had been partially pre-satiated on the diet before drug administration, an effect which was reversible by the benzodiazepine receptor antagonist Ro15-1788. Administered alone, Ro15-1788 (1.25-10.0 mg/kg, IP) had no intrinsic activity in the food consumption test. In contrast, CGS 8216 (2.5-40.0 mg/kg, IP) produced a marked dose-related suppression of food intake. This anorectic effect was shared by two benzodiazepine receptor inverse agonists, FG 7142 and DMCM, which also produced dose-dependent reductions in consumption. The effects on feeding produced by FG 7142 (20 mg/kg, IP) and DMCM (1.25 mg/kg, IP) were reversed by either Ro15-1788 (2.5 and 5.0 mg/kg) or midazolam (5.0 and 10.0 mg/kg). A matched anorectic effect produced by CGS 8216 (40 mg/kg) was not, however, reversed by either Ro15-1788 or midazolam. This suggests that at a high dose CGS 8216 may act by a mechanism different from that of the two inverse agonists. The feeding test described in the report proved sensitive to both hyperphagic and anorectic effects of drugs active at benzodiazepine receptors, pointing to a possible bi-directional control of palatable food consumption.

Selective attenuation of sweetened milk consumption by opiate receptor antagonists in male and female rats of the Roman strains.

Male and female rats of the three Roman strains (Roman High-, Roman Low-, and Roman Control Avoidance; RHA, RLA and RCA, respectively) were familiarized with a highly palatable sweetened milk in a daily 30 min test. The animals were never food- or water-deprived prior to the test. Daily milk intake stabilised at a high level before drug tests were initiated. Effects of naloxone, diprenorphine, WIN 44,441-3, MR2266, MR2267, and ICI 154129 on milk consumption were investigated. Naloxone, diprenorphine and MR2266 each had comparable anorectic effects across strains and sexes. WIN 44,441-3 was relatively ineffective; MR2267 and ICI 154129 were without effect on milk consumption.

The benzodiazepine receptor partial agonist bretazenil and the partial inverse agonist Ro 15-4513: effects on salt preference and aversion in the rat.

The general aim of the present series of experiments was to contrast the effects of the benzodiazepine receptor (BZR) partial agonist bretazenil and those of the partial inverse agonist Ro 15-4513 in two-choice tests between saline (0.9% or 1.8%) and water, using water-deprived rats. Since BZR agonists appear to enhance positive hedonic reactions to taste stimuli selectively, it was hypothesized that bretazenil (and a second BZR partial agonist Ro 17-1812) would selectively enhance intake of a preferred 0.9% salt solution, but not necessarily reduce the relative aversion to a more concentrated 1.8% salt solution, in these choice tests. The results were in general agreement with these hypotheses. Despite an earlier finding that Ro 15-4513 abolished sweet taste preference, there was no evidence here that it reduced the relative preference expressed for 0.9% NaCl solution. Moreover, Ro 15-4513 did not enhance the relative avoidance of the 1.8% NaCl solution. The BZR antagonist, flumazenil, had no effect on either salt preference or aversion. These results indicate that the type of taste stimulus (sweet or salt), the type of behavioural response (preference or aversion) and the type of BZR ligand (agonist, antagonist or inverse agonist) interact to determine the observed behavioural consequences in choice tests.

Pharmacological mechanisms mediating phencyclidine-induced apoptosis of striatopallidal neurons: the roles of glutamate, dopamine, acetylcholine and corticosteroids.

