Real-Time Effects of N-Methyl-d-Aspartic Acid on Dopamine Release in Slices of Rat Caudate Putamen: A Study Using Fast Cyclic Voltammetry

Abstract: The functional role of N-methyl-d -aspartic acid (NMDA) glutamate receptors in the real-time regulation of single electrical pulse (1 p)-stimulated endogenous dopamine release was investigated in slices of rat caudate putamen using fast cyclic voltammetry at a carbon fibre electrode. In the presence of Mg²⁺, 20 µM NMDA had a weak effect on background signals but did not affect 1 p-stimulated dopamine release. Removal of Mg²⁺ increased the background and doubled 1 p-stimulated dopamine release. In the absence of Mg²⁺, 20 µM NMDA caused a transient “release” of dopamine and decreased the background signal. The 1 p-stimulated dopamine release was subsequently reduced. In the presence of 1 µM (±)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), superfusion with 20 µM NMDA did not cause a transient “release” of dopamine, and 1 p-stimulated dopamine release was not subsequently attenuated. In the presence of 1 µM tetrodotoxin, 1 p-stimulated dopamine release was abolished, but 20 µM NMDA still caused a transient “release” of dopamine. Removal of Ca²⁺ from the artificial CSF abolished 1 p-stimulated dopamine release and resulted in a decline in the baseline but did not affect dopamine “release” when 20 µM NMDA was added. The dopamine release-inducing effect of 20 µM NMDA was less pronounced in sites in the caudate putamen where dopamine release increased with frequency of electrical stimulation (hot spots) than in sites where there was little frequency-dependent dopamine release (cold spots). Subsequent 1 p-stimulated dopamine release was less attenuated in cold spots than in hot spots. We conclude that in the absence of Mg²⁺, NMDA induces release of dopamine by acting at CPP-sensitive NMDA receptors in a Ca²⁺-independent manner. This transient release depletes dopamine from a storage site from which dopamine is released by 1 p electrical stimulation. These real-time observations of the effects of NMDA on electrical stimulus-independent and -dependent dopamine release may explain the apparently conflicting observations of the effects of NMDA on dopamine release made in previous studies. They also indicate that dopamine release and storage are heterogeneous at different sites in the rat caudate putamen.     

Potassium-induced insulin release and voltage noise measurements in single mouse islets of Langerhans

Summary Insulin release and membrane potential fluctuations in response to increased extracellular potassium [K⁺] _o have been measured in single perifused islets of Langerhans from normal mice. An increase in [K⁺] _o from 5mm to 50mm induced a transient insulin release with a peak at about 1 min. The peak value was [K⁺] _o -dependent but the half-timet _1/2 for the decline was constant at nearly 1 min. 2.5mm cobalt completely inhibited the potassium-induced stimulation of insulin release. The insulin release elicited by 28 and 50mm [K⁺] _o was similar in terms of peak, total release and half-time from maximum release. Stepwise increase in [K⁺] _o from 10 to 28 to 50mm resulted in a normal response to 28mm but no peak of release after the 28 to 50mm increase. The results indicate good correlation between excess voltage noise, thought to reflect calcium channel activity, and insulin release evoked by changing extracellular potassium.     

ON THE RELATIONSHIP BETWEEN [3H]CHOLINE UPTAKE ACTIVATION AND [3H]ACETYLCHOLINE RELEASE

The depolarization-induced, calcium-dependent release of [³H]ACh from hippocampal synaptosomes was studied in a superfusion system. Release increased, with increasing depolarization. Barium and strontium effectively substituted for calcium during the depolarization, but magnesium inhibited the release. Releasable [³H]ACh is derived from the sodium-dependent component of the [³H]choline uptake which points out the physiologic importance of sodium-dependent choline transport. It is concluded that [³H]ACh release in this system has the same properties as neurotransmitter release in many other systems. Previous studies have shown that treatments which alter the activity of cholinergic neurons in vivo result in parallel changes in sodium-dependent choline uptake in vitro. When synaptosomes were utilized from animals treated to reduce cholinergic activity, there was a reduced release following the reduced uptake. Conversely, when synaptosomes were taken from animals treated to increase sodium-dependent choline uptake, there was an increase in the release. It is concluded that the changes in sodium-dependent choline uptake in vitro consequent to changes in neuronal activity in vivo result in parallel changes in releasable ACh. A comparison was made between the effect of a number of ions and agents on release and their effect on the in vitro, depolarization-induced activation of sodium-dependent choline uptake. Barium and strontium, ions which substitute for calcium in the release process, support the in vitro activation of uptake. Vinblastine and Bay a 1040, compounds which block release, prevented the in vitro activation of sodium-dependent choline uptake. However, magnesium blocked release in a dose-dependent manner, but did not block the activation of uptake in vitro. Rather, magnesium substituted for calcium and supported the activation of uptake in a dose-dependent fashion. It is concluded that acetylcholine release is not necessary for the activation of choline uptake.     

