bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interactive effects of parental age and environmental variation on the breeding performance of Tengmalm’s owls
Authors: Laaksonen Toni , Korpimäki Erkki , Hakkarainen Harri 
Published: March 2003

Summary

Two main mechanisms have been proposed to account for the changes in breeding performance of long‐lived animals with age: progressive appearance or disappearance of different quality individuals within a cohort and within‐individual improvements with age.
We studied age‐related breeding performance of vole‐eating Tengmalm’s owls (Aegolius funereus, L.), whose prey populations fluctuate in a cyclic manner in western Finland. In years of low vole abundance, most yearling owls were not able to breed. In years of initially intermediate but increasing vole abundance, clutch size increased with female age and partners of old males initiated egg‐laying earlier than those of young males. In years of initially high but decreasing vole abundance, the differences in laying dates were still detectable, whereas age‐related differences in clutch size of females tended to disappear.
Within‐cohort analyses did not indicate quality differences between surviving and dying males of the same age in years of increasing vole abundance, whereas in years of decreasing vole abundance early breeding males were more likely to survive than late‐breeding males. This novel finding indicates that quality differences between individuals may induce observed age‐related differences in only some years, and especially that differential mortality may occur in a different year when the difference in breeding performance is detectable.
Within‐individual analyses showed that individual males advanced their nest initiation with age, and there was a trend that females laid larger clutches with increasing age. In nests of long‐lived males, a significant decline in the clutch size from mid‐age (2–4 years) to older age (6–10 years) was found.
We conclude that environmental variation may mask age‐related differences in breeding performance at the population level, since the differences appeared to emerge more clearly in poor and intermediate food conditions. Some evidence for the differential mortality‐hypothesis was found for males, which are mainly responsible for subsisting their families during the entire breeding season. Substantial improvements in competence or increased reproductive effort from 1 to 3 years of age, and deteriorated skills due to senescence at older ages may account for within‐individual changes in breeding performance of males.
Aapa mires as a carbon sink and source during the Holocene
Authors: Mäkilä Markku , Saarnisto Matti , Kankainen Tuovi 
Published: March 2003

Summary

The vertical and horizontal dynamics of peat carbon accumulation in Ruosuo aapa mire, north‐central Finland, were investigated in an attempt to understand variations in carbon accumulation over time.
Paludification began around 8700 BP (9600 cal BP). The long‐term net carbon accumulation rate, based on vertical and lateral growth, was 8.0 g C m−2 year−1. Variations in carbon accumulation rates can be explained to a great extent by natural succession and variations in local conditions, but the role of climate cannot be ignored.
The marked decline in carbon accumulation rates after 6100 BP (7000 cal BP) may indicate a relatively dry and warm climate. The levelling out and subsequent increase in carbon accumulation rates after 4000 BP (4500 cal BP) indicates the development of a cooler and moister climate.
The low long‐term net carbon accumulation rate and the high carbon content per unit volume in the layer underlying the surficial peat is typical for a wet aapa mire. The continuous penetration of roots, mostly sedge, results in carbon input into the underlying peat layer and contributes to the intensive decay of the surficial peat due to high biological activity.
Although one‐third of the apparent carbon has accumulated during the last 2000 years, most of Ruosuo is approaching the stage where primary production does not adequately compensate for overall carbon loss. The declining net carbon accumulation rates from the base up to the depth of 80 cm may indicate a real delayed trend in net carbon accumulation rates.
We suggest that under the present climatic conditions the northern circumpolar wet mires are significant sources of greenhouse gases. In addition to high methane production, northern aapa mires also have lower carbon accumulation rates than more southern raised bogs.
Our results, which are based on horizontal and vertical carbon accumulation rates, suggest that the earlier published carbon accumulation rates in Finnish aapa mires are overestimated.
Effects of streptozotocin‐diabetes on the hippocampal NMDA receptor complex in rats
Authors: Gardoni F. , Kamal A. , Bellone C. , Biessels G. J. , Ramakers G. M. J. , Cattabeni F. , Gispen W. H. , Di Luca M. 
Published: March 2003

