Spatial patterns in the distribution of tropical tree species.

Fully mapped tree census plots of large area, 25 to 52 hectares, have now been completed at six different sites in tropical forests, including dry deciduous to wet evergreen forest on two continents. One of the main goals of these plots has been to evaluate spatial patterns in tropical tree populations. Here the degree of aggregation in the distribution of 1768 tree species is examined based on the average density of conspecific trees in circular neighborhoods around each tree. When all individuals larger than 1 centimeter in stem diameter were included, nearly every species was more aggregated than a random distribution. Considering only larger trees (>/= 10 centimeters in diameter), the pattern persisted, with most species being more aggregated than random. Rare species were more aggregated than common species. All six forests were very similar in all the particulars of these results.

Subunit- and site-specific pharmacology of the NMDA receptor channel.

N-Methyl-D-aspartate (NMDA) receptor channels play important roles in various physiological functions such as synaptic plasticity and synapse formation underlying memory, learning and formation of neural networks during development. They are also important for a variety of pathological states including acute and chronic neurological disorders, psychiatric disorders, and neuropathic pain syndromes. cDNA cloning has revealed the molecular diversity of NMDA receptor channels. The identification of multiple subunits with distinct distributions, properties and regulation, implies that NMDA receptor channels are heterogeneous in their pharmacological properties, depending on the brain region and the developmental stage. Furthermore, mutation studies have revealed a critical role for specific amino acid residues in certain subunits in determining the pharmacological properties of NMDA receptor channels. The molecular heterogeneity of NMDA receptor channels as well as their dual role in physiological and pathological functions makes it necessary to develop subunit- and site-specific drugs for precise and selective therapeutic intervention. This review summarizes from a molecular perspective the recent advances in our understanding of the pharmacological properties of NMDA receptor channels with specific references to agonists binding sites, channel pore regions, allosteric modulation sites for protons, polyamines, redox agents, Zn2+ and protein kinases, phosphatases.

The sensitivity of AMPA-selective glutamate receptor channels to pentobarbital is determined by a single amino acid residue of the alpha 2 subunit.

Clinical concentrations of pentobarbital inhibit the alpha-amino-3-hydroxy-5- methyl-4-isoxazole propionic acid (AMPA)-selective glutamate receptor (GluR) channels. Recently, the AMPA-selective GluR channels that contained the alpha 2 subunit were shown to be more sensitive to pentobarbital block than those without the alpha 2 subunit. Here we demonstrated that replacement by glutamine of the arginine residue in putative transmembrane segment M2 of the alpha 2 subunit (mutation alpha 2-R586Q) drastically reduced the pentobarbital sensitivity of the alpha 2 heteromeric channel to the level comparable to those of the alpha 1 and alpha 2-R586Q homomeric channels. These results suggest that the arginine residue in segment M2 of the alpha 2 subunit is the critical determinant of the sensitivities of the AMPA-selective GluR channels to pentobarbital.

Sensitivity of the N-methyl-D-aspartate receptor channel to butyrophenones is dependent on the epsilon2 subunit.

The effects of three kinds of butyrophenones, haloperidol, droperidol and spiperone, on the N-methyl-D-aspartate (NMDA) receptor channel were examined on the epsilon1/zeta1, epsilon2/zeta1, epsilon3/zeta1 and epsilon4/zeta1 heteromeric NMDA receptor channels, expressed in Xenopus oocytes. Micromolar concentrations of haloperidol selectively inhibited the epsilon2/zeta1 channel, whereas the epsilon1/zeta1, epsilon3/zeta1 and epsilon4/zeta1 channels were enhanced or minimally affected by higher concentrations of haloperidol. Similarly, droperidol and spiperone inhibited the epsilon2/zeta1 channel more strongly than the other epsilon/zeta channels, although sensitivities of the epsilon2/zeta1 channel to droperidol and spiperone were lower than those to haloperidol. These results suggest that the sensitivities of the NMDA receptor channels to butyrophenones are dependent on the epsilon2 subunit. Furthermore, the replacement with glutamine of the conserved asparagine residue in segment M2, which constitutes the Mg2+ block sites, of the epsilon2 and zeta1 subunits (the mutations epsilon2-N589Q and zeta1-N598Q, respectively) reduced the sensitivities to haloperidol. The mutation zeta1-N598Q reduced the sensitivities to haloperidol more effectively than the mutation epsilon2-N589Q. These results, together with previous findings, suggest that the haloperidol block sites of the NMDA receptor channel partially overlap the Mg2+ block sites.