Synergistic Effect of Vespa Amino Acid Mixture on Lipolysis in Rat Adipocytes

The effect of Vespa amino acid mixture (VAAM) on the release of lipolytic products was examined in isolated rat adipocytes. Concentrations of 112.5 to 225 ppm of VAAM showed significantly greater release of non-esterified fatty acids (NEFA) and glycerol than the same concentrations of casein amino acid mixture (CAAM). The integrated relative release of NEFA and glycerol was lower in response to individual administration of amino acids comprising VAAM than to VAAM itself. Further, amino acids mixtures deficient in a single amino acid comprising VAAM showed significantly lower release of lipolytic products than VAAM. These data suggest that the synergistic effect of VAAM on the release of lipolytic products is a function of concurrent exposure to the unique composition of amino acids found in VAAM as compared to the effect of exposure to the same individual un-mixed amino acids or to a mixture lacking one of the amino acids comprising VAAM.     

Effects of release procedures on the primary stress response and post‐release survival and growth of hatchery‐reared spotted seatrout Cynoscion nebulosus

To help explain the apparent poor post‐release success of hatchery‐reared (HR) spotted seatrout Cynoscion nebulosus, this study examined the effects of handling, transport and release procedures on the stress response of two age classes [48 and 80 day post‐hatch (dph)] of HR C. nebulosus, as measured by cortisol concentrations and the post‐release survival and growth of 48 and 80 dph HR C. nebulosus. As a proxy for stress, tissue cortisol was measured at various times during the handling, tagging (80 dph), transport, acclimation and release process. To consider the implications of the pre‐release stressors, growth and survival were monitored in separate field experiments for each age class of acclimated post‐transport C. nebulosus using control C. nebulosus that only experienced anaesthesia, transport, acclimation and a net release v. experimental C. nebulosus that underwent the entire routine procedure, including anaesthesia, tagging, transport, acclimation and gravity release through a pipe. For 48 dph C. nebulosus, mean cortisol varied significantly throughout handling and transport, increasing more than six‐fold from controls before decreasing in mean concentration just prior to release. For 80 dph C. nebulosus, cortisol varied throughout handling, tagging and transport, first increasing more than three‐fold compared with control C. nebulosus, before decreasing and rising slightly just prior to release. For 48 dph C. nebulosus within field enclosures, survival was high and similar for control and experimental groups; experimental C. nebulosus, however, were shorter, lighter and lower in condition than control C. nebulosus. For 80 dph C. nebulosus within field enclosures, fewer experimental C. nebulosus survived and those that did survive were of lower condition than C. nebulosus from the control group. Small untagged C. nebulosus may survive the release procedure better than larger C. nebulosus carrying a coded‐wire tag. These findings document some ways in which pre‐release practices may translate into detrimental effects on post‐release success of HR C. nebulosus.     

Morphine Activates ω-Conotoxin-Sensitive Ca2+ Channels to Release Adenosine from Spinal Cord Synaptosomes

