The Hydraulic Evolution of Groundwater-Fed Pit Lakes After Mine Closure.

Open pit mining frequently requires regional water tables to be lowered to access ore deposits. When mines close, dewatering ceases allowing the water table to recover. In arid and semi-arid mining regions, the developing pit lakes are predominantly fed by groundwater during this recovery phase and pit lakes develop first into "terminal sinks" for the surrounding groundwater system. With time, the re-establishment of regional hydraulic gradients can cause pit lakes to develop into throughflow systems, in which pit lake water outflows into adjacent aquifers. In this study, we use numerical groundwater modeling to aid process understanding of how regional hydraulic gradients, aquifer properties, net evaporation rates, and pit geometry determine the hydraulic evolution of groundwater-fed pit lakes. We find that before the recovery of the regional water table to its new equilibrium, pit lakes frequently transition to throughflow systems. Throughflow from pit lakes to downstream aquifers can develop within two decades following cessation of dewatering even under low hydraulic gradients (e.g., 5 × 10-4) or high net evaporation rates (e.g., 2.5 m/year). Pit lakes remain terminal sinks only under suitable combinations of high evaporation rates, low hydraulic gradients, and low hydraulic conductivities. In addition, we develop an approximate analytical solution for a rapid assessment of the hydraulic status of pit lakes under steady-state conditions. Understanding whether pit lakes remain terminal sinks or transition into throughflow systems largely determines the long-term water quality of pit lakes and downstream aquifers. This knowledge is fundamental for mine closure and planning post-mining land use.

Modelling mercury sorption of a polysulfide coating made from sulfur and limonene.

A polymer made from sulfur and limonene was used to coat silica gel and then evaluated as a mercury sorbent. A kinetic model of mercury uptake was established for a range of pH values and concentrations of sodium chloride. Mercury uptake was generally rapid from pH = 3 to pH = 11. At neutral pH, the sorbent (500 mg with a 10 : 1 ratio of silica to polymer) could remove 90% of mercury within one minute from a 100 mL solution containing 5 ppm HgCl2 and 99% over 5 minutes. It was found that sodium chloride, at concentrations comparable to seawater, dramatically reduced mercury uptake rates and capacity. It was also found that the spent sorbent was stable in acidic and neutral media, but degraded at pH 11 which led to mercury leaching. These results help define the conditions under which the sorbent could be used, which is an important advance for using this material in remediation processes.

Facilitating Open Pit Mine Closure with Managed Aquifer Recharge.

Dewatering of open pit mines can lower the regional water table for distances of several kilometers from the pit. When the mine is closed, dewatering operations usually cease, and the water table near the pit begins to rise. If the pit is backfilled, the water table will eventually recover, but this recovery may take several hundred years. However, if the extracted water is re-injected into the subsurface, then this may accelerate recovery of the water table. We show that there is an optimal distance for re-injection, which is sufficiently far from the mine to minimize the amount of groundwater that flows back to the pit during mine operations (and hence necessitate additional pumping) but is still close enough to speed up the water table recovery post-mine closure. The optimal injection distance increases with the aquifer hydraulic diffusivity and the mine life (duration of dewatering and injection), and typically ranges between about two and nine times the radius of the mine pit. Where the mine pit is not backfilled, the relative reduction in drawdown due to injecting all the pumped water at the optimal distance is between approximately 10% and 50% after a recovery time equal to the mining period, increasing to 30% to 90% after a recovery time five times the mining period. The relative drawdown reduction due to managed aquifer recharge will be even greater for a pit which is backfilled when mining ceases.

The Effect of Undetected Barriers on Groundwater Drawdown and Recovery.

In large-scale pumping projects, such as mine dewatering, predictions are often made about the rate of groundwater level recovery after pumping has ceased. However, these predictions may be impacted by geological uncertainty-including the presence of undetected impermeable barriers. During pumping, an impermeable barrier may be undetected if it is located beyond the maximum extent of the cone of depression; yet it may still control drawdown during the recovery phase. This has implications for regional-scale modeling and monitoring of groundwater level recovery. In this article, non-dimensional solutions are developed to show the conditions under which a barrier may be undetected during pumping but still significantly impact groundwater level recovery. The magnitude of the impact from an undetected barrier will increase as the ratio of pumping rate to aquifer transmissivity increases. The results are exemplified for a hypothetical aquifer with an unknown barrier 3 km from a pumping well. The difference in drawdown between a model with and without a barrier may be <1 m in the 10 years while pumping is occurring, but up to 50 m after pumping has ceased.

Minimizing fouling at hydrogenated conical-tip carbon electrodes during dopamine detection in vivo.