Involvement of the carboxyl-terminal region in modulation by TPA of the NMDA receptor channel.

The epsilon 1/zeta 1 and epsilon 2/zeta 1 heteromeric N-methyl-D-aspartate (NMDA) receptor channels expressed in Xenopus oocytes, but not the epsilon 3/zeta 1 and epsilon 4/zeta 1 channels, are positively modulated by the treatment with 12-O-tetradecanoyl phorbol 13-acetate (TPA). Failure of potentiation in the presence of staurosporine suggests the involvement of protein kinases in the TPA effect. To identify the structural domain involved in the modulation of the NMDA receptor channel by the TPA treatment, we constructed chimeric subunits between the epsilon 2 and epsilon 3 subunits. Functional analysis of heteromeric channels containing chimeric epsilon subunits has shown that the carboxyl-terminal region of the epsilon 2 subunit is responsible for the activation of the epsilon 2/zeta 1 channel by the TPA treatment.

Different sensitivities of NMDA receptor channel subtypes to non-competitive antagonists.

Four kinds of heteromeric N-methyl-D-aspartate (NMDA) receptor channels, the epsilon 1/zeta 1, epsilon 2/zeta 1, epsilon 3/zeta 1 and epsilon 4/zeta 1 channels, were expressed in Xenopus oocytes and their sensitivities to various non-competitive antagonists were examined. The epsilon 1/zeta 1 and epsilon 2/zeta 1 channels were more sensitive to (+)MK-801 (dizocilpine) than the epsilon 3/zeta 1 and epsilon 4/zeta 1 channels, whereas the sensitivities to phencyclidine (PCP), ketamine and N-allylnormetazocine (SKF-10,047) were only slightly variable among the four epsilon/zeta channels. Furthermore, the replacement by glutamine or arginine of the conserved asparagine residue in segment M2 of the epsilon 2 and zeta 1 NMDA receptor channel subunits reduced the sensitivities to PCP, ketamine and SKF-10,047, though to different extents. These results, together with previous findings, suggest that these non-competitive antagonists as well as (+)MK-801 and Mg2+ act on a common site.

The Lurcher mutation reveals Ca(2+) permeability and PKC modification of the GluRdelta channels.

The physiological function of the GluRdelta subfamily which is one of the glutamate receptor (GluR) channel subunits has not yet been clarified, because no GluR channel activity has been detected in heterologous expression systems. The Lurcher mutation, a point mutation of the GluRdelta2 subunit, converts it into a constitutively active and cation-permeating channel. We introduced this mutation into GluRdelta1 and GluRdelta2, AMPA-selective, and NMDA-selective GluR channel subunits, and characterized their channel properties. It was shown that the Lurcher mutation alters the gating properties of AMPA- and NMDA-selective GluR channels, but not their cation permeabilities nor metabolic modulations. These findings support the idea that the Lurcher mutant homomeric GluRdelta1 channels are permeable to Ca(2+) as do the mutant GluRdelta2 channels, reflecting their original channel properties. We also found that cation permeability of the mutant GluRdelta1 channels was decreased by TPA, a protein kinase C activator. It indicates the possibility that phosphorylation by PKC activation may inhibit channel with wild-type GluRdelta1 subunit.

Prior brain injury protects death from local anaesthetic-induced convulsion.

Minor brain injury was inflicted with a small hypodermic needle at four sites from the scalp 7 days before the production of convulsion by i.p. injection of 100 mg/kg lidocaine in mice. The latency to convulsion and survival rate were significantly longer and higher, respectively, in the brain-injured group than in the sham-operated one. Thus, the results suggest that a protective mechanism develops in the injured brain against asphyxia caused by lidocaine convulsion.