Abstract: Morphine-induced release of adenosine from the spinal cord is believed to contribute to spinal antinociception. Although this release is Ca²⁺ dependent, little is known of the nature of this dependence. In this study, the effects of the dihydropyridine L-type Ca²⁺ channel agonist Bay K 8644 and the antagonist nifedipine, the N-type Ca²⁺ channel antagonist ω-conotoxin, and ruthenium red, a blocker of Ca²⁺ influx induced by capsaicin, on release of adenosine evoked by morphine were determined. The effect of partial depolarization with a minimally effective concentration of K⁺ on morphine-evoked release of adenosine also was examined. Morphine 10^?5-10^?4M produced a dose-dependent enhancement of adenosine release from dorsal spinal cord synaptosomes. Following the addition of 6 mM K⁺ (total K⁺ concentration of 10.7 mM), 10^?6M morphine also enhanced release, and an additional component of action at 10^?8M was revealed. Release was Ca²⁺-dependent as it was not observed in the absence of Ca²⁺ and presence of EGTA. Bay K 8644 (10 nM) and nifedipine (100 nM) had no effect on the release of adenosine evoked by morphine, but ω-conotoxin (100 nM) markedly reduced such release in both the absence and the presence of the additional 6 mM K⁺. Morphine-evoked adenosine release was not altered in the presence of a partially effective dose of capsaicin, nor by ruthenium red. These results indicate that morphine can stimulate two distinct phases of adenosine release from the spinal cord (nanomolar and micromolar), and that both phases of release are due to Ca²⁺ entry via ω-conotoxin-sensitive N-type Ca²⁺ channels.     

Fat Depot‐specific Impact of Visceral Obesity on Adipocyte Adiponectin Release in Women

Our objective was to examine omental and subcutaneous adipocyte adiponectin release in women. We tested the hypothesis that adiponectin release would be reduced to a greater extent in omental than in subcutaneous adipocytes of women with visceral obesity. Omental and subcutaneous adipose tissue samples were obtained from 52 women undergoing abdominal hysterectomies (age: 47.1 ± 4.8 years; BMI: 26.7 ± 4.7 kg/m²). Adipocytes were isolated and their adiponectin release in the medium was measured over 2 h. Measures of body fat accumulation and distribution were obtained using dual‐energy X‐ray absorptiometry and computed tomography, respectively. Adiponectin release by omental and subcutaneous adipocytes was similar in lean individuals; however, in subsamples of obese or visceral obese women, adiponectin release by omental adipocytes was significantly reduced while that of subcutaneous adipocytes was not affected. Omental adipocyte adiponectin release was significantly and negatively correlated with total body fat mass (r = ?0.47, P < 0.01), visceral adipose tissue area (r = ?0.50, P < 0.01), omental adipocyte diameter (r = ?0.43, P < 0.01), triglyceride levels (r = ?0.32, P ≤ 0.05), cholesterol/high‐density lipoprotein (HDL)‐cholesterol (r = ?0.31, P ≤ 0.05), fasting glucose (r = ?0.39, P ≤ 0.01), fasting insulin (r = ?0.36, P ≤ 0.05), homeostasis model assessment index (r = ?0.39, P ≤ 0.01), and positively associated with HDL‐cholesterol concentrations (r = 0.33, P ≤ 0.05). Adiponectin release from subcutaneous cells was not associated with any measure of adiposity, lipid profile, or glucose homeostasis. In conclusion, compared to subcutaneous adipocyte adiponectin release, omental adipocyte adiponectin release is reduced to a greater extent in visceral obese women and better predicts obesity‐associated metabolic abnormalities.     

<Emphasis Type="Italic">In Vitro</Emphasis> and <Emphasis Type="Italic">In Vivo</Emphasis> Investigation of Drug-Eluting Implants for the Treatment of Periodontal Disease

This paper developed solvent-free drug-eluting implants for metronidazole delivery for the treatment of periodontal disease and investigated the characteristics of the drug’s release from the implants, both in vitro and in vivo, using an HPLC assay. The metronidazole exhibited a two-stage release behavior in vitro with an initial burst release followed by a diffusion-controlled release and then a secondary burst release. The accumulated drug release reached 100% on the 18th day, and the drug-eluting implant was totally dissolved on the same day. Additionally, the drug-eluting disks were implanted within the sub-gingival space of both lower incisors of six rabbits. The curve of in vivo drug release was smoother and showed a predominantly diffusion-controlled release. The implants were totally dissolved at 2 weeks after implantation. The concentration of metronidazole remained above the MIC₉₀ during the entire investigation.     