AbstractIn animal models of diabetes mellitus, such as the streptozotocin‐diabetic rat (STZ‐rat), spatial learning impairments develop in parallel with a reduced expression of long‐term potentiation (LTP) and enhanced expression of long‐term depression (LTD) in the hippocampus. This study examined the time course of the effects of STZ‐diabetes and insulin treatment on the hippocampal post‐synaptic glutamate N‐methyl‐d‐aspartate (NMDA) receptor complex and other key proteins regulating hippocampal synaptic transmission in the post‐synaptic density (PSD) fraction. In addition, the functional properties of the NMDA‐receptor complex were examined. One month of STZ‐diabetes did not affect the NMDA receptor complex. In contrast, 4 months after induction of diabetes NR2B subunit immunoreactivity, CaMKII and Tyr‐dependent phosphorylation of the NR2A/B subunits of the NMDA receptor were reduced and αCaMKII autophosphorylation and its association to the NMDA receptor complex were impaired in STZ‐rats compared with age‐matched controls. Likewise, NMDA currents in hippocampal pyramidal neurones measured by intracellular recording were reduced in STZ‐rats. Insulin treatment prevented the reduction in kinase activities, NR2B expression levels, CaMKII–NMDA receptor association and NMDA currents. These findings strengthen the hypothesis that altered post‐synaptic glutamatergic transmission is␣related to deficits in learning and plasticity in this animal model.
Elevated hepatic and depressed renal cytochrome P450 activity in the Tg2576 transgenic mouse model of Alzheimer's disease
Authors: Van Ess P. J. , Pedersen W. A. , Culmsee C. , Mattson M. P. , Blouin R. A. 
Published: March 2003

AbstractRecent studies indicate that the Tg2576 transgenic mouse model of Alzheimer's disease [tg(hAPP)] demonstrates disturbances in plasma glucose and neuroendocrine function reminiscent of Alzheimer's disease (AD). Alterations in any one of these systems can have a profound effect on hepatic cytochrome P450 (CYP) expression. Additionally, the recent discovery that amyloid beta 1–42 can induce the expression of CYP reductase in neuronal cultures further suggests that hepatic CYP‐related metabolism may be affected by the expression of mutant human amyloid precursor protein in these tg(hAPP) mice. Therefore, the current study was conducted to investigate the activity and protein content of several CYP isoforms in the livers and kidneys of aged (20‐month‐old) tg(hAPP) mice. tg(hAPP) mice exhibit significant elevations in hepatic CYP2B, CYP2E1‐, CYP3A‐ and CYP4A‐associated activities and CYP4A immunoreactive protein compared with wild‐type. In contrast to the liver, a significant depression in renal CYP2E1‐ and CYP4A‐associated activities were demonstrated in tg(hAPP) mice. The presence of the mutant hAPP protein was detected in the brain, kidney and livers of tg(hAPP) mice.
Lithium protection against glutamate excitotoxicity in rat cerebral cortical neurons: involvement of NMDA receptor inhibition possibly by decreasing NR2B tyrosine phosphorylation
Authors: Hashimoto Ryota , Hough Christopher , Nakazawa Takanobu , Yamamoto Tadashi , Chuang De‐Maw 
Published: March 2003

AbstractThe therapeutic mechanisms of lithium for treating bipolar mood disorder remain poorly understood. Recent studies demonstrate that lithium has neuroprotective actions against a variety of insults. Here, we studied neuroprotective effects of lithium against excitotoxicity in cultured cerebral cortical neurons. Glutamate‐induced excitotoxicity in cortical neurons was exclusively mediated by NMDA receptors. Pre‐treatment of cortical neurons with LiCl time‐dependently suppressed excitotoxicity with maximal protection after 6 days of pre‐treatment. Significant protection was observed at the therapeutic and subtherapeutic concentration of 0.2–1.6 mm LiCl with almost complete protection at 1 mm. Neuroprotection was␣also elicited by valproate, another major mood‐stabilizer. The neuroprotective effects of lithium coincided with inhibition␣of␣NMDA receptor‐mediated calcium influx. Lithium pre‐treatment did not alter total protein levels of NR1, NR2A and NR2B subunits of NMDA receptors. However, it did markedly reduce the level of NR2B phosphorylation at Tyr1472 and this was temporally associated with its neuroprotective effect. Because NR2B tyrosine phosphorylation has been positively correlated with NMDA receptor‐mediated synaptic activity and excitotoxicity, the suppression of NR2B phosphorylation by lithium is likely to result in the inactivation of NMDA receptors and contributes to neuroprotection against excitotoxicity. This action could also be relevant to its clinical efficacy for bipolar patients.
The human histamine H2‐receptor couples more efficiently to Sf9 insect cell Gs‐proteins than to insect cell Gq‐proteins: limitations	of Sf9 cells for the analysis of receptor/Gq‐protein coupling
Authors: Houston Christine , Wenzel‐Seifert Katharina , Bürckstümmer Tilmann , Seifert Roland 
Published: March 2003

