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The mammalian retina contains around 30 morphological varieties of amacrine cell types. These interneurons receive excitatory glutamatergic input from bipolar cells and provide GABA- and glycinergic inhibition to other cells in the retina. Amacrine cells exhibit widely varying light evoked responses, in large part defined by their presynaptic partners. We wondered whether amacrine functional diversity is based on a differential expression of glutamate receptors among cell populations and types. In whole cell patch-clamp experiments on mouse retinal slices, we used selective agonists and antagonists to discriminate responses mediated by NMDA/ non-NMDA (NBQX) and AMPA/ KA receptors (cyclothiazide, GYKI 52466, GYKI 53655, SYM 2081). We sampled a large variety of individual cell types, which were classified by their dendritic field size into either narrow-field or wide-field cells after filling with Lucifer yellow or neurobiotin. In addition, we used transgenic GlyT2-EGFP mice, whose glycinergic neurons express EGFP. This allowed us to classify amacrines on basis of their neurotransmitter into either glycinergic or GABAergic cells. All cells (n = 300) had good responses to non-NMDA agonists. Specific AMPA receptor responses could be obtained from almost all cells recorded: 94% of the AII (n = 17), 87% of the narrow-field (n = 45), 81% of the wide-field (n = 21), 85% of the glycinergic (n = 20) and 78% of the GABAergic cells (n = 9). KA receptor selective drugs were also effective on the majority of the AII (79%, n = 14), narrow-field (93%, n = 43), wide-field (85%, n = 26), glycinergic (94%, n = 16) and GABAergic amacrine cells (100%, n = 6). Among the cells tested for the two receptors (n = 65), we encountered both exclusive expression of AMPA or KA receptors and co-expression of the two types. Most narrow-field (70%, n = 27), glycinergic (81%, n = 16) and GABAergic cells (67%, n = 6) were found to have both AMPA and KA receptors. In contrast, only less than half of the wide-field cells (43%, n = 14) were found to co-express AMPA and KA receptors, most of them expressing exclusively AMPA (36%) or KA receptors (21%). We could elicit small NMDA responses from most of the wide-field (75%, n = 13) and GABAergic cells (67%, n = 3), whereas only 47% of the narrow-field (n = 15), 14% of the AII (n = 22) and no glycinergic cell (n = 2) reacted to NMDA. Abstract 83 Our data suggest that AMPA, KA and NMDA receptors are differentially expressed among different types of amacrine cells rather than among populations with different neurotransmitters or different dendritic coverage of the retina. Selective expression of kinetically different glutamate receptors among amacrine types may be involved in generating transient and sustained inhibitory pathways in the retina. Since AMPA and KA receptors are not generally clustered at the same postsynaptic sites, a single amacrine cell expressing both AMPA and KA receptors may provide inhibition with different temporal characteristics to individual synaptic partners.
Life of Varroa destructor, Anderson and Trueman, an ectoparasitic mite of honeybees, is divided into a reproductive phase in the bee brood and a phoretic phase during which the mite is attached to the adult bee. Phoretic mites leave the colony with workers involved in foraging tasks. Little information is available on the mortality of mites outside the colony. Mites may or not return to the colony as a result of death of the infested foragers, host change by drifting of foragers, or removal of mites outside the colony. That mites do not return to the colony was indicated by substantially higher infestation of outflying workers compared to the infestation of returning workers (Kutschker, 1999). The main objective of the study was to provide information whether V. destructor influences flight behaviour of foragers and consequently returning frequency of foragers to the colony. I first repeated the experiment of Kutschker (1999) examining the infestation of outflying and returning workers. Further, I registered flight duration of foragers using a video method. In this experiment I compared also the infestation and flight duration of bees of different genetic origin, Carnica from Oberursel and bees from Primorsky region. I investigated returning time of workers, returning frequency until evening, drifting to other colonies and orientation toward the nest entrance in the experiments in which workers were released in close vicinity of the colony. At last, I measured the loss of foragers in relation to colony infestation using a Bee Scan. Results from this study, listed below, showed considerable influence of V. destructor on flight behavior of foragers translating into loss of mites. Loss of mites with foragers add substantial component to mite mortality and was underestimated in previous studies. Such loss might be viewed as a mechanism of resistance against V. destructor. a) The mean infestation