川南地区毛竹和林下植被芒箕细根分解特征

揭示竹林与其林下植被细根单独和混合分解特征,探讨竹林细根与其林下植被细根之间相互影响的潜在机制,为毛竹林林下植被的合理经营管理提供理论参考。采用原位分解袋法研究了四川长宁毛竹(Phyllostachys edulis)与林下植被芒箕(Dicranopteris pedata)细根分解和养分释放过程,试验周期为1年。结果表明(1)毛竹和芒箕细根初始化学组分有着明显差异,碳(C)含量、碳氮比(C/N)和碳磷比(C/P)毛竹显著高于芒箕(P0.05),而氮(N)含量、磷(P)含量和氮磷比(N/P)均芒箕高于毛竹(P0.05)。(2)毛竹和芒箕细根分解系数(k)分别为0.66±0.04和0.42±0.41,毛竹细根分解速率显著高于芒箕;土壤温度与分解速率呈显著正相关,是影响细根分解速率的关键环境因子。(3)毛竹和芒箕细根碳(C)、氮(N)、磷(P)养分释放均表现为净释放,毛竹细根碳(C)释放速率高于芒箕,但细根氮(N)和磷(P)释放率均低于芒箕。(4)混合分解的实测值和期望值对比结果表明毛竹和芒箕细根混合对分解速率和磷(P)元素的释放没有显著影响,但显著促进了碳(C)元素的释放,抑制了分解初期氮(N)元素的释放。毛竹与林下植被芒箕单独细根分解和养分释放特征均表现不同;细根混合分解速率无显著混合效应,但养分释放的混合效应表现出不同阶段性和不同方向(正或负),说明林下植被通过影响细根养分释放而影响竹林生态系统的养分循环。     

Mivazerol, a Novel α2-Agonist and Potential Anti-Ischemic Drug, Inhibits KCl-Stimulated Neurotransmitter Release in Rat Nervous Tissue Preparations

Abstract: In this study, we have investigated the effect of mivazerol, [3-(1H-imidazol-4-yl)methyl-1]-2-hydroxy-benzamide hydrochloride, a new α₂-agonist lacking hypotensive properties and a potential anti-ischemic drug, on the evoked release of norepinephrine, aspartate, and glutamate in tissue preparations from hippocampus, spinal cord T1–T5 section, rostrolateral ventricular medulla, and nucleus tractus solitarii of the brainstem of rat. A simple and efficient in vitro procedure to study pharmacologically the release of norepinephrine and glutamate is described. Tissues were chopped into (0.3 × 0.2 × 0.2 mm³) sections and the resulting minces were used for this study. Exposure to KCl (10–75 mM) for 5 min served as a stimulus for the release response. One, S (for aspartate and for glutamate release), or two such stimuli, S₁ and S₂ (for norepinephrine release) were conducted. The release of norepinephrine (+150% above baseline) was inhibited in a dose-dependent manner by mivazerol in hippocampus (IC₅₀ = 1.5 × 10^?8M), spinal cord (IC₅₀ = 5 × 10^?8M), rostrolateral ventricular medulla (IC₅₀ = 10^?7M), and nucleus tractus solitarii (IC₅₀ = 7.5 × 10^?8M), and by clonidine in hippocampus (IC₅₀ = 5 × 10^?8M), spinal cord (IC₅₀ = 4.5 × 10^?8M), rostrolateral ventricular medulla (IC₅₀ = 2.5 × 10^?7M), and nucleus tractus solitarii (IC₅₀ = 10^?7M). This effect was counteracted by the selective α₂-antagonists yohimbine and rauwolscine. A significant glutamate and aspartate release response was also induced by KCl (35 mmol/L) in hippocampus (+250 and +135%, respectively) and spinal cord (+120 and +55%, respectively), in vitro. However, neither mivazerol nor clonidine, at doses up to 10 µM, had any significant effect on KCl-induced glutamate release in spinal cord, whereas mivazerol blocked completely the release of both amino acids in hippocampus and only the release of aspartate in spinal cord. On the other hand, clonidine (1 µM) was only effective in reducing by 40% the release of aspartate in hippocampus. These data indicate that (1) inhibition of KCl-induced norepinephrine release by mivazerol is mediated by its action on α₂-adrenergic receptors; (2) at concentrations selective for α₂-adrenergic receptors, only mivazerol was effective in blocking the KCl-induced glutamate release in hippocampal tissue; and (3) at the same concentrations, both mivazerol and clonidine were unable to inhibit glutamate release in the spinal cord. These data suggest that prevention of hyperadrenergic activity by mivazerol in perioperative patients may be mediated through its effect on the release of norepinephrine and/or the release of glutamate and aspartate in regions of the CNS that are involved in the control of cardiovascular homeostasis.     

