Spreading depression (SD) waves in the brainstem can be elicited after blockade of potassium channels – evidence for the role of extracellular potassium ions as a driving force?

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S438-S438
Author(s):  
Frank Richter ◽  
Alfred Lehmenkühler ◽  
Hans-Georg Schaible
Author(s):  
Tina Hu

Cortical spreading depression (CSD), a phenomenon underlying stroke and head trauma, involves the depolarization of neurons in one localized area that rapidly propagates to and depolarizes surrounding cells. CSD is characterized by a sudden increased concentration of extracellular potassium ions (K+), which is also generated by cellular stressors like anoxia. The purpose of this study is to examine the role of biogenic amines in the time to succumb and time to recover from anoxic coma in Locusta migratoria, a locust which is regularly exposed to anoxia in its natural environment and survive by entering a reversible coma (a spreading‐depression like event). Locusts were first immersed in water for 30 minutes and the time to succumb, ventilate, and stand upright were measured. There were 5 treatment groups with each one paired to a control group using saline injections: 1) octopamine (OA) and its antagonist epinastine (EP), 2) dopamine (DA) and its antagonist haloperidol, 3) serotonin (5‐HT) and its antagonist mianserin, 4) tyramine (TA) and its antagonist yohimbine, and 5) histamine (HA) and its antagonist pyrilamine maleate salt. Results indicated that EP‐injected locusts took significantly longer to succumb, ventilate, and stand upright compared to controls. Mianserin‐injected locusts also took significantly longer to succumb, ventilate, and stand upright.


1999 ◽  
Vol 82 (4) ◽  
pp. 1728-1739 ◽  
Author(s):  
Nikita G. Grigoriev ◽  
J. David Spafford ◽  
Andrew N. Spencer

The amplitude of an A-like potassium current ( I Kfast) in identified cultured motor neurons isolated from the jellyfish Polyorchis penicillatus was found to be strongly modulated by extracellular potassium ([K+]out). When expressed in Xenopus oocytes, two jellyfish Shaker-like genes, jShak1 and jShak2, coding for potassium channels, exhibited similar modulation by [K+]out over a range of concentrations from 0 to 100 mM. jShak2-encoded channels also showed a decreased rate of inactivation and an increased rate of recovery from inactivation at high [K+]out. Using site-directed mutagenesis we show that inactivation of jShak2 can be ascribed to an unusual combination of a weak “implicit” N-type inactivation mechanism and a strong, fast, potassium-sensitive C-type mechanism. Interaction between the two forms of inactivation is responsible for the potassium dependence of cumulative inactivation. Inactivation of jShak1 was determined primarily by a strong “ball and chain” mechanism similar to fruit fly Shaker channels. Experiments using fast perfusion of outside-out patches with jShak2 channels were used to establish that the effects of [K+]out on the peak current amplitude and inactivation were due to processes occurring at either different sites located at the external channel mouth with different retention times for potassium ions, or at the same site(s) where retention time is determined by state-dependent conformations of the channel protein. The possible physiological implications of potassium sensitivity of high-threshold potassium A-like currents is discussed.


2015 ◽  
Vol 114 (6) ◽  
pp. 3111-3120 ◽  
Author(s):  
Kristin E. Spong ◽  
Brittany Chin ◽  
Kelsey L. M. Witiuk ◽  
R. Meldrum Robertson

Progressive accumulation of extracellular potassium ions can trigger propagating waves of spreading depression (SD), which are associated with dramatic increases in extracellular potassium levels ([K+]o) and arrest in neural activity. In the central nervous system the restricted nature of the extracellular compartment creates an environment that is vulnerable to disturbances in ionic homeostasis. Here we investigate how changes in the size of the extracellular space induced by alterations in extracellular osmolarity affect locust SD. We found that hypotonic exposure increased susceptibility to experimentally induced SD evidenced by a decrease in the latency to onset and period between individual events. Hypertonic exposure was observed to delay the onset of SD or prevent the occurrence altogether. Additionally, the magnitude of extracellular K+ concentration ([K+]o) disturbance during individual SD events was significantly greater and they were observed to propagate more quickly under hypotonic conditions compared with hypertonic conditions. Our results are consistent with a conclusion that hypotonic exposure reduced the size of the extracellular compartment by causing cell swelling and thus facilitated the accumulation of K+ ions. Lastly, we found that pharmacologically reducing the accumulation of extracellular K+ using the K+ channel blocker tetraethylammonium slowed the rate of SD propagation while increasing [K+]o through inhibition of the Na-K-2Cl cotransporter increased propagation rates. Overall our findings indicate that treatments or conditions that act to reduce the accumulation of extracellular K+ help to protect against the development of SD and attenuate the spread of ionic disturbance adding to the evidence that diffusion of K+ is a leading event during locust SD.


