Governance in contemporary Germany:the semisovereign State revisited

Throughout the 1970s and 1980s, West Germany was considered to be one of the world’s most successful economic and political systems. In his seminal 1987 analysis of West Germany’s ‘semisovereign’ system of governance, Peter Katzenstein attributed this success to a combination of a fragmented polity, consensus politics and incremental policy changes. However, unification in 1990 has both changed Germany’s institutional configuration and created economic and social challenges on a huge scale. This volume therefore asks whether semisovereignty still exists in contemporary Germany and, crucially, whether it remains an asset in terms of addressing these challenges. By shadowing and building on the original study, an eminent team of British, German and American scholars analyses institutional changes and the resulting policy developments in key sectors, with Peter Katzenstein himself providing the conclusion. Together, the chapters provide a landmark assessment of the outcomes produced by one of the world’s most important countries. Contents: 1. Introduction: semisovereignty challenged Simon Green and William E. Paterson; 2. Institutional transfer: can semisovereignty be transferred? The political economy of Eastern Germany Wade Jacoby; 3. Political parties Thomas Saalfeld; 4. Federalism: the new territorialism Charlie Jeffery; 5. Shock-absorbers under stress. Parapublic institutions and the double challenges of German unification and European integration Andreas Busch; 6. Economic policy management: catastrophic equilibrium, tipping points and crisis interventions Kenneth Dyson; 7. Industrial relations: from state weakness as strength to state weakness as weakness. Welfare corporatism and the private use of the public interest Wolfgang Streeck; 8. Social policy: crisis and transformation Roland Czada; 9. Immigration and integration policy: between incrementalism and non-decisions Simon Green; 10. Environmental policy: the law of diminishing returns? Charles Lees; 11. Administrative reform Kluas H. Goetz; 12. European policy-making: between associated sovereignty and semisovereignty William E. Paterson; 13. Conclusion: semisovereignty in United Germany Peter J. Katzenstein.

On the mechanisms of cerebellar synaptic plasticity

Changes in the strength of signalling between neurones are thought to provide a cellular substrate for learning and memory. In the cerebellar cortex, raising the frequency and the strength of parallel fibre (PF) stimulation leads to a long-term depression (LTD) of the strength of signalling at the synapse between PFs and Purkinje cells (PCs), which spreads to distant synapses to the same cell via a nitric oxide (NO) dependent mechanism. At the same synapse, but under conditions of reduced post-synaptic calcium activity, raised frequency stimulation (RFS) of PFs triggers a long-term potentiation of synaptic transmission. The aims of the work described in this thesis were to investigate the conditions necessary for LTD and LTP at this synapse following RFS and to identify the origins and second messenger cascades involved in the induction and spread of LTP and LTD. In thin, parasagittal cerebellar slices whole cell patch clamp recordings were made from PCs and the effects of RFS of one of two, independent PF inputs to the same PC were examined under a range of experimental conditions. Under conditions designed to reduce post-synaptic calcium activity, RFS to a single PF input led to LTP and a decreases in paired pulse facilitation (PPF) in both pathways. This heterosynaptic potentiation was prevented by inhibition of protein kinase A (PKA) or by inhibition of NO synthase with either 7-nitroindazole (7-NI) or NG Nitro-L-argenine methyl ester. Inhibition of guanylate cyclase (GC) or protein kinase G (PKG) had no effect. A similar potentiation was observed upon application of the adenylyl cyclase (AC) activator forskolin or the NO donor spermine NONOate. Both of these treatments also resulted in an increase in the frequency of mEPSCs, which provides further evidence for a presynaptic origin of LTP. Forskolin induced potentiation and the increase in mEPSC frequency were blocked by 7-NI. The styryl dye FM1-43, a fluorescent reporter of endo- and exocytosis, was also used to further examine the possible pre-synaptic origins of LTP. RFS or forskolin application enhanced FM1-43 de-staining and NOS inhibitors blocked this effect. Application of NONOate also enhanced FM1-43 de-staining. When post-synaptic calcium activity was less strictly buffered, RFS to a single PF input led to a transient potentiation that was succeeded by LTD in both pathways. This LTD, which resembled previously described forms, was prevented by inhibition of the NO/cGMP/PKG cascade. Modification of the AC/cAMP/PKA cascade had no effect. In summary, the direction of synaptic plasticity at the PF-PC synapse in response to RFS depends largely on the level of post-synaptic calcium activity. LTP and LTD were non-input specific and both forms of plasticity were dependent on NOS activity. Induction of LTP was mediated by a presynaptic mechanism and depended on NO and cAMP production. LTD on the other hand was a post-synaptic process and required activity of the NO/cGMP/PKG signalling cascade.