Reintroducing a keystone bioturbator can facilitate microbial bioremediation in urban polluted sediments.

Anthropogenic environmental stressors have significantly reduced biodiversity and the capacity of remnant natural habitats to deliver ecosystem functions and services in urban areas. To mitigate these impacts and recover biodiversity and function, ecological restoration strategies are needed. While habitat restoration is proliferating in rural and peri-urban areas, strategies purposely designed to succeed under the environmental, social and political pressures of urban areas are lacking. Here, we propose that ecosystem health in marine urban areas can be improved by restoring biodiversity to the most dominant habitat, unvegetated sediments. We reintroduced a native ecosystem engineer, the sediment bioturbating worm Diopatra aciculata, and assessed their effects on microbial biodiversity and function. Results showed that worms can affect the diversity of microbes, but effects varied between locations. Worms caused shifts in microbial community composition and function at all locations. Specifically, the abundance of microbes capable of chlorophyll production (i.e. benthic microalgae) increased and the abundance of microbes capable of methane production decreased. Moreover, worms increased the abundances of microbes capable of denitrification in the site with lowest sediment oxygenation. Worms also affected microbes capable of degrading the polycyclic aromatic hydrocarbon toluene, although the direction of that effect was site-specific. This study provides evidence that a simple intervention such as the reintroduction of a single species can enhance sediment functions important for the amelioration of contamination and eutrophication, although further studies are needed to understand the variation in outcomes between sites. Nevertheless, restoration strategies targeting unvegetated sediments provide an opportunity to combat anthropogenic stressors in urban ecosystems and may be used for precondition before more traditional forms of habitat restoration such as seagrass, mangrove and shellfish restoration.

Validity and reliability of the Moxy oxygen monitor during incremental cycling exercise.

INTRODUCTION: The Moxy is a novel, cutaneously placed muscle oxygen monitor which claims to measure local oxygen saturation (SmO2) and total haemoglobin (THb) using near-infrared spectroscopy. If shown to be reliable, its data storage and telemetric capability will be useful for assessing localised O2 usage during field-based exercise. This study investigated the reliability of the Moxy during cycling and assessed the correlations between its measurements, whole-body O2 consumption (VO2) and heart rate (HR). METHODS: Ten highly trained cyclists performed an incremental, step-wise cycling protocol on two occasions while wearing the Moxy. SmO2, THb, VO2 and HR were recorded in the final minute of each five-minute stage. Data were analysed using Spearman's Order-Rank Coefficient (SROC), Intraclass Correlation (ICC), and Coefficient of Variance (COV). Significance was set at p ≤ .05. RESULTS: SmO2 showed a 'strong' or 'very large' correlation between trials (SROC: r = 0.842-0.993, ICC: r = 0.773-0.992, p ≤ .01) and was moderately correlated with VO2 and HR (r = -0.71-0.73, p ≤ .01). SmO2 showed a moderate to high reliability at low intensities, but this decreased as relative exercise intensity increased. THb showed poor correlations between tests and with the other measured variables, but was highly reliable at all power outputs. CONCLUSIONS: The Moxy is a reliable device to measure SmO2 at low to moderate intensities, but at higher intensities, greater variation in measurements occurs, likely due to tissue ischaemia or increased movement artefacts due to more frequent muscular contractions. THb has low variation during exercise, and does not appear to be a valid indicator of muscle oxygenation.

Differential proteomic responses of selectively bred and wild-type Sydney rock oyster populations exposed to elevated CO2.

Previous work suggests that larvae from Sydney rock oysters that have been selectively bred for fast growth and disease resistance are more resilient to the impacts of ocean acidification than nonselected, wild-type oysters. In this study, we used proteomics to investigate the molecular differences between oyster populations in adult Sydney rock oysters and to identify whether these form the basis for observations seen in larvae. Adult oysters from a selective breeding line (B2) and nonselected wild types (WT) were exposed for 4 weeks to elevated pCO2 (856 µatm) before their proteomes were compared to those of oysters held under ambient conditions (375 µatm pCO2 ). Exposure to elevated pCO2 resulted in substantial changes in the proteomes of oysters from both the selectively bred and wild-type populations. When biological functions were assigned, these differential proteins fell into five broad, potentially interrelated categories of subcellular functions, in both oyster populations. These functional categories were energy production, cellular stress responses, the cytoskeleton, protein synthesis and cell signalling. In the wild-type population, proteins were predominantly upregulated. However, unexpectedly, these cellular systems were downregulated in the selectively bred oyster population, indicating cellular dysfunction. We argue that this reflects a trade-off, whereby an adaptive capacity for enhanced mitochondrial energy production in the selectively bred population may help to protect larvae from the effects of elevated CO2 , whilst being deleterious to adult oysters.