Chronic Nicotine Administration Differentially Affects Neurotransmitter Release from Rat Striatal Slices

Abstract: The objective of these experiments was to determine whether the chronic administration of nicotine, at a dose regimen that increases the density of nicotine binding sites, alters the nicotine-induced release of [³H]dopamine ([³H]DA), [³H]norepinephrine ([³H]NE), [³H]serotonin ([³H]5-HT), or [³H]acetylcholine ([³H]ACh) from rat striatal slices. For these experiments, rats received subcutaneous injections of either saline or nicotine bitartrate [1.76 mg (3.6 µmol)/kg, dissolved in saline] twice daily for 10 days, and neurotransmitter release was measured following preloading of the tissues with [³H]DA, [³H]NE, [³H]5-HT, or [³H]choline. Chronic nicotine administration did not affect the accumulation of tritium by striatal slices, the basal release of radioactivity, or the 25 mM KCl-evoked release of neurotransmitter. Superfusion of striatal slices with 1, 10, and 100 µM nicotine increased [³H]DA release in a concentration-dependent manner, and release from slices from nicotine-injected animals was significantly (p < 0.05) greater than release from saline-injected controls; release from the former increased to 132, 191, and 172% of release from the controls following superfusion with 1, 10, and 100 µM nicotine, respectively. Similarly, [³H]5-HT release increased in a concentration-related manner following superfusion with nicotine, and release from slices from nicotine-injected rats was significantly (p < 0.05) greater than that from controls. [³H]5-HT release from slices from nicotine-injected rats evoked by superfusion with 1 and 10 µM nicotine increased to 453 and 217%, respectively, of release from slices from saline-injected animals. The nicotine-induced release of [³H]NE from striatal slices was also concentration dependent but was unaffected by chronic nicotine administration. [³H]ACh release from striatal slices could not be detected when samples were superfused with nicotine but was measurable when tissues were incubated with nicotine. The release of [³H]ACh from slices from nicotine-injected rats was significantly (p < 0.05) less than release from controls and decreased to 36, 83, and 77% of control values following incubation with 1, 10, or 100 µM nicotine, respectively. This decreased [³H]ACh release could not be attributed to methodological differences because slices from nicotine-injected rats incubated with nicotine exhibited an increased [³H]DA release, similar to results from superfusion studies. In addition, it is unlikely that the decreased release of [³H]ACh from striatal slices from nicotine-injected rats was secondary to increased DA release because [³H]ACh release from slices from hippocampus, which is not tonically inhibited by DA, also decreased significantly (p < 0.05) in response to nicotine; hippocampal slices from nicotine-injected rats incubated with 1 and 10 µM nicotine decreased to 42 and 70%, respectively, of release from slices from saline-injected animals. Results indicate that the chronic administration of nicotine increases the ability of nicotine to induce the release of [³H]DA and [³H]5-HT and decreases the ability of nicotine to evoke the release of [³H]ACh but does not alter the nicotine-induced release of [³H]NE from brain slices.     

Biological Control ofBemisia argentifolii(Homoptera: Aleyrodidae) on Poinsettia with Inundative Releases ofEncarsia formosa(Hymenoptera: Aphelinidae): Are Higher Release Rates Necessarily Better?

The effectiveness of inundative releases of the parasitoidEncarsia formosafor control ofBemisia argentifoliion poinsettia was determined in replicated experimental greenhouses. We evaluated two release rates ofE. formosa:a low release rate (1 wasp/plant/week, released in two greenhouses, in spring 1995) and a high release rate (3 wasps/plant/week, released in two greenhouses, in fall 1993), each over a 14-week growing season. Each release trial had one or two control greenhouses in whichB. argentifoliideveloped on poinsettia in the absence ofE. formosa.Life-tables were constructed forB. argentifoliiin the presence and absence ofE. formosaby using a photographic technique to follow cohorts of whiteflies on poinsettia leaves. Weekly population counts of the whitefly were also made. In the absence ofE. formosa,egg to adult survivorship ofB. argentifoliion poinsettia was 75–81%. At the low release rate, egg to survivorship ofB. argentifoliiwas 5% and parasitism was 13%. At the high release rate, egg to adult survivorship forB. argentifoliiwas 8% and parasitism was 23%. The net reproductive rates (R₀) forB. argentifoliipopulations in the absence ofE. formosaranged from 18.01–26.12, indicating a rapidly increasing population. Net reproductive rates for whitefly populations subject to wasp releases were 1.54 for the low release rate greenhouses and 2.11 for the high release rate greenhouses, indicating substantially reducedB. argentifoliipopulation growth. The low release rate provided better control ofB. argentifoliithan the high release rate. This difference was attributed to higher levels of mortality of whiteflies at the low release rate in the first 5–6 weeks of the growing period. We suggest that mutual interference may also have affected observed levels of mortality and parasitism.     