In this paper, physically small conical-tip carbon electrodes (∼2-5 µm diameter and ∼4 µm axial length) were hydrogenated to develop a probe capable of withstanding fouling during dopamine detection in vivo. Upon hydrogenation, the resultant hydrophobic sp(3) carbon surface deters adsorption of amphiphilic lipids, proteins, and peptides present in extracellular fluid and hence minimizes electrode fouling. These hydrogenated carbon electrodes showed a 35% decrease in sensitivity but little change in the limit of detection for dopamine over a 7-day incubation in a synthetic laboratory solution containing 1.0% (v/v) caproic acid (a lipid), 0.1% (w/v) bovine serum albumin and 0.01% (w/v) cytochrome C (both are proteins), and 0.002% (w/v) human fibrinopeptide B (a peptide). Subsequently, during dopamine detection in vivo, over 70% of the dopamine oxidation current remained after the first 30 min of a 60-min experiment, and at least 50% remained over the next half-period at the hydrogenated carbon electrodes. On the basis of these results, an initial average electrode surface fouling rate of 1.2% min(-1) was estimated, which gradually declined to 0.7% min(-1). These results support minimal fouling at hydrogenated carbon electrodes applied to dopamine detection in vivo.

M5 muscarinic receptors mediate striatal dopamine activation by ventral tegmental morphine and pedunculopontine stimulation in mice.

Opiates, like other addictive drugs, elevate forebrain dopamine levels and are thought to do so mainly by inhibiting GABA neurons near the ventral tegmental area (VTA), in turn leading to a disinhibition of dopamine neurons. However, cholinergic inputs from the laterodorsal (LDT) and pedunculopontine (PPT) tegmental nucleus to the VTA and substantia nigra (SN) importantly contribute, as either LDT or PPT lesions strongly attenuate morphine-induced forebrain dopamine elevations. Pharmacological blockade of muscarinic acetylcholine receptors in the VTA or SN has similar effects. M5 muscarinic receptors are the only muscarinic receptor subtype associated with VTA and SN dopamine neurons. Here we tested the contribution of M5 muscarinic receptors to morphine-induced dopamine elevations by measuring nucleus accumbens dopamine efflux in response to intra-VTA morphine infusion using in vivo chronoamperometry. Intra-VTA morphine increased nucleus accumbens dopamine efflux in urethane-anesthetized wildtype mice starting at 10 min after infusion. These increases were absent in M5 knockout mice and were similarly blocked by pre-treatment with VTA scopolamine in wildtype mice. Furthermore, in wildtype mice electrical stimulation of the PPT evoked an initial, short-lasting increase in striatal dopamine efflux, followed 5 min later by a second prolonged increase in dopamine efflux. In M5 knockout mice, or following systemic pre-treatment with scopolamine in wildtype mice, the prolonged increase in striatal dopamine efflux was absent. The time course of increased accumbal dopamine efflux in wildtype mice following VTA morphine was consistent with both the prolonged M5-mediated excitation of striatal dopamine efflux following PPT electrical stimulation and accumbal dopamine efflux following LDT electrical stimulation. Therefore, M5 receptors appear critical for prolonged PPT excitation of dopamine efflux and for dopamine efflux induced by intra-VTA morphine.

Muscarinic receptor blockade in the ventral tegmental area attenuates cocaine enhancement of laterodorsal tegmentum stimulation-evoked accumbens dopamine efflux in the mouse.

The reinforcing properties of cocaine have been related to increased extracellular concentrations of dopamine in the nucleus accumbens (NAc). M5 muscarinic acetylcholine receptors (mAChRs) on dopamine cells in the ventral tegmental area (VTA) facilitate mesoaccumbens dopamine transmission and are critically involved in mediating natural and drug reinforcement. We investigated the effects of pharmacological blockade of mAChRs in the VTA on cocaine's ability to enhance electrically evoked NAc dopamine efflux. Using fixed potential amperometry together with carbon fiber recording microelectrodes positioned in the NAc core, we quantified dopamine oxidation currents (dopamine efflux) evoked by brief stimulation (15 monophasic pulses at 50 Hz every 30 s) of the laterodorsal tegmentum (LDT) in urethane (1.5 g/kg, i.p.) anesthetized mice. Compared to predrug baseline responses, cocaine (5 or 10 mg/kg, i.p.) dose-dependently enhanced LDT stimulation-evoked NAc dopamine efflux, whereas the nonsubtype selective mAChR antagonist scopolamine (10 microg/0.5 microl) microinfused into the VTA diminished LDT-evoked NAc dopamine efflux. Preinfusion of scopolamine into the VTA diminished the facilitatory actions of cocaine on LDT stimulation-evoked NAc dopamine efflux, and when infused at the peak effect of cocaine attenuated LDT-evoked dopamine efflux to below predrug baseline levels. These findings suggest that LDT cholinergic inputs to dopamine neurons in the VTA, via activation of mAChRs (probably of the M5 subtype), are involved in modulating the facilitatory effects of cocaine on NAc dopamine neurotransmission. They also suggest that the development of antagonists aimed at selectively disrupting M5 receptor function may be valuable in reducing abuse liability of psychostimulants.