AbstractThe human histamine H2‐receptor (hH2R) couples to	Gs‐proteins to activate adenylyl cyclase and to Gq‐proteins to activate phospholipase C, but phospholipase C activation has not consistently been observed. The aim of this study was to compare coupling of hH2R to insect and mammalian Gs‐ and Gq‐proteins in Spodoptera frugiperda (Sf9) cells. Interaction of hH2R with mammalian G proteins was assessed with coexpressed proteins or receptor‐Gα fusion proteins that enhance coupling efficiency. hH2R efficiently coupled to insect Gs‐proteins to activate adenylyl cyclase. However, hH2R poorly coupled to insect Gq‐proteins as assessed by the lack of enhancement of histamine‐stimulated steady‐state GTP hydrolysis by regulators of G protein signaling (RGS proteins). In contrast, RGS‐proteins efficiently enhanced GTP hydrolysis stimulated by the human platelet‐activating factor receptor (PAFR) and the histamine H1‐receptor (H1R) from man and guinea pig. The measurement of intracellular free Ca2+ concentration was not useful for studying receptor/Gq‐protein coupling. hH2R also efficiently interacted with mammalian Gs‐proteins, specifically with fused Gsα as assessed by guanosine 5′‐O‐(3‐thiotriphosphate) (GTPγS)‐sensitive high‐affinity agonist binding, agonist‐stimulated [35S]GTPγS binding and adenylyl cyclase activation. In contrast, coupling of hH2R to coexpressed and fused mammalian Gqα was poor. However, our inability to reconstitute efficient coupling of PAFR and H1R to mammalian Gqα indicated that a large portion of the expressed G protein was functionally inactive. Taken together, our data show that hH2R couples more efficiently to insect cell Gs‐proteins than to insect cell Gq‐proteins. Unfortunately, there are significant limitations in the usefulness of Sf9 cells for comparing the coupling of receptors to mammalian Gs‐ and Gq‐proteins and assessing Gq‐mediated activation of effector systems.
A homeostatic mechanism counteracting K+‐evoked choline release in adult brain
Authors: Klein Jochen , Weichel Oksana , Ruhr Judith , Dvorak Claudia , Löffelholz Konrad 
Published: March 2003

AbstractCholine (Ch) is an essential nutrient as the biosynthetic precursor of acetylcholine (ACh) and phospholipids. Under resting conditions, the intracellular accumulation of Ch (above 10‐fold), which is positively charged, is governed by the membrane potential and follows the Nernst equation. Accordingly, in synaptosomes from adult rats during depolarization, we observed a linear relationship between release of free cytoplasmic Ch and KCl concentration (2.7–120 mm). The K+‐evoked Ch release was Ca2+‐independent and did not originate from ACh or phospholipid hydrolysis. In superfused brain slices of adult rats, however, a K+‐induced Ch efflux was absent. Also, under in vivo conditions, 30–60 mm KCl failed to increase the extracellular Ch level as shown by microdialysis in adult rat hippocampus. On the contrary, in brain slices from 1‐week‐old rats, high K+ as well as 4‐aminopyridine evoked a marked Ch efflux in a concentration‐dependent fashion. This phenomenon faded within 1 week. Hemicholinium‐3 (HC‐3, 1␣and 10 µm), a blocker of cellular choline uptake, caused a marked efflux of choline from adult rat slices but no or significantly less release from immature slices. We conclude that depolarization of synaptic endings causes a Ca2+‐independent release of free cytoplasmic Ch into the extracellular space. In adult rat brain, this elevation of Ch is counteracted by a homeostatic mechanism such as uptake into brain cells.
Effect of depleting vesicular and cytoplasmic dopamine on methylenedioxymethamphetamine neurotoxicity
Authors: Yuan Jie , Cord Branden J. , McCann Una D. , Callahan Brian T. , Ricaurte George A. 
Published: March 2003