The pepsinogen releasing effect of Helicobacter pylori lipopolysaccharide

Background. Helicobacter pylori lipopolysaccharide (LPS) affects pepsinogen release by a nontoxic mechanism. We hypothesized that this effect was characteristic of the organism and related to the clinical status of the strain. Materials and methods. LPS was isolated from 11 H. pylori strains whose pathogenic profile was known and four other nongastric bacteria. The effects of luminal LPS on guinea pig gastric mucosal pepsinogen release was evaluated using the Ussing chamber technique. CCK‐8 (10^?9M) was used as a positive control. Results. H. pylori LPS dose‐dependently stimulated pepsinogen release with a maximal stimulation at 250 µg/ml (~4500%; p < .001 vs. control). LPS from other Helicobacter or Campylobacter species had no effect on pepsinogen release. ANOVA demonstrated significant differences in the efficacies of pepsinogen release between the 11 clinical H. pylori strains (p < .0001) despite the fact that they were all cagA⁺ and 90% had the cytotoxic vacA subtype s1. Physical and chemical disruption of the LPS suggested that both the structure and the carbohydrate composition of this molecule may play a critical role in pepsinogen release. Polymyxin B partly (p < .03) inhibited and dephosphorylation completely inhibited (p = .0002) LPS‐stimulated pepsinogen release. Conclusion. Pepsinogen release is an innate property of all cagA⁺H. pylori LPS. The structure of the molecule and composition of side‐chains are important in this response which appears to be partially lipid A driven.     

N-Methyl-d-Aspartic Acid/Glycine Interactions on the Control of 5-Hydroxytryptamine Release in Raphe Primary Cultures

Abstract: Glutamic acid and glycine were quantified in cells and medium of cultured rostral rhombencephalic neurons derived from fetal rats. In the presence of 1 mM Mg²⁺, NMDA (50 μM) significantly stimulated (by 69%) release of newly synthesized 5-[³H]hydroxytryptamine ([³H]5-HT). d -2-Amino-5-phosphonopentanoate (AP-5; 50 μM) blocked the stimulatory effect of NMDA. AP-5 by itself inhibited [³H]5-HT release (by 25%), suggesting a tonic control of 5-HT by glutamate. In the absence of Mg²⁺, basal [³H]5-HT release was 60% higher as compared with release with Mg²⁺. AP-5 blocked the increased [³H]5-HT release observed without Mg²⁺, suggesting that this effect was due to the stimulation of NMDA receptors by endogenous glutamate. Glycine (100 μM) inhibited [³H]5-HT release in the absence of Mg²⁺. Strychnine (50 μM) blocked the inhibitory effect of glycine, indicating an action through strychnine-sensitive inhibitory glycine receptors. The [³H]5-HT release stimulated by NMDA was unaffected by glycine. In contrast, when tested in the presence of strychnine, glycine increased NMDA-evoked [³H]5-HT release (by 22%), and this effect was prevented by a selective antagonist of the NMDA-associated glycine receptor, 7-chlorokynurenate (100 μM). 7-Chlorokynuren-ate by itself induced a drastic decrease in [³H]5-HT release, indicating that under basal conditions these sites were stimulated by endogenous glycine. These results indicate that NMDA stimulated [³H]5-HT release in both the presence or absence of Mg²⁺. Use of selective antagonists allowed differentiation of a strychnine-sensitive glycine response (inhibition of [³H]5-HT release) from a 7-chlorokynurenate-sensitive response (potentiation of NMDA-evoked [³H]5-HT release).     