NMDA induces a biphasic change in intracellular pH in rat hippocampal slices.

As alterations in intracellular pH (pH(i)) tend to exert a profound effect on the properties of cells, this study was undertaken to examine NMDA-induced changes in pH(i) in rat hippocampal slices using the BCECF fluorescent technique. The 'resting' pH(i) in the CA1 pyramidal cell layers was 6.93 +/- 0.07 (mean +/- S.D., n = 72 slices) in 25 mM HCO3-/5% CO2-buffered solution at 37 degrees C. Exposure of hippocampal slices to NMDA in the range of 10-1000 microM produced a biphasic change in pH(i): an initial transient alkaline shift was followed by a long-lasting acid shift. Dizocilpine (10 microM) but not CNQX (40 microM) blocked the NMDA-induced changes in pH(i). In 0 Ca medium (0 mM Ca2+ supplemented 1 mM EGTA, referred to as 0 Ca), pH(i) acid shift caused by NMDA (20 microM) declined by about 11%, whereas the initial alkaline shift almost completely disappeared. In an independent experiment, the NMDA-induced increase in intracellular Ca2+ ([Ca2+]i) was reduced by more than 80% in 0 Ca medium. Glucose substitution using equimolar pyruvate (as an energy-yielding substrate) suppressed this NMDA-induced pH(i) acid shift by two-thirds, while the NMDA-induced pH(i) alkaline shift was enhanced. Fluoride (10 mM), a glycolytic inhibitor, abolished NMDA-induced pH(i) acid shift. Furthermore, the lactate content of hippocampal slices was markedly increased following exposure to NMDA. In conclusion, activation of NMDA receptors in rat hippocampal slices evokes a biphasic change in pH(i). The initial alkaline shift is suggested to be associated with calcium influx, and the following acid shift may be caused by an increase in lactate production through the acceleration of glycolysis, as well as the increased [Ca2+]i. The pH(i) acid shift produced by the increased lactate may contribute to proton modulation of the NMDA receptor and NMDA-induced cell injury or death.

Effects of propofol on various AMPA-, kainate- and NMDA-selective glutamate receptor channels expressed in Xenopus oocytes.

Effects of a general intravenous anesthetic 2,6-diisopropylphenol (propofol) on various glutamate receptor (GluR) channels were examined on the alpha 1 and alpha 1/alpha 2 GluR channels selective for alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), the beta 2/gamma 2 GluR channels selective for kainate, and the epsilon 2/zeta 1 and epsilon 3/zeta 1 N-methyl-D-aspartate (NMDA) receptor channels expressed in Xenopus oocytes. Propofol suppressed the current responses of the alpha 1/alpha 2, beta 2/gamma 2, epsilon 2/zeta 1 and epsilon 3/zeta 1 channels in a dose-dependent manner, whereas it enhanced the current responses of the alpha 1 channel. The extents of inhibition were in the order epsilon 2/zeta 1 > epsilon 3/zeta 1 > beta 2/gamma 2 > alpha 1/alpha 2 channels. During perfusion of 500 microM propofol, the alpha 1/alpha 2, beta 2/gamma 2, epsilon 2/zeta 1 and epsilon 3/zeta 1 channels were progressively suppressed. Furthermore, 10 min perfusion of 20 microM propofol inhibited the epsilon 2/zeta 1 channel by 24%. These results suggest that clinical concentrations (approximately 35 microM) of propofol suppress the NMDA receptor channels slightly.

Sublethal cerebral ischemia inhibits caspase-3 activation induced by subsequent prolonged ischemia in the C57Black/Crj6 strain mouse.