AbstractThe mechanism by which 3,4‐methylenedioxymethamphetamine (MDMA) produces serotonin (5‐HT) neurotoxicity is unknown but considerable evidence suggests that endogenous brain dopamine (DA) is involved. However, it has recently become apparent that some of the data implicating brain DA in MDMA neurotoxicity may be confounded by drug effects on thermoregulation. The purpose of the present studies was to examine the role of DA in MDMA neurotoxicity, while controlling for possible confounding effects of drug‐ induced changes in core temperature. Rats were treated with reserpine, alone and in combination with α‐methyl‐p‐tyrosine (AMPT), to deplete vesicular and cytoplasmic stores of DA. When drug‐induced hypothermia was averted (by raising ambient temperature), the 5‐HT neuroprotective effects of reserpine and AMPT were no longer apparent. The lack of neuroprotection by AMPT and reserpine, alone and in combination, in studies that control for the effects of these drugs on core temperature, suggests that DA per se is not essential for the expression of MDMA‐induced 5‐HT neurotoxicity.
PK 11195 attenuates kainic acid‐induced seizures and alterations in peripheral‐type benzodiazepine receptor (PBR) protein components in the rat brain
Authors: Veenman L. , Leschiner S. , Spanier I. , Weisinger G. , Weizman A. , Gavish M. 
Published: March 2003

AbstractPeripheral‐type benzodiazepine receptors (PBR) are located in glial cells in the brain and in peripheral tissues. Mitochondria form the primary location for PBR. Functional PBR appear to require at least three components: an isoquinoline binding protein, a voltage‐dependent anion channel, and an adenine nucleotide carrier. In the present study, rats received intraperitoneal kainic acid injections, which are known to cause seizures, neurodegeneration, hyperactivity, gliosis, and a fivefold increase in PBR ligand binding density in the hippocampus. In the forebrain of control rats, hippocampal voltage‐dependent anion channel and adenine nucleotide carrier abundance was relatively low, while isoquinoline binding protein abundance did not differ between hippocampus and the rest of the forebrain. One week after kainic acid injection, isoquinoline binding protein abundance was increased more than 20‐fold in the hippocampal mitochondrial fraction. No significant changes were detected regarding hippocampal voltage‐dependent anion channel and adenine nucleotide carrier abundance. Pre‐treatment with the isoquinoline PK11195, a specific PBR ligand, attenuated the occurrence of seizures, hyperactivity, and increases in isoquinoline binding protein levels in the hippocampus, which usually follow kainic acid application. These data suggest that isoquinoline binding protein may be involved in these effects of kainic acid injections.
Direct evidence that release‐stimulating α7* nicotinic cholinergic receptors are localized on human and rat brain glutamatergic axon terminals
Authors: Marchi Mario , Risso Francesca , Viola Concetta , Cavazzani Paolo , Raiteri Maurizio 
Published: March 2003

AbstractThe existence on glutamatergic nerve endings of nicotinic acetylcholine receptors (nAChRs) mediating enhancement of glutamate release has often been suggested but not demonstrated directly. Here, we study the effects of nAChR agonists on [3H]‐d‐aspartate ([3H]‐d‐ASP) release from synaptosomes superfused in conditions known to prevent indirect effects. Nicotinic receptor agonists, while unable to modify the basal [3H]‐d‐ASP release from human neocortex or rat striatal synaptosomes, enhanced the Ca2+‐dependent exocytotic release evoked by K+ (12 mm) depolarization. Their rank order of potency were anatoxin‐a > epibatidine > nicotine > ACh (+ atropine). The anatoxin‐a effect, both in human and rat synaptosomes, was antagonized by mecamylamine, α‐bungarotoxin or methyllycaconitine. The basal release of [3H]ACh from human cortical synaptosomes was increased by (–)‐nicotine (EC50 = 1.16 ± 0.33 µm) or by ACh plus atropine (EC50 = 2.0 ± 0.04 µm). The effect of ACh plus atropine was␣insensitive to α‐bungarotoxin, methyllycaconitine or α‐conotoxin MII, whereas it was totally antagonized by mecamylamine or dihydro‐β‐erythroidine. To conclude, glutamatergic axon terminals in human neocortex and in rat striatum possess α7* nicotinic heteroreceptors mediating enhancement of glutamate release. Release‐enhancing cholinergic autoreceptors in human neocortex are nAChRs with a pharmacological profile compatible with the α4β2 subunit combination.
Intrinsic water‐use efficiency and heterotrophic investment in tropical leaf growth of two Neotropical pioneer tree species as estimated from δ13C values
Authors: Terwilliger V. J. , Kitajima K. , Le Roux‐Swarthout D. J. , Mulkey S. , Wright S. J. 
Published: March 2003