of outflying workers (0.019±0.018) was twice as the mean infestation of returning workers (0.009±0.018). The difference in the infestation between outflying and returning workers was more marked in highly infested colonies. b) Investigation of individually tagged workers by use of a two camera video recording device showed significantly higher infestation of outflying workers compared to returning workers. Mites were lost by the non returning of infested foragers (22%) and by loss of mites from foragers that returned to the colony without the mite (20%). A small portion of mites (1.8%) was gained. Loss of mites significantly exceeded mite gain. c) The flight duration of infested workers determined by using the same two camera video system was significantly higher in infested compared to uninfested workers of the same age that flew closest at time. The median flight duration of infested workers was 1.7 higher (214s) than the median duration of unifested workers (128s). d) Infested workers took 2.3 times longer to return to the colony than uninfested workers of the same age when released from the same locations, closest at time. The returning time increased with the distance of release. In a group of bees released simultaneously the infestation was higher in bees returning later and in those that did not return in the observation period of 15 min. e) Released workers did not return to the colony 1.5 more frequently than uninfested workers in evening. The difference in returning was significant for locations of 20 and 50m from the colony. No difference in returning between infested and uninfested workers were observed for the most distant location of 400m. f) No significant difference was found in returning time and/or in the returning frequency until evening between workers artificially infested overnight and naturally infested workers. Artificially infested workers returned later and less frequently than a control group indicating rapid influence of V. destructor on flight behavior of foragers. g) The orientation ability of infested workers toward the nest entrance was impaired. Infested workers compared to uninfested workers twice as often approached a dummy entrance before finding the nest entrance. h) No significant differences were found in drifting between infested and uninfested workers. Drifting in the neighboring nucleus colony occurred in about 1% occasions after release of marked workers. Similarly, more infested, but not significantly more infested workers (2.6%) entered a different colored hive than the same colored hive (1.9%). However, the number of drifting bees were to low to make results conclusive. i) The comparison between Carnica and Primorsky workers revealed higher infestation in Carnica compared to Primorsky. Further, Primorsky workers lost more mites during foraging due to mite loss from foragers and non returning of infested workers. No significant differences in flight duration were observed between the two bee stocks. j) Loss of foragers, as determined by the Bee Scan counts of outflying and returning foragers, and the infestation of outflying bees increased significantly over a period of 70 days. A colony with 7.7. higher infestation of outflying foragers lost 2.2. time more bees per flight per day compared to a low infested colony. k) The estimates of mite loss with foragers from mite population per day up to 3.1% exceeds approximately mite mortality of 1% within the colony as represented by counting dead mites on bottom board inserts.
Cold target recoil ion momentum spectroscopy (COLTRIM) has been employed to image the momentum distributions of continuum electrons liberated in the impact of slow He2+ on He and H2. The distributions were measured for fully determined motion of the nuclei that is as a function of the impact parameter and in a well de ned scattering plane The single ionization (SI) of H2 leading to H2+ recoil ions in nondissociative states (He2+ + H+ -> He2+ + H+ + e-) and the transfer ionization (TI) of H2 leading to H2 dissociation into two free protons (He2+ H2 -> He+ + H+ + H+ + e-) were investigated. Similar measurements have been carried out for He target, the corresponding atomic two electron system, i.e. the single ionization (SI) (He2+ + He -> He+ + He2+ e- and the transfer ionization (TI) (He2+ + He -> He+ + He2+ + e-). These measurements have been exploited to understand the results obtained for H target. In comparing the continuum electron momentum distributions for H2 with that for He, a high degree of similarity is observed. In the case of transfer ionization of H2, the electron momentum distributions generated for parallel and perpendicular molecular orientations revealed no orientation dependence. The in scattering plane electron momentum distributions for the transfer ionization of H2 by He2+ and for the transfer ionization of He by He2e showed that the salient feature of these distributions for both collisions systems consists in the appearance of two groups of electrons