Caspase-3 activation has been implicated in ischemic neuronal death. In the present study, we examined if cerebral ischemic tolerance induced by sublethal ischemia is associated with an attenuation of caspase-3 activation in a mouse forebrain ischemia model. Forebrain ischemia in C57Black/Crj6 strain mice was induced by bilateral common carotid artery occlusion (BCCAO) for 18 min. Two episodes of 6-min ischemia were carried out as preconditioning 48 and 72 h before the 18-min BCCAO. Caspase-3-like activity was determined by fluorescently monitoring the release of amino-4-methylcoumarin from N-acetyl-Asp-Glu-Val-Asp-7-amino-4-methylcoumarin in the striatal protein extracts at 4, 24, and 72 h after reperfusion. The results showed that the ischemic preconditioning significantly attenuated caspase-3 activation at 4, 24, and 72 h after reperfusion, and reduced neuronal loss caused by the 18-min ischemia as examined on the 7th day after reperfusion. The present results suggest that the neuroprotection achieved by ischemic preconditioning is related to an attenuation of caspase-3 activation.

[Anesthetic managements for pericardiectomy of three patients with constrictive pericarditis].

We experienced three patients with constrictive pericarditis who underwent pericardiectomy. Percutaneous cardiopulmonary support (PCPS) was carried out in two patients because of unstable hemodynamics caused by massive bleeding or cardiac compression due to surgical manipulation. In the other patient with severe tachycardia, we prepared PCPS before the induction of anesthesia, and could manage the whole course of anesthesia satisfactorily. It is suggested that PCPS is the most reliable way to support hemodynamics during anesthesia in patients with constrictive pericarditis.

Tree allometry and improved estimation of carbon stocks and balance in tropical forests.

Tropical forests hold large stores of carbon, yet uncertainty remains regarding their quantitative contribution to the global carbon cycle. One approach to quantifying carbon biomass stores consists in inferring changes from long-term forest inventory plots. Regression models are used to convert inventory data into an estimate of aboveground biomass (AGB). We provide a critical reassessment of the quality and the robustness of these models across tropical forest types, using a large dataset of 2,410 trees >or= 5 cm diameter, directly harvested in 27 study sites across the tropics. Proportional relationships between aboveground biomass and the product of wood density, trunk cross-sectional area, and total height are constructed. We also develop a regression model involving wood density and stem diameter only. Our models were tested for secondary and old-growth forests, for dry, moist and wet forests, for lowland and montane forests, and for mangrove forests. The most important predictors of AGB of a tree were, in decreasing order of importance, its trunk diameter, wood specific gravity, total height, and forest type (dry, moist, or wet). Overestimates prevailed, giving a bias of 0.5-6.5% when errors were averaged across all stands. Our regression models can be used reliably to predict aboveground tree biomass across a broad range of tropical forests. Because they are based on an unprecedented dataset, these models should improve the quality of tropical biomass estimates, and bring consensus about the contribution of the tropical forest biome and tropical deforestation to the global carbon cycle.

Seasonal change in nagilactone contents in leaves inPodocarpus nagi forest.

Nagilactones isolated fromPodocarpus nagi (Thunb.) Zoll. et Moritz. are known by their physiological activities as a plant growth inhibitor or antiherbivory substance. As the first step in clarifying the nagilactone dynamics in a forest canopy, the seasonal variations in nagilactone contents in leaves and mass of nagilactones accumulated in the canopy were examined at Mt. Mikasa, Nara City, central Japan. Nagilactone content in mature leaves dropped sharply in May, when new leaves flushed. The nagilactone content of new leaves was far greater than that of mature leaves, implying a translocation of nagilactones from old leaves to new leaves. The total mass of nagilactones in the canopy was 3.9 kg/ha.

The stereoselective effects of ketamine isomers on heteromeric N-methyl-D-aspartate receptor channels.

UNLABELLED: The effects of S(+)- and R(-)-ketamine on heteromeric N-methyl-D-aspartate receptor channels were investigated on the epsilon1/zeta1, epsilon2/zeta1, epsilon3/zeta1, and epsilon4/zeta1 channels expressed in Xenopus oocytes. S(+)-ketamine inhibited all four epsilon/zeta channels more effectively than R(-)-ketamine. The inhibitor concentrations for half-control response for S(+)-ketamine were quite similar among the four channels with 0.44-0.56 microM. However, the inhibitor concentrations for half-control response for R(-)-ketamine varied slightly among the four channels with 1.0 microM for epsilon2/zeta1 and epsilon3/zeta1 channels and 1.9-2.0 microM for epsilon1/zeta1 and epsilon4/zeta1 channels. Thus, the potency ratio of S(+)- and R(-)-ketamine for heteromeric channels was only slightly different among the epsilon/zeta channels. IMPLICATIONS: The potency order and ratio of ketamine isomers for inhibition of N-methyl-D-aspartate receptor channels may not be so different between the brain region and the developmental stage.

