Exp Brain Res (2003) 152:221–228 DOI 10.1007/s00221-003-1545-y RESEARCH ARTICLE Yuliya A. Dahlem · Markus A. Dahlem · Thomas Mair · Katharina Braun · Stefan C. Müller Extracellular potassium alters frequency and profile of retinal spreading depression waves Received: 1 October 2002 / Accepted: 14 May 2003 / Published online: 23 July 2003  Springer-Verlag 2003 Abstract The phenomenon of spreading depression (SD) was observed in chicken retina by means of optical registration via a microscope and a CCD camera applying modern methods of image processing for optimized evaluation of the wave profiles. The propagation dynam- ics of SD waves was investigated as a function of extracellular potassium. Two main findings were ob- tained. Firstly, the frequency of spontaneous wave generation increased with the increase of K + concentra- tion. Secondly, there was an effect of potassium on the wave profile. In particular, the recovery zone of SD waves was shortened at increased K + . This effect was not only due to the dispersion relation of waves in excitable media as shown by the result of the mechanically induced wave trains. Applying the basic principles of chemical excit- ability for the interpretation of the data led us to the conclusion that these potassium effects are due to perturbations of an autocatalytic reaction to be further explored. Keywords Excitability · Refractory period · Intrinsic optical signal · Chicken Introduction Spreading depression (SD) is a wave phenomenon that propagates in gray matter of nervous tissue with a velocity of 2–5 mm/min (Le¼o 1944; BureÐ et al. 1984). Its spread involves a large number of cellular processes. Among them is a nearly total depolarization of the neurons and glia cells caused by a drastic ion redistribu- tion between extra- and intracellular compartments (Somjen and Aitken 1984). These changes are accompa- nied by cellular swelling and by the block of action potentials in a sizable population of brain cells (for review see Somjen et al. 1992; Parsons 1998; Somjen 2001). SD waves have been linked to the pathophysiology of the migraine aura (Lauritzen 1994; Bolay et al. 2002) and may produce an expansion of a neuronal lesion after ischemic stroke (Hossman 1996). A simplified model of a reaction-transport mechanism of SD is as follows: an initial excess of a so-called activator in the extracellular space (ECS) causes a super- threshold depolarization of the cell membrane, which leads to an autocatalytic release of the activator. Possible activators are potassium (Grafstein 1956) or glutamate (van Harreveld 1978). In both cases, intracellular K + is released into the ECS. This autocatalytic rise in the extracellular potassium concentration ([K + ] o ) is partially cleared by active uptake, extracellular diffusion, and a redistribution of K + through the network of glial cells. If sufficient K + is transported to neighboring cell groups, then the same excitation cycle is initiated there and a wave of excitation spreads via reaction-diffusion coupling through the neuronal tissue followed by a prolonged depression of neuronal activity. Spreading depression is the only phenomenon known where K + rises from its resting level of 3 mM much above the normally well- preserved ceiling level of 10 mM (Heinemann and Lux 1977) up to an extracellular concentration as high as 50 mM (Sugaya et al. 1975). Note that throughout this article we refer to 10 mM K + as the ceiling level, even though during SD this level is actually overshot. Y. A. Dahlem · M. A. Dahlem · T. Mair · S. C. Müller Institut für Experimentelle Physik, Abteilung Biophysik, Otto-von-Guericke-Universität Magdeburg, Universitätsplatz 2, 39016 Magdeburg, Germany K. Braun Institut für Biologie, Abteilung Entwicklungsbiologie, Otto-von-Guericke-Universität Magdeburg, Brenneckestraße 6, 39118 Magdeburg, Germany Y. A. Dahlem ( ) ) Medizinische Fakultät, Institut für Medizinische Neurobiologie, Otto-von-Guericke-Universität Magdeburg, Leipziger Straße 44, 39120 Magdeburg, Germany e-mail: yuliya.dahlem@medizin.uni-magdeburg.de Tel.: +49-391-6714368 Fax: +49-391-6714365