The longitudinal effects of resisted sprint training using weighted sleds vs. weighted vests.

The purpose of this study was to determine the longitudinal effects of weighted sled (WS) and weighted vest (WV) sprint training on maximum velocity sprint performance and kinematics. Twenty male collegiate lacrosse players were randomly assigned to a WS group (n = 7) towing 10% body mass, a WV group (n = 6) loaded with 18.5% body mass, or an unresisted (UR) active control group (n = 7). All subjects completed 13 training sessions over 7 weeks. Pre- and post-test measures of sprint time and average velocity across the distance interval of 18.3 to 54.9 m were used to assess sprint performance, whereas high-speed video (300 Hz) and motion-analysis software were used to analyze stride length, stride rate, ground contact time, and flight time. A 3 × 2 repeated measures analysis of variance was performed for each dependent variable and revealed no significant between-group differences for any of the sprint performance or kinematic stride cycle measures. Effect size statistics suggested small improvements in 18.3- to 54.9-m sprint time and average velocity for the UR group but only trivial improvements for the WS and WV groups. With regard to sprint performance, the results indicate that WS and WV training had no beneficial effect compared with UR training. In fact, for the loads used by WS and WV in this study, UR training may actually be superior for improving sprint performance in the 18.3- to 54.9-m interval.

Increased amphetamine-induced locomotor activity, sensitization, and accumbal dopamine release in M5 muscarinic receptor knockout mice.

INTRODUCTION: Muscarinic M(5) receptors are the only muscarinic receptor subtype expressed by dopamine-containing neurons of the ventral tegmental area. These cells play an important role for the reinforcing properties of psychostimulants and M(5) receptors modulate their activity. Previous studies showed that M(5) receptor knockout (M (5) (-/-) ) mice are less sensitive to the reinforcing properties of addictive drugs. MATERIALS AND METHODS: Here, we investigate the role of M(5) receptors in the effects of amphetamine and cocaine on locomotor activity, locomotor sensitization, and dopamine release using M (5) (-/-) mice backcrossed to the C57BL/6NTac strain. STATISTICAL ANALYSES: Sensitization of the locomotor response is considered a model for chronic adaptations to repeated substance exposure, which might be related to drug craving and relapse. The effects of amphetamine on locomotor activity and locomotor sensitization were enhanced in M (5) (-/-) mice, while the effects of cocaine were similar in M (5) (-/-) and wild-type mice. RESULTS: Consistent with the behavioral results, amphetamine-, but not cocaine, -elicited dopamine release in nucleus accumbens was enhanced in M (5) (-/-) mice. DISCUSSION: The different effects of amphetamine and cocaine in M (5) (-/-) mice may be due to the divergent pharmacological profile of the two drugs, where amphetamine, but not cocaine, is able to release intracellular stores of dopamine. In conclusion, we show here for the first time that amphetamine-induced hyperactivity and dopamine release as well as amphetamine sensitization are enhanced in mice lacking the M(5) receptor. These results support the concept that the M(5) receptor modulates effects of addictive drugs.

Differential corticosteroid receptor regulation of mesoaccumbens dopamine efflux during the peak and nadir of the circadian rhythm: a molecular equilibrium in the midbrain?

Corticosteroid receptor modulation of mesoaccumbens dopamine neurotransmission is believed to be a key neurobiological mechanism mediating the effects of stress in addiction. Importantly, nucleus accumbens (NAc) subregions (core and shell) are reported to respond differentially to fluctuating basal levels of glucocorticoids, with dopaminergic responses in the core of the NAc being somewhat impervious to fluctuating levels of glucocorticoids relative to the shell. To investigate the corticosteroid receptor mechanisms mediating basal dopamine efflux in the core of the NAc, we have used chronoamperometry in combination with stearate-modified graphite paste electrodes in urethane anesthetized male Long-Evans rats during the peak and nadir of the circadian cycle. Blockade of ventral tegmental area low-affinity glucocorticoid (GR) or high-affinity mineralocorticoid (MR) receptors with mifepristone (1 microg/microl) or spironolactone (0.2 microg/microl), respectively, indicated that endogenous phase-dependent corticosteroid receptor activation (GRs during peak; MRs during nadir) facilitated extracellular NAc dopamine efflux. Conversely, the alternate receptor's actions appeared inhibitory at these time points (MRs during peak; GRs during nadir). Pharmacological activation of either the GR or MR with corticosterone (2 microg/microl) or aldosterone (0.2 microg/microl), respectively, potentiated NAc dopamine efflux, irrespective of circadian phase. Together, these data suggest that dominant corticosteroid receptor activation stimulates tonic mesoaccumbens dopamine transmission, enabling MRs and GRs to differentially maintain basal NAc dopamine release over the course of the circadian cycle. This points to an important molecular mechanism through which relatively stable NAc core dopamine extracellular levels could be maintained in the face of fluctuating corticosterone circadian rhythms.