Effects of gaseous anesthetics nitrous oxide and xenon on ligand-gated ion channels. Comparison with isoflurane and ethanol.

BACKGROUND: Ligand-gated ion channels are considered to be potential general anesthetic targets. Although most general anesthetics potentiate the function of gamma-aminobutyric acid receptor type A (GABAA), the gaseous anesthetics nitrous oxide and xenon are reported to have little effect on GABAA receptors but inhibit N-methyl-d-aspartate (NMDA) receptors. To define the spectrum of effects of nitrous oxide and xenon on receptors thought to be important in anesthesia, the authors tested these anesthetics on a variety of recombinant brain receptors. METHODS: The glycine, GABAA, GABA receptor type C (GABAC), NMDA, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), kainate, 5-hydroxytryptamine3 (5-HT3), and nicotinic acetylcholine (nACh) receptors were expressed in Xenopus oocytes and effects of nitrous oxide and xenon, and as equipotent concentrations of isoflurane and ethanol, were studied using the two-electrode voltage clamp. RESULTS: Nitrous oxide (0.58 atmosphere [atm]) and xenon (0.46 atm) exhibited similar effects on various receptors. Glycine and GABAA receptors were potentiated by gaseous anesthetics much less than by isoflurane, whereas nitrous oxide inhibited GABAC receptors. Glutamate receptors were inhibited by gaseous anesthetics more markedly than by isoflurane, but less than by ethanol. NMDA receptors were the most sensitive among glutamate receptors and were inhibited by nitrous oxide by 31%. 5-HT3 receptors were slightly inhibited by nitrous oxide. The nACh receptors were inhibited by gaseous and volatile anesthetics, but ethanol potentiated them. The sensitivity was different between alpha4beta2 and alpha4beta4 nACh receptors; alpha4beta2 receptors were inhibited by nitrous oxide by 39%, whereas alpha4beta4 receptors were inhibited by 7%. The inhibition of NMDA and nACh receptors by nitrous oxide was noncompetitive and was slightly different depending on membrane potentials for NMDA receptors, but not for nACh receptors. CONCLUSIONS: Nitrous oxide and xenon displayed a similar spectrum of receptor actions, but this spectrum is distinct from that of isoflurane or ethanol. These results suggest that NMDA receptors and nACh receptors composed of beta2 subunits are likely targets for nitrous oxide and xenon.

N-methyl-D-aspartate receptor channel block by meperidine is dependent on extracellular pH.

UNLABELLED: Large concentrations of meperidine inhibit N-methyl-D-aspartate-(NMDA) receptor channels by channel block mechanisms. Extracellular pH regulates the activity and drug sensitivity of NMDA-receptor channels. We examined the influence of extracellular pH on sensitivity to meperidine of epsilon/zeta heteromeric NMDA-receptor channels expressed in Xenopus oocytes. Inhibition of epsilon1/zeta1, epsilon2/zeta1, epsilon3/zeta1, and epsilon4/zeta1 channels by meperidine was dependent on pH, with more inhibition at acidic pH and less inhibition at alkaline pH. The degree of voltage-dependence of meperidine block was only slightly affected by changes in pH, whereas affinity for meperidine was greatly reduced at alkaline pH. Furthermore, interaction of meperidine with Mg(2+) block was reduced at alkaline pH. Because the percentage of the protonated form of meperidine is only slightly affected by pH, changes in properties of the meperidine binding site may be involved in mechanisms of alteration of meperidine potency by pH. IMPLICATIONS: At acidic pH the potency of meperidine for N-methyl-D-aspartate-receptor channels was increased. Any antinociceptive and neuroprotective benefit from the N-methyl-D-aspartate-receptor antagonist property of meperidine may be pH dependent.