Estrogen mediated effects in the Sydney rock oyster, Saccostrea glomerata, following field exposures to sewage effluent containing estrogenic compounds and activity.

The Sydney rock oyster, Saccostrea glomerata, has been demonstrated as a useful biomonitor of estrogenic compounds following laboratory exposures, yet its utility in the assessment of estrogenic exposure and effects under field conditions requires investigation. To achieve this aim, S. glomerata were deployed in Newcastle, Australia in the effluent receiving marine waters of Burwood Beach WWTP (Burwood Beach "near", <50 m from outfall and Burwood Beach "far", 100-150 m from outfall) and reference locations (Redhead, Fingal Island 1 and Fingal Island 2) at depths of 4, 8 and 12 m for six weeks. Effluent receiving waters of Burwood Beach WWTP were found to be a suitable impact location, demonstrated via measurement of estrogenic compounds and activity throughout the deployment. Estrogenic compounds were detected (average of combined solids and liquid fractions) at average concentrations of: 1.42 ng/L for estrone, 0.69 ng/L for 17ß estradiol, 3.83 ng/L for estriol (E3), 0.56 ng/L for 17α-ethynylestradiol, 64.2 ng/L for bisphenol A, 7.51 ng/L for 4-nonylphenol and 5.93 ng/L for 4-tert-octylphenol. Total estrogenic activity was estimated at 4.48 ng/L EEQ via the Yeast Estrogen Screen (YES(®)) assay (average of combined solid and liquid fractions). Female vitellogenin gene expression was highest at Burwood Beach locations, yet no significant differences were detected among locations for either sex. Vitellogenin protein was significantly higher (p<0.05) in S. glomerata at Burwood Beach Near compared to reference locations for the 4 and 12 m depths. Increased proportions of females were found at Burwood Beach Near, at 4m depth (p<0.05). Both Burwood Beach locations had higher proportions of mature female gonadal development stages compared to reference locations (p<0.05). Oocyte area was highest at both Burwood Beach locations, but no significant differences were detected among locations. Findings provided further evidence that female S. glomerata may be a suitable candidate species for assessment of effects of estrogenic compounds in Australian waters.

Exposure to 17α-ethynylestradiol causes dose and temporally dependent changes in intersex, females and vitellogenin production in the Sydney rock oyster.

Although mounting evidence suggests exposure to estrogenic contaminants increases vitellogenin production in molluscs, demonstration of dose-response relationships and knowledge of the temporal nature of the vitellogenin response with continual exposure is currently lacking for biomarker utility. To address this knowledge gap, adult Sydney rock oysters, Saccostrea glomerata, were exposed to a range of environmentally relevant concentrations of 17α-ethynylestradiol (EE2) (0, 6.25, 12.5, 25 or 50 ng/l) in seawater under laboratory conditions. Vitellogenin induction and gonadal development was assessed following 4, 21 and 49 days exposure to EE2. Vitellogenin was found to increase in a dose dependent manner with EE2 exposure for females (4 and 49 days) and males (4 and 21 days). Histological examination of gonads revealed a number of individuals exhibited intersex (ovotestis) in 50 ng/l EE2 (after 21 days) and in 6.25 and 12.5 ng/l EE2 (after 49 days). Furthermore, a significant shift towards females was observed following 49 days exposure at 50 ng/l EE2 suggesting estrogenic exposure is capable of facilitating a progression for protandric males from male-intersex-female gametal status. Increases in female vitellogenin (4 days) were predictive of later increases in female developmental stages at 21 days and increases in oocyte area following 49 days. Male vitellogenin (4 days) was predictive of decreased male percentages and lower male developmental stages at 49 days. Vitellogenin in S. glomerata is a predictive biomarker of estrogenic exposure and effect if sampled soon after exposure and at the commencement of a gonadal development cycle.

