The present book is the outcome of a symposium on cal- cium electrogenesis and neuronal functioning, held in January 1985 in the Ringberg Castle of the Max Planck Society, located at the Tegernsee in Bavaria. People from various fields in the neurosciences came together in order to discuss the physiological characteris- tics of calcium currents in nerve cells and the implications for an improved understanding of the physiology and pathophysiology of the central nervous system. The chap- ters deal with the physical and pharmacological properties of calcium currents, the role of calcium in neurotransmis- sion and secretion, aspects of neuroplasticity, epilepsy, and their behavioral implications. The 60th anniversary of Hans Dieter Lux served as the occasion to gather a substantial number of his colleagues to one of the most fascinating fields in present neuroscience. We felt that this was the appropriate way to honour Hans Dieter Lux for his impor- tant contributions to our understanding of the central nerv- ous system. We gratefully acknowledge the support of the Volkswagen-Stiftung, the German EEG Society, and the Max Planck Society for their support of the symposium. We also wish to express our gratitude to the following com- panies for sponsoring this volume: Fa. List Elektronik, Darmstadt; Fa. Zeiss, Oberkochen; Fa. Sandoz, Basel; Fa. Janssen, Neuss; Fa. Bayer, Leverkusen; Fa. Knoll, Ludwigs- hafen; Fa. Merck, Darmstadt. The editors gratefully acknowledge the support of the Springer-Verlag in editing this book, and the expert secre- tarial assistance of G. Trinkel, U. Roessler, and B.

This volume is based on an advanced course on epileptogenic and excitotoxic mechanisms with emphasis on development. Information on partial and generalised epileptogenesis, derived from different experimental models, is comprehensively reviewed. Special sections are devoted to anatomical, biochemical and functional aspects of the maturing brain and to their interaction with epileptogenic agents. Several seizure-related factors, for example an intracellular rise of calcium, can lead to excitotoxic cellular damage. Despite some protective mechanisms, this risk is particularly worrying in the immature brain due to the over-expression and facilitation of NMDA receptors, the depolarising effect of GAGA and the immaturity of ionic homoeostasis. Seizures in early developmental stages can thus result in permanent defects and epileptic sequelae. Our present understanding of basic mechanisms of the epilepsies allows pharmacologists to design new drugs with specific pharmacological action targeted on crucial epileptogenic factors. These results, together with those of developmental studies of excitotoxicity, provide a basis for new therapeutic strategies aimed at preventing the development of severe infantile epileptic encephalopathies and at alleviating their dramatic consequences. The authors have combined their personal experience with a comprehensive review of the literature, providing the reader, either scientist or clinician, with an updated and exhaustive account of every topic.