Midbrain acetylcholine and glutamate receptors modulate accumbal dopamine release.

This study determined the role of ventral tegmental area acetylcholine and glutamate receptors in modulating laterodorsal tegmentum stimulation-evoked dopamine efflux in the nucleus accumbens. Rapid changes in dopamine oxidation current were measured at carbon fiber microelectrodes using fixed potential amperometry in urethane anesthetized male mice. Intraventral tegmental area infusions of the muscarinic acetylcholine receptor antagonist scopolamine, the nicotinic acetylcholine receptor antagonist mecamylamine, or the ionotropic glutamate receptor antagonist kynurenate significantly diminished dopamine efflux in the nucleus accumbens evoked by brief electrical stimulation of the laterodorsal tegmentum. These findings suggest that acetylcholine and ionotropic glutamate receptors influence rapid dopaminergic activity and thus the communication of behaviorally relevant information from ventral tegmental area dopamine cells to forebrain areas.

Midbrain muscarinic receptor mechanisms underlying regulation of mesoaccumbens and nigrostriatal dopaminergic transmission in the rat.

Laterodorsal (LDT) and pedunculopontine (PPT) tegmental nuclei in the mesopontine project cholinergic inputs to the midbrain ventral tegmental area (VTA) and substantia nigra pars compacta (SNc), respectively, to directly and indirectly influence the activity of dopamine neuronal cells via actions on muscarinic and nicotinic receptors. The present study investigated the role of midbrain muscarinic receptors in the functional modulation of VTA and SNc dopamine cell activity as reflected by alterations in, respectively, nucleus accumbens (NAc) and striataldopamine efflux. In vivo chronoamperometry was used to measure changes in basal dopamine efflux via stearate-graphite paste electrodes implanted unilaterally in the NAc or striatum of urethane-anaesthetized rats, following blockade or activation of, respectively, VTA or SNc muscarinic receptors. Intra-VTA or -SNc infusion of the muscarinic antagonist scopolamine (200 microg/microL) reduced, respectively, NAc and striatal dopamine efflux while infusion of the muscarinic and nicotinic agonist carbachol (0.5 microg/microL) or the prototypical muscarinic agonist muscarine (0.5 microg/microL) increased NAc and striatal dopamine efflux. Transient decreases in dopamine efflux preceded these increases selectively in the striatum, suggesting a reduction in excitatory or increase in inhibitory drive to the SNc by preferential activation of M3 muscarinic receptors on GABA interneurons and glutamatergic inputs. This was confirmed by showing that selective blockade of M3 receptors with p-F-HHSiD (0.5 microg/microL) increased striatal, but not NAc, dopamine efflux. Together, these findings suggest that midbrain muscarinic receptors, probably M5 subtypes on VTA and SNc dopamine neurons, contribute to the tonic excitatory regulation of forebrain basal dopamine transmission whereas presynaptic M3 receptors serve to counter excessive excitation of nigral dopamine cell activity.

Nigrostriatal dopamine release modulated by mesopontine muscarinic receptors.

The present study investigated the regulation of substantia nigra pars compacta (SNc) dopamine neuronal activity by pedunculopontine (PPT) cholinergic neurons. Changes in dopamine efflux following chemical activation or blockade of muscarinic acetylcholine receptors in the PPT were measured at stearate-carbon paste electrodes in the striatum of urethane (1.5 g/kg) anaesthetized male rats using in vivo chronoamperometry (30 s sampling rate). Intra-PPT infusions of a mixed muscarinic/nicotinic (carbachol 8 microg/microl) or M2/4-selective muscarinic (oxotremorine 0.5 microg/microl) receptor agonist attenuated striatal dopamine efflux, whereas a non-selective (scopolamine 100 microg/microl) or M2/4-selective (methoctramine 50 microg/microl) muscarinic receptor antagonist enhanced striatal dopamine efflux. These results suggest that M2/4 muscarinic receptors in the mesopontine tonically influence SNc basal dopamine cell activity and striatal dopamine release.