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.

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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.

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