Decomposition and nutrient release by green manures in a tropical hillside agroecosystem

The decomposition and nutrient release of 12 plant materials were assessed in a 20-week litterbag field study in hillsides from Cauca, Colombia. Leaves of Tithonia diversifolia (TTH) and Indigofera constricta (IND) decomposed quickly (k=0.035±0.002 d^–1), while those of Cratylia argentea (CRA) and the stems evaluated decomposed slowly (k=0.007±0.002 d^–1). Potassium presented the highest release rates (k>0.085 d^–1). Rates of N and P release were high for all leaf materials evaluated (k>0.028 d^–1) with the exception of CRA (N and P), TTH and IND (P). While Mg release rates ranged from 0.013 to 0.122 d^–1, Ca release was generally slower (k=0.008–0.041 d^–1). Initial quality parameters that best correlated with decomposition (P>0.001) were neutral detergent fibre, NDF (r=–0.96) and in vitro dry matter digestibility, IVDMD (r=0.87). It is argued that NDF or IVDMD could be useful lab-based tests during screening of plant materials as green manures. Significant correlations (P>0.05) were also found for initial quality parameters and nutrient release, being most important the lignin/N ratio (r=–0.71) and (lignin+polyphenol)/N ratios (r=–0.70) for N release, the C/N (r=0.70) and N/P ratios (r=–0.66) for P release, the hemicellulose content (r=–0.75) for K release, the Ca content (r=0.82) for Ca release, and the C/P ratio (r=0.65) for Mg release. After 20 weeks, the leaves of Mucuna deerengianum released the highest amounts of N and P (144.5 and 11.4 kg ha^–1, respectively), while TTH released the highest amounts of K, Ca and Mg (129.3, 112.6 and 25.9 kg ha^–1, respectively). These results show the potential of some plant materials studied as sources of nutrients in tropical hillside agroecosystems.     

The relationship between handling time and cortisol release rates changes as a function of brain parasite densities in California killifish Fundulus parvipinnis

This study validated a technique for non‐invasive hormone measurements in California killifish Fundulus parvipinnis, and looked for associations between cortisol (a stress hormone) and 11‐ketotestosterone (KT, an androgen) release rates and the density or intensity of the trematode parasites Euhaplorchis californiensis (EUHA) and Renicola buchanani (RENB) in wild‐caught, naturally infected F. parvipinnis. In experiment 1, F. parvipinnis were exposed to an acute stressor by lowering water levels to dorsal‐fin height and repeatedly handling the fish over the course of an hour. Neither parasite was found to influence cortisol release rates in response to this acute stressor. In experiment 2, different F. parvipinnis were exposed on four consecutive days to the procedure for collecting water‐borne hormone levels and release rates of 11‐KT and cortisol were quantified. This design examined whether F. parvipinnis perceived the water‐borne collection procedure to be a stressor, while also exploring how parasites influenced hormone release rates under conditions less stressful than those in experiment 1. No association was found between RENB and hormone release rates, or between EUHA and 11‐KT release rates. The interaction between EUHA density and handling time, however, was an important predictor of cortisol release rates. The relationship between handling time and cortisol release rates was negative for F. parvipinnis harbouring low or intermediate density infections, and became positive for fish harbouring high densities of EUHA.     

Influence of the introduced parasitoid Torymus sinensis (Hymenoptera: Torymidae) on T. koreanus and T. beneficus as indigenous parasitoids of the chestnut gall wasp Dryocosmuskuriphilus (Hymenoptera: Cynipidae) on chestnut trees in Nagano Prefecture, Japan

We describe here the parasitoid wasps Torymus sinensis Kamijo and T. beneficus Yasumatsu & Kamijo (early-spring and late-spring strains), which are introduced and indigenous natural enemies of the chestnut gall wasp Dryocosmus kuriphilus Yasumatsu, an invasive chestnut pest in Japan. We recently discovered specimens of T. koreanus Kamijo, endemic in Korea, among Torymus parasitoids collected from D. kuriphilus galls in a Japanese chestnut orchard. In this study we compare the composition of Torymus parasitoids emerging from D. kuriphilus galls before and after the release of T. sinensis. Before the release of T. sinensis, early-spring and late-spring strains of T. beneficus predominated (58.3 and 20.8% of specimens collected). However, a few years after the release, both T. beneficus strains had been almost completely displaced by T. sinensis. In contrast to the rapid decrease in T. beneficus, T. koreanus did not decrease drastically before and even after the release of T. sinensis (approximately 10–20% of specimens collected). These results suggest that not a few T. koreanus were present in the Japanese chestnut orchard investigated at least several years after the release of T. sinensis, although both the T. beneficus strains were rapidly displaced by T. sinensis during this period.     