with difeerent structures. In addition to the group of the saddle electrons forming two jets separated by a valley along the projectile axis we nd a new group of electrons moving with a velocity higher than the projectile velocity These new fast forward electrons result from a narrow range of impact parameters and appear as image saddle in the projectile frame. In contrast to the transfer ionization of He, the fast forward electrons group disappears in the in scattering plane electron momentum distribution generated for the single ionization of He. Instead of this group another new group of electrons appear These electrons exhibit an amount of backscattering These backward elec trons appear as image saddle in the target frame The structures that the saddle electrons show are owing to the quasi molecular nature of the collision process For the TI of H2, the TI of He and the SI of He, a pi-orbital shape of the electron momentum distribution is observed This indicates the importance of the rotational coupling 2-p-theta -> 2p-pi in the initial promotion of the ground state followed by further promotions to the continuum The backward electrons as well as the fast forward electrons are not discussed in the theoretical literature at all. However, a number of obvious indications of the existence of the backward and fast forward electrons could be seen in the experimental works of Abdallah et al. as well as in the theoretical calculations of Sidky et al One might speculate that electrons which are promoted on the saddle for some time during the collision could finally swing around the He+ ion in the way out of the collision, i.e. either around the projectile in the forward direction as in the TI case forming the fast forward electrons or around the recoil ion in the backward direction as in the SI case forming the backward electrons. This might be a result of the strong gradient, and hence the large acceleration of the screened He+ potential.
Alzheimer’s disease (AD) is the most common neurodegenerative disorder world wide, causing presenile dementia and death of millions of people. During AD damage and massive loss of brain cells occur. Alzheimer’s disease is genetically heterogeneous and may therefore represent a common phenotype that results from various genetic and environmental influences and risk factors. In approximately 10% of patients, changes of the genetic information were detected (gene mutations). In these cases, Alzheimer’s disease is inherited as an autosomal dominant trait (familial Alzheimer’s disease, FAD). In rare cases of familial Alzheimer’s disease (about 1-3%), mutations have been detected in genes on chromosomes 14 and 1 (encoding for Presenilin 1 and 2, respectively), and on chromosome 21 encoding for the amyloid precursor protein (APP), which is responsible for the release of the cell-damaging protein amyloid-beta (ß-amyloid, Aß). Familial forms of early-onset Alzheimer’s disease are rare; however, their importance extends far beyond their frequency, because they allow to identify some of the critical pathogenetic pathways of the disease. All familial Alzheimer mutations share a common feature: they lead to an enhanced production of the Aß, which is the major constituent of senile plaques in brains of AD patients. New data indicates that Aß promotes neuronal degeneration. Therefore, one aim of these thesis was to elucidate the neurotoxic biochemical pathways induced by Aß, investigating the effect of the FAD Swedish APP double mutation (APPsw) on oxidative stress-induced cell death mechanisms. This mutation results in a three- to sixfold increased Aß production compared to wild-type APP (APPwt). As cell models, the neuronal PC12 (rat pheochromocytoma) and the HEK (human embryonic kidney 293) cell lines were used, which have been transfected with human wiltyp APP or human APP containing the Swedish double mutation. The used cell models offer two important advantages. First, compared to experiments using high concentrations of Aß at micromolar levels applied extracellularly to cells, PC12 APPsw cells secret low Aß levels similar to the situation in FAD brains. Thus, this cell model represents a very suitable approach to elucidate the AD-specific cell death pathways mimicking physiological conditions. Second, these two cell lines (PC12 and HEK APPwt and APPsw) with different production levels of Aß may additionally allow to study dose-dependent effects of Aß. The here obtained results provide evidence for the enhanced cell vulnerability caused by the Swedish APP mutation and elucidate the cell death mechanism probably initiated by intracellulary produced Aß. Here it seems likely that increased production of Aß at physiological levels primes APPsw PC12 cells to undergo cell death only after additional stress, while chronic high levels in HEK cells already lead to enhanced basal apoptotic levels. Crucial effects of the Swedish APP mutation include the impairments of cellular energy metabolism affecting mitochondrial