Protein markers of Marteilia sydneyi infection in Sydney rock oysters, Saccostrea glomerata.

Marteilia sydneyi is the causative agent of QX disease in Sydney rock oyster, Saccostrea glomerata. It is responsible for disease outbreaks among oysters that occur during summer and can result in up to 95% mortality. QX disease has significantly decreased S. glomerata production in some areas of Australia's eastern seaboard over the past 30 years. Marteilia sydneyi sporulates in the digestive gland of oysters leading to complete disorganization of the infected tissues. The current study used proteomics to identify potential molecular markers of sporulating M. sydneyi infection during a field trial undertaken in the Georges River, Sydney, between December 2006 and May 2007. Early stages of M. sydneyi infection were detected by polymerase chain reaction, whilst cytological examination was used to identify sporulating M. sydneyi in the gut. Protein expression in oyster haemolymph was assessed during the M. sydneyi infection period by two dimensional electrophoresis. Proteome maps identified significant differences in the expression of four proteins in oysters with sporulating M. sydneyi infections.

Bayesian estimation of synaptic physiology from the spectral responses of neural masses.

We describe a Bayesian inference scheme for quantifying the active physiology of neuronal ensembles using local field recordings of synaptic potentials. This entails the inversion of a generative neural mass model of steady-state spectral activity. The inversion uses Expectation Maximization (EM) to furnish the posterior probability of key synaptic parameters and the marginal likelihood of the model itself. The neural mass model embeds prior knowledge pertaining to both the anatomical [synaptic] circuitry and plausible trajectories of neuronal dynamics. This model comprises a population of excitatory pyramidal cells, under local interneuron inhibition and driving excitation from layer IV stellate cells. Under quasi-stationary assumptions, the model can predict the spectral profile of local field potentials (LFP). This means model parameters can be optimised given real electrophysiological observations. The validity of inferences about synaptic parameters is demonstrated using simulated data and experimental recordings from the medial prefrontal cortex of control and isolation-reared Wistar rats. Specifically, we examined the maximum a posteriori estimates of parameters describing synaptic function in the two groups and tested predictions derived from concomitant microdialysis measures. The modelling of the LFP recordings revealed (i) a sensitization of post-synaptic excitatory responses, particularly marked in pyramidal cells, in the medial prefrontal cortex of socially isolated rats and (ii) increased neuronal adaptation. These inferences were consistent with predictions derived from experimental microdialysis measures of extracellular glutamate levels.

Effects of 4-nonylphenol and 17alpha-ethynylestradiol exposure in the Sydney rock oyster, Saccostrea glomerata: Vitellogenin induction and gonadal development.

Adult Saccostrea glomerata were exposed to environmentally relevant concentrations of 4-nonylphenol (1microg/L and 100microg/L) and 17alpha-ethynylestradiol (5ng/L and 50ng/L) in seawater over 8 weeks. Exposures were performed to assess effects on vitellogenin induction and gonadal development during reproductive conditioning. Chronic direct estrogenicity within gonadal tissue was assessed via an estrogen receptor-mediated, chemical-activated luciferase reporter gene-expression assay (ER-CALUX). Estradiol equivalents (EEQ) were greatest in the 100microg/L 4-nonylphenol exposure (28.7+/-2.3ng/g tissue EEQ) while 17alpha-ethynylestradiol at concentrations of 50ng/L were 2.2+/-1.5ng/g tissue EEQ. Results suggest 4-nonylphenol may be accumulated in tissue and is partly resistant to biotransformation; maintaining its potential for chronic estrogenic action, while 17alpha-ethynylestradiol, although exhibiting greater estrogenic potency on biological endpoints possibly exerts its estrogenic action before being rapidly metabolised and/or excreted. A novel methodology was developed to assess vitellogenin using high-performance liquid chromatography (HPLC). Exposure to both 17alpha-ethynylestradiol (50ng/L) and 4-nonylphenol (100microg/L) produced increases in vitellogenin for females, whereas males exhibited increases in vitellogenin when exposed to 50ng/L 17alpha-ethynylestradiol only. Females exhibited greater vitellogenin responses than males at 50ng/L 17alpha-ethynylestradiol only. Histological examination of gonads revealed a number of individuals exhibiting intersex (ovotestis) in 50ng/L 17alpha-ethynylestradiol exposures. Male individuals in 1microg/L and 100microg/L 4-nonylphenol exposures and 5ng/L 17alpha-ethynylestradiol were at earlier stages of spermatogenic development than corresponding controls.