Structure-activity relationship of polyphenols on inhibition of chemical mediator release from rat peritoneal exudate cells

Summary The effect of phenolic compounds in foodstuffs on histamine and leukotriene B₄ (LTB₄) release from rat peritoneal exudate cells and their antioxidative activity were examined to assess their antiallergenic activities. Among them, triphenols such as pyrogallol and gallic acid inhibited histamine release from the cells, but diphenols did not. On the other hand, o- and p-diphenols such as catechol and hydroquinone with strong antioxidative activity inhibited LTB₄ release as strongly as pyrogallol, but an m-derivative resorcinol with weak antioxidative activity did not. Though carboxylated compounds and their noncarboxylated counterparts were antioxidative, the former exerted a much weaker inhibitory effect on the LTB₄ release than the latter. In flavonols, only myricetin with a triphenolic B ring strongly inhibited histamine release, but all flavonols strongly suppressed LTB₄ release irrespective of the number of OH groups in the B ring. Among flavonoids with an o-diphenolic B ring, flavonol and flavone with a C₄-carbonyl group strongly inhibited LTB₄ release, whereas the activity of anthocyan without C₄-carbonyl was much weaker than the above compounds. These results suggest that triphenolic structure is essential for the inhibition of histamine release. On the other hand, antioxidative activity and membrane permeability of phenolic compounds seemed to be essential for the inhibition of LTB₄ release. In addition, the C₄-carbonyl group seemed to be important for strongly inhibiting LTB₄ release.     

A Single Compartment Quantal Response Model with an Inspection Process

In a single compartment quantal response model, besides the input and release processes, an inspection process, assumed to be independent of the input and release processes, is considered. Each time when a release occurs, we assume the amount of release is randomly proportional to the amount present and the proportional rates form a sequence of independent and identically distributed random variables with support on [0, 1]. The input policy we consider is a modification of (s, S) input policy in the inventory model. More precisely, let 0 ≦s₂ ≦s₁ ≦s ≦ S, if after a release, the amount of the drug in subject's body is less than a level s₂ which is small enough, then there will be an input immediately with probability 1 — p and no more inputs thereafter with probability p, also there will be an input immediately if the dose level is in the interval [s₂, s₁). If the dose level is in the interval [s₁, s) there will be no input unless the inspector arrives. On the other hand, if the dose level is greater than or equal to s, then there will be no input. We consider a stochastic model as described above, and obtain the expressions for some quantities of interest. A Monte Carlo study has also been carried out to demonstrate some behaviors of our quantal response process.     

Adenosine and Glutamate Modulate Each Other's Release from Rat Hippocampal Synaptosomes

Abstract: In rat hippocampal synaptosomes, adenosine decreased the K⁺ (15 mM) or the kainate (1 mM) evoked release of glutamate and aspartate. An even more pronounced effect was observed in the presence of the stable adenosine analogue, R-phenylisopropyladenosine. All these effects were reversed by the selective adenosine A₁ receptor antagonist 8-cyclo-pentyltheophylline. In the same synaptosomal preparation, K⁺ (30 mM) strongly stimulated the release of the preloaded [³H]adenosine in a partially Ca²⁺-dependent and tetrodotoxin (TTX)-sensitive manner. Moreover, in the same experimental conditions, both l -glutamate and l -aspartate enhanced the release of [³H]adenosine derivatives ([³H]ADD). The gluta-mate-evoked release was dose dependent and appeared to be Ca²⁺ independent and tetrodotoxin insensitive. This effect was not due to metabolism because even the nonmetabolizable isomers d -glutamate and d -aspartate were able to stimulate [³H]ADD release. In contrast, the specific glutamate agonists N-methyl-d -aspartate, kainate, and quisqualate failed to stimulate [³H]ADD release, suggesting that glutamate and aspartate effects were not mediated by known excitatory amino acid receptors. Moreover, NMDA was also ineffective in the absence of Mg²⁺ and l -glutamate-evoked release was not inhibited by adding the specific antagonists 2-amino-5-phosphonovaleric acid or 6–7-dinitroquinoxaline-2, 3-dione. The stimulatory effect did not appear specific for only excitatory amino acids, as γ-anunobutyric acid stimulated [³H]ADD release in a dose-related manner. These results suggest that, at least in synaptosomal preparations from rat hippocampus, adenosine and glutamate modulate each other's release. The exact mechanism of such interplay, although still, unknown, could help in the understanding of excitatory amino acid neurotoxicity.