Summary

13C enrichment in emerging leaves and its effect on carbon isotopic composition (δ13C) of mature leaves were investigated in the neotropical pioneer tree species, Cecropia longipes and Urera caracasana, in Panama.
Leaves of all ages were analysed for δ13C, gas exchange, nitrogen, and leaf mass per area. Low intercellular to atmospheric carbon dioxide (CO2) partial pressure (pi : pa); and high δ13C of CO2 in air, intrinsic water‐use efficiency, internal resistance, and carboxylation capacity were discounted as causes of 13C enrichment.
13C enrichment might occur when leaf growth is from imported organic carbon but might not reflect δ13C values at the leaf producing the carbon. Results support hypotheses that: de novo sucrose synthesis causes 13C enrichment of mobile sugars after export from source leaves; and high ratios of PEP carboxylase (PEPc) : PEPc + Rubisco cause emerging leaves to be 13C enriched relative to their growth substrate. Carbon contributions of 13C‐enriched early growth could yield inaccurate pi : pa estimates from δ13C in mature leaves.
A model estimated investment of imported organic carbon to leaf growth and improved estimates of pi : pa from mature leaves. With such adjustment, δ13C analyses provide valuable information about age‐related source–sink relations in leaves.
Remobilized old‐leaf nitrogen predominates for spring growth in two temperate grasses
Authors: Bausenwein Ursula , Millard Peter , Raven John A. 
Published: March 2003

Summary

The importance of N derived from internal remobilization and root uptake to growth in spring is reported here for the perennial grasses Festuca rubra and Agrostis capillaris derived from seminatural grasslands in Scotland, UK.
Plants grown in sand culture, received 15N‐enriched nutrient solution during the first year of growth and nutrient solution with N at natural abundance during the subsequent spring and summer when destructive harvests were taken.
Labelled N was recovered in new growth of overwintering tillers and new tillers. Remobilized N contributed 70% and 82% for F. rubra and A. capillaris, respectively, to the total N in new above‐ground growth in early spring, declining to 34% and 45%, respectively, by mid June. Species showed similar patterns of remobilization on a new growth biomass basis. The root system did not remobilize N to support new above‐ground growth. Labelled N was derived from senescing leaves present on overwintering tillers. Net balances of labelled N suggest that N was translocated between tillers; reproductive tillers acted as sinks, vegetative tillers as the source of N.
Initial growth in spring is largely independent of N uptake from the soil, provided that overwintering leaves are present on the plants.
Functional genomics: tools of the trade
Authors: Colebatch G. , Trevaskis B. , Udvardi M. 
Published: March 2003

SummaryFunctional genomics is transforming the way biological research is done in the 21st century. Functional genomics brings together high‐throughput genetics with multiparallel analyses of gene transcripts, proteins, and metabolites to answer the ultimate question posed by all genome‐sequencing projects: what is the biological function of each and every gene? Functional genomics is driving a shift in the research paradigm away from vertical analysis of single genes, proteins, or metabolites, towards horizontal analysis of full suites of genes, proteins, and metabolites. By identifying and measuring many, if not all of the molecular players that participate in a given biological process, functional genomics offers the prospect of obtaining a truly holistic picture of life. This review describes the tools that are currently being used for functional genomics work and considers the impact that this new discipline is likely to have in the future.
Specification of stomatal fate in Arabidopsis: evidences for cellular interactions
Authors: Serna Laura , Torres‐Contreras Javier , Fenoll Carmen 
Published: March 2003

SummaryStomata are bi‐celled epidermal structures distributed in predictable patterns providing plants with pathways for gas exchange with the atmosphere. In Arabidopsis thaliana, stomatal formation is emerging as an elegant and powerful model system to study the genetic and molecular control of cell fate specification and pattern formation in multicellular organisms. In this review, we describe the mechanisms that regulate stomatal distribution in this model plant. The emerging view indicates that cellular interactions play a relevant role during stomatal pattern formation. These cellular interactions are not restricted to a cell layer and signalling within the epidermis, between the epidermis and the underlying tissues and between organs seem to play a relevant role during stomatal formation. Whatever the nature of the different signals, the stomatal pattern must arise as the result of the integration by the epidermal cells of multiple inputs. Uncovering the molecular nature of such signals and understanding the specific role during stomatal development provides a formidable task for the future.