Phencyclidine (PCP) has recently been shown to induce apoptosis of a subpopulation of striatopallidal neurons which lie in the dorsomedial caudate-putamen. The pharmacological mechanisms underlying this PCP-induced striatal death were investigated in a series of small experiments. Striatal silver-methenamine-stained sections from rats injected acutely with dizocilpine (MK-801; 1.5-5 mg/kg, i.p.) were analysed to determine whether other non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists could induce apoptotic-like changes in striatal cells. The effects of amphetamine (3-12 mg/kg, i.p.) were similarly investigated as PCP can elevate extracellular dopamine levels and dopamine has the potential to be neurotoxic. The potential involvement of dopamine transmission in PCP-induced striatal apoptosis was also tested by determining the effect of co-administering SCH23390 (D1 dopamine receptor antagonist) and quinpirole (D2 dopamine receptor agonist) on PCP (80 mg/kg, s.c.)-induced striatal apoptotic-like cell death. Equivalent experiments were performed using scopolamine (cholinergic antagonist) as this drug blocks PCP-induced damage of the retrosplenial cortex and RU38486 (corticosteroid receptor antagonist) as a similar subpopulation of striatal neurons undergoes apoptosis following dexamethasone administration. Injection of neither MK-801 nor amphetamine induced elevations of apoptotic-like cells in the striatum nor did co-administration of SCH23390 or scopolamine affect the levels of PCP-induced striatal cell death. In contrast, quinpirole elevated the levels of PCP-induced apoptotic-like striatal cell death and RU38486 markedly reduced it. Within the retrosplenial cortex, scopolamine lowered PCP-induced apoptotic-like cell death whereas RU38486 was without effect. These results suggest that PCP-induced striatal apoptosis results from a corticosteroid-dependent mechanism. The results further demonstrate that different pathological mechanisms underlie PCP-induced neuronal damage in the striatum and the retrosplenial cortex.

Effects of dl-fenfluramine and xylamidine on gastric emptying of maintenance diet in freely feeding rats.

Freely feeding rats received an anorexigenic dose of dl-fenfluramine HCl (5 mg/kg). Two hours following injection, their stomachs retained significantly greater dry weight contents than saline-injected controls. The same dose of fenfluramine decreased the rate of gastric emptying over a 2 h period to a similar extent in mildly food-deprived rats. The peripherally acting serotonin antagonist xylamidine counteracted the effect of fenfluramine in prolonging the satiating effect of an ad libitum meal of a given size. We propose therefore that the principal mechanism by which fenfluramine reduces food consumption in freely feeding rats is through a prolongation of the satiating effect of absorption as a result of slowing of gastric emptying, presumably via enhanced release of serotonin from nerve terminals in the wall of the gastrointestinal tract.

SCH 23390-induced hypophagia is blocked by the selective CCK-A receptor antagonist devazepide, but not by the CCK-B/gastrin receptor antagonist L-365,260.

The selective dopamine D-1 receptor antagonist SCH 23390 (30 micrograms/kg, SC) significantly reduced palatable food consumption by nondeprived rats in a 30-min test period. Prior administration of the selective CCK-A receptor antagonist devazepide (MK 329; L-364,718) blocked the hypophagic effect of SCH 23390. In contrast, prior administration of the selective CCK-B/gastrin receptor antagonist L-365,260 had no effect. Devazepide did not antagonize a matched hypophagic effect produced by the dopamine D-2 receptor antagonist raclopride (0.1 mg/kg, SC). These data direct attention to possible dopamine-cholecystokinin interactions in relation to the control of ingestional responses, and, more specifically, indicate possible functional relationships between D-1 and CCK-A receptor mechanisms.

Studies on paracetamol-induced lipid peroxidation.

Post-mitochondrial supernatants isolated from livers of rats given a single large oral dose of paracetamol (800 mg/kg) showed rapid rates of lipid peroxidation when incubated in vitro. As a result of paracetamol administration the level of reduced glutathione (GSH) declined to approx. 20-25% of the peak physiological value. Addition of reduced GSH to the supernatant inhibited the peroxidation. Paracetamol-induced lipid peroxidation was inhibited in vitro by antioxidants (e.g. vitamin E) but was unaffected by superoxide dismutase and mannitol. N-acetyl cysteine and cysteamine inhibited lipid peroxidation in vitro in a cytosol-dependent manner in the absence of glutathione. Lipid peroxidation probably occurs simultaneously with the proposed covalent binding of the active metabolite of paracetamol. Since the former process is known to cause severe and extensive membrane damage, it may be a very important factor in paracetamol-induced liver necrosis.

Yawning induced by the selective dopamine D2 agonist N-0437 is blocked by the selective dopamine autoreceptor antagonist (+)-UH 232.

Yawning and stretching responses were elicited in rats by a small dose (0.3 mg/kg) of the highly selective dopamine D2 agonist, N-0437. The responses were blocked by the highly selective dopamine autoreceptor antagonist, (+)-UH 232 (3.0 mg/kg), but not by raclopride at a dose which selectively blocks postsynaptic D2 receptors. The results strongly confirm the view that yawning and stretching are behavioral responses elicited by stimulation of presynaptic D2 receptors.