Adenosine modulates synaptic transmission by acting on inhibitory A(1) and facilitatory A(2A) receptors, the densities of which are modified in aged animals. We investigated how A(2A) receptor activation influences A(1) receptor function and whether this interaction is modified in aged rats. In hippocampal and cortical nerve terminals from young adult (6 wk), but not old rats (24 mo), the A(2A) receptor agonist, 2-[4-(2-carboxyethyl) phenethylamino]-5'-N-ethylcarboxamidoadenosine (CGS 21680; 30 nM) decreased the binding affinity of a selective A(1) receptor agonist, cyclopentyladenosine (CPA), an effect prevented by the A(2A) antagonist, (4-(2-[7-amino-2-(2-furyl (1,2,4)-triazolo(2,3-a (1,3,5)triazin-5-yl-aminoethyl)phenol (ZM 241385, 20 nM). This effect of CGS 21680 required intact nerve terminals and was also observed in the absence of Ca(2+). This A(2A)-induced "desensitization" of A(1) receptors was prevented by the protein kinase C inhibitor, chelerythrine (6 microM), and was not detected in the presence of the protein kinase C activator, phorbol-12,13-didecanoate (250 nM), which itself caused a reduction in binding affinity for CPA. The protein kinase A inhibitor, N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (10 microM), and the protein kinase A activator, 8-Br-cAMP (1 mM), had no effects on the A(2A)-induced A(1) receptor desensitization. This A(2A)-induced A(1) receptor desensitization had a functional correlation because CGS 21680 (10 nM) attenuated by 40% the inhibition caused by CPA (10 nM) on CA1 area population spike amplitude in hippocampal slices. This A(2A)/A(1) interaction may explain the attenuation by adenosine deaminase (2 U/ml), which removes tonic A(1) inhibition, of the facilitatory effect of CGS 21680 on synaptic transmission. The requirement of tonic A(1) receptor activation for CGS 21680 to induce facilitation of synaptic transmission was reinforced by the observation that the A(1) receptor antagonist, 1, 3-dipropyl-8-cyclopentylxanthine (20 nM) prevented CGS 21680 (10 nM) facilitation of population spike amplitude. The present results show the ability of A(2A) receptors to control A(1) receptor function in a manner mediated by protein kinase C, but not protein kinase A, in young adult but not in aged rats.
PurposeTo explore the contributions made by two strands of institutional research that have been applied to the study of management accounting change: “old institutional economics” and “new institutional sociology”. To propose ways of developing these theories, and in general to develop an institutional understanding of management accounting change.Design/methodology/approachAnalysis of the literature on management accounting change, with a special emphasis on the literature drawing on institutional theory. Theoretical discussion based on the concept of the “circuits of power”. Illustration with observations made during a case study of an organisation in which attempts to promote change in management accounting were conducted in recent years.FindingsIdentification of some complementarities between these two strands of institutional theorising, and suggestions of how they can be developed by drawing on insights from the “circuits of power” framework.Research limitations/implicationsThe case study analysis is limited to an illustration of the theoretical discussion. A building of bridges between the various developments in institutional approaches to management accounting change is necessary.Originality/valueThe paper is of value to researchers studying management accounting change. It clarifies the theoretical underpinnings of the institutional frameworks and suggests areas for institutional research into management accounting change.
Kainate receptors are a subtype of ionotropic glutamate receptors, permeable to cations and thus expected to have an excitatory depolarizing action on neurons. However, kainate receptor activation inhibits ␥-aminobutyric acid release in the hippocampus through activation of protein kinase C in a pertussis toxin-dependent manner, suggesting a coupling of kainate receptors to G proteins. Thus, we directly investigated the G protein coupling of kainate receptors in the rat hippocampus by using a selective kainate receptor agonist, [ 3
Purpose – The purpose of this paper is to discuss and analyse how intellectual capital (IC) is created and deteriorated in a meta-organization by assessing the interdependency between the collective IC of the meta-organization and the individual IC of its members. Design/methodology/approach – A case study conducted in a seaport is adopted to explore how creation or deterioration of IC at one level of analysis affects the IC at the other. Four different illustrations are provided, depicting different instances of articulation between both types of IC. Findings – Evidence suggests that, in a meta-organization, IC appears as a function of both individual and collective IC dimensions. Changes in the meta-organization’s IC or in its members’ IC may have different impacts on each other, generating intellectual assets or intellectual liabilities at both levels. Evidence also suggests that those changes in IC should be analysed in a longitudinal way, since both levels affect each other in different ways over time. Research limitations/implications – Despite the validity of the interpretations provided in the context of the case study, generalization to other situations should be conducted only in a theoretically framed manner. Practical implications – This study provides important strategic and managerial implications for meta-organizations and their members, who are concerned with their performance. Originality/value – Although there have been some efforts to apply the traditional IC methodologies to a bigger scope, such as regions or nations, some meso level empirical contexts are yet far unexplored, such as the case of meta-organizations. Furthermore there is a gap in management sciences’ research on seaports.
Adenosine modulates long-term synaptic plasticity. Application of adenosine A 1 receptor agonists attenuates long-term potentiation (LTP) in the hippocampus. Endogenous adenosine exerts a tonic inhibitory effect on LTP, since A 1 receptor antagonists consistently facilitate LTP. Adenosine also modulates the reciprocal phenomenon of synaptic plasticity, long-term depression (LTD), and depotentiation in a way that depends on the specific induction protocol. Application of adenosine A 2A receptor agonists can facilitate LTP, but the role of endogenous adenosine mediated through A 2A receptors in the modulation of synaptic plasticity is still the subject of controversy. The effects of adenosine on synaptic plasticity mediated through A 3 receptors have been described. In accordance with the notion that synaptic plasticity is the basis for learning and memory in different brain areas, adenosine correspondingly modulates behavior in various learning and memory paradigms. The effects of adenosine on synaptic plasticity should be relevant for the enhancement of intellectual performance related to caffeine intake. Adenosinergic compounds might prove helpful in the treatment of memory disorders. Drug Dev. Res. 52:283-290, 2001.
Purpose The purpose of this paper is to examine differences in corporate social responsibility (CSR) reporting on the websites of football clubs based in five European countries with different levels of football corporatisation. Design/methodology/approach The study examines CSR reporting on the internet by football clubs based in five European countries. Multiple regression analysis is used to analyse some factors which influence reporting and test a set of hypotheses. Findings The findings suggest that clubs from countries in which the level of corporatisation is higher disclose more CSR information. Also, clubs with higher public visibility disclose a higher variety of CSR information. Originality/value This study adds to the scarce research on CSR reporting in professional sports leagues by providing new empirical data and by extending prior research comparing such practices within different international frameworks of CSR.
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