The non-L-glutamate (L-Glu) receptor component of D-aspartate (D-Asp) currents in Aplysia californica buccal S cluster (BSC) neurons was studied with whole cell voltage clamp to differentiate it from receptors activated by other well-known agonists of the Aplysia nervous system and investigate modulatory mechanisms of D-Asp currents associated with synaptic plasticity. Acetylcholine (ACh) and serotonin (5-HT) activated whole cell excitatory currents with similar current voltage relationships to D-Asp. These currents, however, were pharmacologically distinct from D-Asp. ACh currents were blocked by hexamethonium (C6) and tubocurarine (d-TC), while D-Asp currents were unaffected. 5-HT currents were blocked by granisetron and methysergide (MES), while D-Asp currents were unaffected. Conversely, while (2S,3R)-1-(Phenanthren-2-carbonyl)piperazine-2,3-dicarboxylic acid(PPDA) blocked D-Asp currents, it had no effect on ACh or 5-HT currents. Comparison of the charge area described by currents induced by ACh or 5-HT separately from, or with, D-Asp suggests activation of distinct receptors by all 3 agonists. Charge area comparisons with L-Glu, however, suggested some overlap between L-Gluand D-Asp receptors. Ten minute exposure to 5-HT induced facilitation of D-Asp-evoked responses in BSC neurons. This effect was mimicked by phorbol ester, suggesting that protein kinase C (PKC) was involved.

D-Aspartate (D-Asp) activates a nonspecific cation current of unknown identity independent of L-glutamate (L-Glu) in neurons of Aplysia californica. Whole-cell voltage clamp studies were conducted using primary cultures of Aplysia buccal S cluster (BSC) neurons to characterize these receptor channels pharmacologically. The N-methyl-D-aspartate receptor (NMDAR) coagonist glycine potentiated D-Asp currents only at −30 mV, while D-serine did not potentiate D-Asp currents at any amplitude. Portions of D-Asp currents were blocked by the L-Glu antagonists kynurenate, DL-2-amino-5-phosphonopentanoic acid (APV), (2S,3R)-1-(phenanthren-2-carbonyl)piperazine-2,3-dicarboxylic acid (PPDA), and 1,3-dihydro-5-[3-[4-(phenylmethyl)-1–2H-benzimidazol-2-one (TCS46b), suggesting that L-Glu channels, particularly NMDAR-like channels, may partially contribute to D-Asp whole-cell currents. In contrast, L-Glu currents were unaffected by APV, and showed greater block by kynurenate, suggesting that D-Asp and L-Glu act, in part, at different sites. The excitatory amino acid transport blocker DL-threo-b-Benzyloxyaspartic acid (TBOA) blocked a fraction of D-Asp currents, suggesting that currents associated with these transporters also contribute. Non-NMDA L-GluR antagonists that preferentially block alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionic acid (AMPA)/kainate receptors significantly increased D-Asp currents, suggesting a possible allosteric potentiating effect of these antagonists on D-Asp receptors. L-Glu-induced currents were significantly reduced in the presence of bath-applied D-Asp, whereas bath-applied L-Glu had no effect on D-Asp-induced currents. The mixed effects of these agents on D-Asp-induced currents in Aplysia illustrate that the underlying channels are not uniformly characteristic of any known agonist associated channel type.

D-Aspartate (D-Asp) can substitute for L-Glutamate (L-Glu) at excitatory Glu receptors, and occurs as free D-Asp in the mammalian brain. D-Asp electrophysiological responses were studied as a potential correlate of aging in the California sea hare, Aplysia californica. Whole cell voltage- and current clamp measurements were made from primary neuron cultures of the pleural ganglion (PVC) and buccal ganglion S cluster (BSC) in 3 egg cohorts at sexual maturity and senescence. D-Asp activated an inward current at the hyperpolarized voltage of −70 mV, where molluscan NMDA receptors open free of constitutive block by Mg2+. Half of the cells responded to both D-Asp and L-Glu while the remainder responded only to D-Asp or L-Glu, suggesting that D-Asp activated non-Glu channels in a subpopulation of these cells. The frequency of D-Asp-induced currents and their density were significantly decreased in senescent PVC cells but not in senescent BSC cells. These changes in sensory neurons of the tail predict functional deficits that may contribute to an overall decline in reflexive movement in aged Aplysia.

Earlier studies documented the loss of wood preservatives from new wood. The objective of this study was to evaluate losses from weathered treated wood under field conditions by collecting rainfall leachate from 5 different wood types, all with a surface area of 0.21 m2. Wood samples included weathered chromate copper arsenate (CCA) treated wood at low (2.7 kg/m3), medium (4.8 kg/m3) and high (35.4 kg/m3) retention levels, new alkaline copper quat (ACQ) treated wood (1.1 kg/m3 as CuO) and new untreated wood. Arsenic was found to leach at a higher rate (100 mg in 1 year for low retention) than chromium and copper (<40 mg) in all CCA treated wood samples. Copper leached at the highest rate from the ACQ sample (670 mg). Overall results suggest that metals’ leaching is a continuous process driven by rainfall, and that the mechanism of release from the wood matrix changes as wood weathers.

A novel modulator of sodium ion currents was synthesized in 6 steps from a protected dihydroxypyrrolidine nitrone, via 1,3-dipolar cycloaddition reaction with acrylamide. Sodium ion currents in B50 cells were evaluated in comparison to saxitoxin and tetrodotoxin, and revealed an IC50 of 15.7 μM. The new compound shows no evidence of binding to the C-lobe of the saxitoxin-binding protein saxiphilin.

Laboratory column leaching experiments were conducted to investigate the transport and interaction of As, Cr, and Cu associated with CCA-treated wood in sand with and without peat amendment. Results showed that leaching behavior of As, Cr, and Cu in these substrates were totally different. Substrate characteristics and microorganism activity posed distinct effects on the transport and transformation of these three elements. Arsenic was rapidly leached out from the columns with or without the amendment of peat, while Cr remained in all columns during the entire experimental period (215 days). Copper was leached out only in the substrate column without peat. The presence of microorganism clearly facilitated the transport of As, while it did not show obvious effects on the transport of Cr and Cu. Interactions among these three elements were observed during the processes of adsorption and transport. The adsorption of Cu on soil was enhanced with the adsorption of As, likely caused by a more negatively charged soil surface because of As adsorption. The adsorption of Cr on soil increased the adsorption of As due to the additional As binding sites induced by Cr adsorption. These results suggest that As concentrations in the soil affected by CCA-treated wood could largely exceed predictions based on soil adsorption capacity for As. The evaluation of the impact on human health associated with CCA-treated wood should take consideration of the distinct transport characteristics of three elements and their interactions in soils.