membrane potential and ATP levels as well as the additional activation of caspase 2, caspase 8 and JNK in response to oxidative stress. Thereby ,the following model can be proposed: PC12 cells harboring the Swedish APP mutation have a reduced energy metabolism compared to APPwt or control cells. However, this effect does not leads to enhanced basal apoptotic levels of cultured cells. An exposure of PC12 cells to oxidative stress leads to mitochondrial dysfunction, e.g., decrease in mitochondrial membrane potential and depletion in ATP. The consequence is the activation of the intrinsic apoptotic pathway releasing cytochrome c and Smac resulting in the activation of caspase 9. This effect is amplified by the overexpression of APP, since both APPsw and APPwt PC12 cells show enhanced cytochrome c and Smac release as well as enhanced caspase 9 activity as vector transfected control. In APPsw PC12 cells a parallel pathway is additionally emphased. Due to reduced ATP levels or enhanced Aß production JNK is activated. Furthermore, the extrinsic apoptotic pathway is enhanced, since caspase 8 and caspase 2 activation was clearly enhanced by the Swedish APP mutation. Both pathways may then converge by activating the effector enzyme, caspase 3, and the execution of cell death. In addition, caspase independent effects also needs to be considered. One possibility could be the implication of AIF since AIF expression was found to be induced by the Swedish APP mutation. In APPsw HEK cells high chronic Aß levels leads to enhanced apoptotic levels, reduce mitochondrial membrane potential and ATP levels even under basal conditions. Summarizing, a hypothetical sequence of events is proposed linking FAD, Aß production, JNK-activation, mitochondrial dysfunction with caspase pathway and neuronal loss for our cell model. The brain has a high metabolic rate and is exposured to gradually rising levels of oxidative stress during life. In Swedish FAD patients the levels of oxidative stress are increased in the temporal inferior cortex. This study using a cell model mimicking the in vivo situation in AD brains indicates that probably both, increased Aß production and the gradual rise of oxidative stress throughout life converge at a final common pathway of an increased vulnerability of neurons to apoptotic cell death from FAD patients. Presenilin (PS) 1 is an aspartyl protease, involved in the gamma-secretase mediated proteolysis of Amyloid-ß-protein (Aß), the major constituent of senile plaques in brains of Alzheimer’s disease (AD) patients. Recent studies have suggested an additional role for presenilin proteins in apoptotic cell death observed in AD. Since PS 1 is proteolytic cleaved by caspase 3, it has been prosposed that the resulting C-terminal fragment of PS1 (PSCas) could play a role in signal transduction during apoptosis. Moreover, it was shown that mutant presenilins causing early-onset of familial Alzheimer's disease (FAD) may render cells vulnerable to apoptosis. The mechanism by which PS1 regulates apoptotic cell death is yet not understood. Therefore one aim of our present study was to clarify the involvement of PS1 in the proteolytic cascade of apoptosis and if the cleavage of PS1 by caspase 3 has an regulatory function. Here it is demonstrated that both, PS1 and PS1Cas lead to a reduced vulnerability of PC12 and Jurkat cells to different apoptotic stimuli. However a mutation at the caspase 3 recognition site (D345A/ PSmut), which inhibits cleavage of PS1 by caspase 3, show no differences in the effect of PS1 or PSCas towards apoptotic stimuli. This suggest that proteolysis of PS1 by caspase 3 is not a determinant, but only a secondary effect during apoptosis. Since several FAD mutation distributed through the whole PS1 gene lead to enhanced apoptosis, an abolishment of the antiapoptotic effect of PS1 might contribute to the massive neurodegeneration in early age of FAD patients. Here, the regulate properties of PS1 in apoptosis may not be through an caspase 3 dependent cleavage and generation of PSCas, but rather through interaction of PS1 with other proteins involved in apoptosis.
The German financial market is often characterized as a bank-based system with strong bank-customer relationships. The corresponding notion of a housebank is closely related to the theoretical idea of relationship lending. It is the objective of this paper to provide a direct comparison between housebanks and "normal" banks as to their credit policy. Therefore, we analyze a new data set, representing a random sample of borrowers drawn from the credit portfolios of five leading German banks over a period of five years. We use credit-file data rather than industry survey data and, thus, focus the analysis on information that is directly related to actual credit decisions. In particular, we use bank-internal borrower rating data to evaluate borrower quality, and the bank's own assessment of its housebank status to control for information-intensive relationships.