The Akoya pearl oyster shell as an archival monitor of lead exposure.

The Akoya pearl oyster (Pinctada imbricata) was experimentally exposed to (a) constant levels of lead (Pb) at 180 microg L(-1) for nine weeks, or (b) two short term (pulse) exposures of Pb at 180 microg L(-1) (three weeks each) with an intervening depuration period (three weeks), to assess its utility as an (i) accumulative monitor of Pb contamination and an (ii) archival monitor for discriminating constant versus pulsed Pb exposure events. P. imbricata showed similar reductions in growth (based on shell morphology and wet weight) and Pb accumulation patterns for whole tissue and shell in response to both Pb exposure regimes. Thus the whole oyster was deemed an inappropriate accumulative monitor for assessing short-term temporal variation of Pb exposure and effect. However, using secondary ion mass spectrometry, Pb was shown to accumulate in the successively deposited nacreous layers of the shell of P. imbricata, documenting the exposure history of constant versus pulsed Pb events. Patterns of Pb deposition not only reflected the frequency of Pb exposure events but also their relative durations. Thus, the shell of P. imbricata may be employed as a suitable biological archive of Pb exposure.

Quantification of in situ nutrient and heavy metal remediation by a small pearl oyster (Pinctada imbricata) farm at Port Stephens, Australia.

The use of pearl oysters has recently been proposed as an environmental remediation tool in coastal ecosystems. This study quantified the nitrogen, phosphorus and heavy metal content of the tissue and shell of pearl oysters harvested from a small pearl oyster farm at Port Stephens, Australia. Each tonne of pearl oyster material harvested resulted in approximately 703 g metals, 7452 g nitrogen, and 545 g phosphorus being removed from the waters of Port Stephens. Increasing current farm production of 9.8 tyr(-1) to 499 tyr(-1) would balance current nitrogen loads entering Port Stephens from a small Sewage Treatment Plant (STP) located on its southern shores. Furthermore, manipulation of harvest dates to coincide with oyster condition would likely remove substantially greater quantities of nutrients. This study demonstrates that pearl aquaculture may be used to assist in the removal of pollutants from coastal waters while producing a commercially profitable commodity.

Evidence for a selective prefrontal cortical GABA(B) receptor-mediated inhibition of glutamate release in the ventral tegmental area: a dual probe microdialysis study in the awake rat.

Glutamate-containing pyramidal neurons in the medial prefrontal cortex (mPfc) project to the ventral tegmental area (VTA) where they synapse on mesocorticolimbic dopamine containing cell bodies and GABA interneurons. In the present study we employed dual probe microdialysis in intact conscious rat brain to investigate the effects of intra-mPfc perfusion with a depolarising concentration of potassium chloride (KCl) (100 mM, 20 min) alone and in the presence of local GABA(A) and GABA(B) receptor blockade on VTA glutamate release. Intra-mPfc KCl transiently increased VTA glutamate release (+71.48+/-14.29%, 20 min). Intra-mPfc perfusion with a concentration of the GABA(A) receptor antagonist bicuculline (10 microM, 120 min) did not influence the intra-mPfc KCl-induced increase in VTA glutamate release (+102.35+/-33.61%, 20 min). In contrast, intra-mPfc perfusion with a concentration of the GABA(B) receptor antagonist CGP35348 (100 microM, 120 min) which when given alone did not influence basal glutamate levels in the VTA was associated with an enhanced KCl-induced stimulation of VTA glutamate release (+375.19+/-89.69%, 40 min). Furthermore, this enhancement was reversed in the presence of the selective GABA(B) receptor agonist baclofen (10 microM, 120 min). The present findings suggest a key role for the prefrontal cortex in the regulation of glutamate release in the VTA. Furthermore, we demonstrate a selective cortical GABA(B) receptor-mediated inhibition of glutamate transmission in the VTA. These findings may be important in the context of abnormalities in amino acid neurotransmission at the network level in schizophrenia.

Evidence for a differential medial prefrontal dopamine D1 and D2 receptor regulation of local and ventral tegmental glutamate and GABA release: a dual probe microdialysis study in the awake rat.

The effects of perfusion with two selective dopamine receptor agonists SKF38393 and pergolide into the medial prefrontal cortex (mPfc) on local and ventral tegmental area (VTA) glutamate and gamma-aminobutyric acid (GABA) release were investigated using dual probe microdialysis in the awake rat. Intracortical SKF38393 (10, 100, 500 microM, 60 min) decreased glutamate and increased GABA release in the mPfc but had no effect on either amino acid neurotransmitter in the VTA. Intracortical perfusion with the selective GABA(A) receptor antagonist bicuculline (0.1 microM, 140 min) reversed the SKF38393 (100 microM, 60 min)-induced decrease in local glutamate release, while the selective GABA(B) receptor antagonist CGP35348 (100 microM, 140 min) was without effect. Intracortical pergolide (1 microM, 60 min) was associated with a prolonged reversible decrease in local and VTA glutamate release that was also associated with a decrease in VTA GABA release, which was reversed in the presence of intracortical raclopride (10 microM, 140 min). Taken together, the present findings indicate a differential regulation of glutamate and GABA release in the mPfc and VTA by dopamine D(1) and D(2) receptors in the mPfc whereby (a) activation of the dopamine D(1) receptor in the mPfc decreases local glutamate release possibly via a feed-forward activation of the local GABA interneurons; (b) activation of the dopamine D(2) receptor in the mPfc inhibits both local glutamate release and the excitatory glutamate drive on the VTA.

Pearl aquaculture-profitable environmental remediation?

Bivalve molluscs are filter feeders, with pearl oysters able to filter water at rates up to 25 lh(-1)g(-1) of dry wt. tissue. Since this process leads to rapid bioaccumulation of recalcitrant pollutants such as heavy metals, organochlorine pesticides and hydrocarbons from impacted sites, it has prompted the widespread use of molluscs as biomonitors to quantify levels of marine pollution. This paper proposes pearl oyster deployment as a novel bioremediation technology for impacted sites to remove toxic contaminants, reduce nutrient loads and lower concentrations of microbial pathogens. Estimates extrapolated from the literature suggest that a modest pearl oyster farm of 100 t oyster material per year could remove 300 kg heavy metals plus 24 kg of organic contaminants via deposition into the tissue and shell. Furthermore, it was estimated that up to 19 kg of nitrogen may be removed from the coastal ecosystem per tonne of pearl oyster harvested. Pearl oysters are also likely to filter substantial amounts of sewage associated microbial pathogens from the water column. Method of cultivation and site selection are the key to minimising negative environmental impacts of bivalve cultivation. Deployment of oysters at sites with high nutrient and contaminant loadings would be advantageous, as these compounds would be removed from the ecosystem whilst generating a value-added product. Future potential may exist for harvesting bio-concentrated elements for commercial production.

Hippocampal microdialysis during spontaneous intraoperative epileptiform activity.