This paper reviews the factors that will determine the shape of financial markets under EMU. It argues that financial markets will not be unified by the introduction of the euro. National central banks have a vested interest in preserving local idiosyncracies (e.g. the Wechsels in Germany) and they might be allowed to do so by promoting the use of so-called tier two assets under the common monetary policy. Moreover, a host of national regulations (prudential and fiscal) will make assets expressed in euro imperfect substitutes across borders. Prudential control will also continue to be handled differently from country to country. In the long run these national idiosyncracies cannot survive competitive pressures in the euro area. The year 1999 will thus see the beginning of a process of unification of financial markets that will be irresistible in the long run, but might still take some time to complete.
In this paper we analyze the relation between fund performance and market share. Using three performance measures we first establish that significant differences in the risk-adjusted returns of the funds in the sample exist. Thus, investors may react to past fund performance when making their investment decisions. We estimated a model relating past performance to changes in market share and found that past performance has a significant positive effect on market share. The results of a specification test indicate that investors react to risk-adjusted returns rather than to raw returns. This suggests that investors may be more sophisticated than is often assumed.
From the mid-seventies on, the central banks of most major industrial countries switched to monetary targeting. The Bundesbank was the first central bank to take this step, making the switch at the end of 1974. This changeover to monetary targeting was due to the difficulties which the Bundesbank - like other central banks - was facing in pursuing its original strategy, and whichcame to a head in the early seventies, when inflation escalated. A second factor was the collapse of the Bretton Woods system of fixed exchange rates, which created the necessary scope for national monetary targeting. Finally, the advance of monetarist ideas fostered the explicit turn towards monetary targets, although the Bundesbank did not implement these in a mechanistic way. Whereas the Bundesbank has adhered to its policy of monetary targeting up to the present, nowadays monetary targeting plays only a minor role worldwide. Many central banks have switched to the strategy of direct inflation targeting. Others favour a more discretionary approach or a policy which is geared to the exchange rate. In the academic debate, monetary targeting is often presented as an outdated approach which has long since lost its basis of stable money demand. These findings give riseto a number of questions: Has monetary targeting actually become outdated? Which role is played by the concrete design of this strategy, and, against this background, how easily can it be transferred to European monetary union? This paper aims to answer these questions, drawing on the particular experience which the Bundesbank has gained of monetary targeting. It seems appropriate to discuss monetary targeting by using a specific example, since this notion is not very precise. This applies, for example, to the money definition used, the way the target is derived, the stringency applied in pursuing the target and the monetary management procedure.
In this speech (given at the CFSresearch conference on the Implementation of Price Stability held at the Bundesbank Frankfurt am Main, 10. - 12. Sept 1998), John Vickers discusses theoretical and practical issues relating to inflation targeting as used in the United Kingdom doing the past six years. After outlining the role of the Bank s Monetary Policy Committee, he considers the Committee s task from a theoretical perspective, beforediscussing the concept and measurement of domestically generated inflation.
Credit Unions are cooperative financial institutions specializing in the basic financial needs of certain groups of consumers. A distinguishing feature of credit unions is the legal requirement that members share a common bond. This organizing principle recently became the focus of national attention as the Supreme Court and the U.S. Congress took opposite sides in a controversy regarding the number of common bonds that could co-exist within the membership of a single credit union. Despite its importance, little research has been done into how common bonds affect how credit unions actually operate. We frame the issues with a simple theoretical model of credit-union formation and consolidation. To provide intuition into the flexibility of multiple-group credit unions in serving members, we simulate the model and present some comparative-static results. We then apply a semi-parametric empirical model to a large dataset drawn from federally chartered occupational credit unions in 1996 to investigate the effects of common bonds. Our results suggest that credit unions with multiple common bonds have higher participation rates than credit unions that are otherwise similar but whose membership shares a single common bond.