BACKGROUND: The actual mechanisms underlying human hippocampal epileptogenicity, a process ultimately mediated by neurochemical events, remains to be fully elucidated. We submit early insight data regarding microdialysis (MD) recovery of the neuroactive amino acids glutamate, aspartate and gamma-aminobutyric acid (GABA) from the intraoperative and intact, spontaneously epileptiform human hippocampus. METHOD: Generally anaesthetised temporal lobe epilepsy (TLE) patients (N=7) undergoing therapeutic and anatomically standardised resective surgery were also subjected to ipsilateral anterior hippocampal MD with concomitant hippocampal electrocorticography (ECoG). Recovered 10-min dialysate samples were quantified for glutamate, aspartate and GABA using high-performance liquid chromatography; corresponding ECoG data was assessed for epileptiform activity (EA); mesial resection tissue was postoperatively examined and graded for hippocampal sclerosis. FINDINGS: Mean 'Sample 3' dialysate absolute recovery of glutamate, aspartate and GABA from hippocampi with minimal EA (N=5) was ( micro M+/-SEM): 6.406+/-2.143, 0.600+/-0.215, and 0.357+/-0.093, respectively. In contrast, 'Sample 3' dialysate absolute glutamate, aspartate and GABA levels ( micro M) from the hippocampi of two patients with vigorous EA were: 101.099 and 211.861, 21.860 and 14.482, and 4.241 and 4.817, respectively. Mesial resection tissue in all cases demonstrated hippocampal sclerosis, though the histopathological degree of sclerosis varied between patients. INTERPRETATION: These preliminary intraoperative findings suggest that dialysate glutamate, aspartate, and GABA levels from the sclerotic anterior hippocampus likely reflects the functional status of the sampled tissue - i.e., lower levels of these neuroactive amino acids are to be expected during quiescent or minimal EA versus considerably higher levels corresponding to vigorous EA.

Schizophrenia: a review of neuropharmacology.

BACKGROUND: The last few decades have seen significant advances in our understanding of the neurochemical basis of schizophrenia. AIMS: To describe the neurotransmitter systems and nerve circuits implicated in schizophrenia; to compare the neuropharmacology of typical and atypical anti-psychotic agents; and to describe recent developments in the pharmacological treatment of schizophrenia. METHODS: Relevant pharmacological, neurophysiological and psychiatric literature was examined and reviewed. RESULTS: Schizophrenia is associated with abnormalities of multiple neurotransmitter systems, including dopamine, serotonin, gamma-aminobutyric acid and glutamate. Typical and atypical antipsychotic agents differ in their receptor-binding affinities, which are related to their differing side-effect profiles. Novel therapeutic strategies include normalisation of synaptic dopamine or serotonin levels, serotonin receptor antagonism and modulation of cerebral protein synthesis. CONCLUSIONS: The ideal treatment for schizophrenia may not be a single pharmacological agent but several agents that match the different expressions of the illness, in combination with psycho-social interventions.

Elevated extracellular levels of glutamate, aspartate and gamma-aminobutyric acid within the intraoperative, spontaneously epileptiform human hippocampus.

We report preliminary results from four patients subjected to hippocampal electrocorticography and microdialysis during temporal lobe epilepsy surgery. In two cases, spontaneously vigorous hippocampal epileptiform activity (EA) was identified; basal dialysate levels for hippocampal glutamate, aspartate, and gamma-aminobutyric acid ranged from approximately 23- to 84-fold, 19- to 33-fold and 10- to 34-fold higher, respectively, compared to the two cases of minimal hippocampal EA. These findings represent the first intraoperative evidence of elevated extracellular levels of neuroactive amino acids within the spontaneously epileptiform human hippocampus.

Evidence for dysfunction of the nigrostriatal pathway in the R6/1 line of transgenic Huntington's disease mice.

The present multidisciplinary study examined nigrostriatal dopamine and striatal amino acid transmission in the R6/1 line of transgenic Huntington's disease (HD) mice expressing exon 1 of the HD gene with 115 CAG repeats. Although the number of tyrosine hydroxylase-positive neurons was not reduced and nigrostriatal connectivity remained intact in 16-week-old R6/1 mice, the size of tyrosine hydroxylase-positive neurons in the substantia nigra was reduced by 15%, and approximately 30% of these cells exhibited aggregated huntingtin. In addition, using in vivo microdialysis, we found that basal extracellular striatal dopamine levels were reduced by 70% in R6/1 mice compared to their wild-type littermates. Intrastriatal perfusion with malonate in R6/1 mice resulted in a short-lasting, attenuated increase in local dopamine release compared to wild-type mice. Furthermore, the size of the malonate-induced striatal lesion was 80% smaller in these animals. Taken together, these findings suggest that a functional deficit in nigrostriatal dopamine transmission may contribute to the behavioral phenotype and the resistance to malonate-induced neurotoxicity characteristic of R6/1 HD mice.

A comparison of situational and dispositional predictors of perceptions of organizational politics.

The present study is an investigation of situational and dispositional characteristics that may predispose an employee to perceive his or her organization as political. Participants were 501 regular members, civilian members, and public servants of the Royal Canadian Mounted Police. Measures used for this research were the Formalization Scale (G. R. Oldham & J. R. Hackman, 1981), the Job Autonomy Scale (H. P. Sims, A. D. Szilagyi, & R. T. Keller, 1976), the Mach IV (A. Zook & G. J. Sipps, 1986), the Dominance subscale from the Manifest Needs Questionnaire (R. M. Steers & D. N. Braunstein, 1976), the Survey of Organizational Climate (J. C. Taylor & D. G. Bowers, 1972), the Perceptions of Organizational Politics Scale (G. R. Ferris & K. M. Kacmar, 1992), and the Work Locus of Control Scale (P. E. Spector, 1988). Results indicated that organizational climate, formalization, work locus of control (both internal and external measures), and Machiavellianism were significant predictors, accounting for 52% of the variance in participants' perceptions of organizational politics. Limitations of the present study and directions for future research are outlined.

Cannabinoid receptor agonist WIN 55,212-2 inhibits rat cortical dialysate gamma-aminobutyric acid levels.

The effects of the cannabinoid receptor agonist WIN 55,212-2 (0.1-5 mg/kg i.p.) on endogenous extracellular gamma-aminobutyric acid (GABA) levels in the cerebral cortex of the awake rat was investigated by using microdialysis. WIN 55,212-2 (1 and 5 mg/kg i.p.) was associated with a concentration-dependent decrease in dialysate GABA levels (-16% +/- 4% and -26% +/- 4% of basal values, respectively). The WIN 55,212-2 (5 mg/kg i.p.) induced-inhibition was counteracted by a dose (0.1 mg/kg i.p.) of the CB(1) receptor antagonist SR141716A, which by itself was without effect on cortical GABA levels. These findings suggest that cannabinoids decrease cortical GABA levels in vivo, an action that might underlie some of the cognitive and behavioral effects of acute exposure to marijuana.

gamma-Hydroxybutyrate modulation of glutamate levels in the hippocampus: an in vivo and in vitro study.

The effect of gamma-hydroxybutyric acid on extracellular glutamate levels in the hippocampus was studied by microdialysis in freely moving rats and in isolated hippocampal synaptosomes. Intra-hippocampal (CA1) perfusion with gamma-hydroxybutyric acid (10 nM-1 mM) concentration-dependently influenced glutamate levels: gamma-hydroxybutyric acid (100 and 500 nM) increased glutamate levels; 100 and 300 microM concentrations were ineffective; whereas the highest 1 mM concentration reduced local glutamate levels. The stimulant effect of gamma-hydroxybutyric acid (100 nM) was suppressed by the locally co-perfused gamma-hydroxybutyric acid receptor antagonist NCS-382 (10 microM) but not by the GABA(B) receptor antagonist CGP-35348 (500 microM). Furthermore, the gamma-hydroxybutyric acid (1 mM)-induced reduction in CA1 glutamate levels was counteracted by NCS-382 (10 microM), and it was also reversed into an increase by CGP-35348. Given alone, neither NCS-382 nor CGP-35348 modified glutamate levels. In hippocampal synaptosomes, gamma-hydroxybutyric acid (50 and 100 nM) enhanced both the spontaneous and K(+)-evoked glutamate efflux, respectively, both effects being counteracted by NCS-382 (100 nM), but not by CGP-35348 (100 microM). These findings indicate that gamma-hydroxybutyric acid exerts a concentration-dependent regulation of hippocampal glutamate transmission via two opposing mechanisms, whereby a direct gamma-hydroxybutyric acid receptor mediated facilitation is observed at nanomolar gamma-hydroxybutyric acid concentrations, and an indirect GABA(B) receptor mediated inhibition predominates at millimolar concentrations.