1986 ◽  
Vol 56 (2) ◽  
pp. 424-438 ◽  
Author(s):  
Y. Yaari ◽  
A. Konnerth ◽  
U. Heinemann

The role of extracellular K+ (K+o) in nonsynaptic epileptogenesis induced in the CA1 area of rat hippocampal slices by lowering [Ca2]o was studied with K+-selective microelectrodes (KSMs). Extracellular field potentials and [K+]o were recorded simultaneously with 1-2 KSMs in the CA1 stratum pyramidale. In slices perfused with an oxygenated standard physiological solution (containing 2 mM Ca2+), base-line [K+]o was stable for several hours. The washout of Ca2+o was accompanied by a gradual tonic rise of [K+]o. Spontaneous and stimulus-evoked maximal seizurelike events (SLEs) appeared when [K+]o was approximately 0.5 mM above the initial 5 mM base line. These changes were reversible in normal medium. When K+o was pressure ejected in the CA1 stratum pyramidale of spontaneously active slices, a local rise in [K+]o of approximately 0.5 mM was necessary to trigger a SLE. A similar apparent [K+]o "threshold" was associated with SLEs evoked by electrical stimulation. Increasing [K+] in the perfusing solution by small increments (1 mM) markedly enhanced SLEs frequency and velocity of spread and decreased the period of absolute refractoriness that succeeded each paroxysm. Similar changes occurred during periods of transient hypoxia. Small [K+] decreases in the perfusate had the converse effects. Spontaneous SLEs were associated with phasic increases in [K+]o. In simultaneous [K+]o recordings from two layers, these transients were largest (up to 3.5 mM above base line) and rose more steeply at the stratum pyramidale. Toward the outer dendritic layers they became smaller, slower in time course, and delayed in onset. We conclude that the main source for these [K+]o transients are the hippocampal pyramidal cell bodies, which discharge intensely during a SLE, and that excess K+o is spatially dispersed around the discharge zone of the paroxysm. [K+]o continued to rise, though at a slower rate, throughout the course of a SLE. Following SLE termination, [K+]o decayed slowly to base line. The invasion of a CA1 region by a propagating SLE was preceded quite often by a slow rise in [K+]o. A sudden transition to a steeply rising [K+]o marked the explosive recruitment of this region into the discharge zone of the spreading paroxysm. The total (tonic and phasic) increase in [K+]o during SLEs did not surpass a maximal level of approximately 9 mM, which was the ceiling level of [K+]o in low [Ca2+]o. However, when spreading depression occurred, [K+]o rose up to 30-40 mM for several minutes. Spreading depression rarely appeared spontaneously despite the recurrence of SLEs, but could be provoked by repetitive electrical stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)


2009 ◽  
Vol 258 (2) ◽  
pp. 219-228 ◽  
Author(s):  
Gerson Florence ◽  
Markus A. Dahlem ◽  
Antônio-Carlos G. Almeida ◽  
José W.M. Bassani ◽  
Jürgen Kurths

2006 ◽  
pp. 20-37 ◽  
Author(s):  
M. Ershov

The economic growth, which is underway in Russia, raises new questions to be addressed. How to improve the quality of growth, increasing the role of new competitive sectors and transforming them into the driving force of growth? How can progressive structural changes be implemented without hampering the rate of growth in general? What are the main external and internal risks, which may undermine positive trends of development? The author looks upon financial, monetary and foreign exchange aspects of the problem and comes up with some suggestions on how to make growth more competitive and sustainable.


2011 ◽  
Vol 162 (7) ◽  
pp. 209-215
Author(s):  
Jean-François Métraux

In the years since 2000, the authorities in charge of forests in canton Vaud have made some substantial changes as a reaction to the political decisions arising from the Swiss Forest Programme and the projected revision of the Federal forestry Law, as well as to the deterioration of the economic situation in forestry enterprises. This article gives a survey of the directions taken. Thus the canton recognises the primordial role of wood production as a driving force behind the creation of a multifunctional forest. The Service for Forests, Wildlife and Nature has invested a great deal in planning, and has redefined the management plan to be an instrument intended for forest owners and forest managers. The canton has innovated by introducing forestry groups and a scheme of equalisation of forestry costs between communes. Hence the conception of forestry management in canton Vaud is resolutely that of a multifunctional natural heritage.


Author(s):  
Andrea Harris

The Conclusion briefly examines the current state of the New York City Ballet under the auspices of industrial billionaire David H. Koch at Lincoln Center. In so doing, it to introduces a series of questions, warranting still more exploration, about the rapid and profound evolution of the structure, funding, and role of the arts in America through the course of the twentieth century. It revisits the historiographical problem that drives Making Ballet American: the narrative that George Balanchine was the sole creative genius who finally created an “American” ballet. In contrast to that hagiography, the Conclusion reiterates the book’s major contribution: illuminating the historical construction of our received idea of American neoclassical ballet within a specific set of social, political, and cultural circumstances. The Conclusion stresses that the history of American neoclassicism must be seen as a complex narrative involving several authors and discourses and crossing national and disciplinary borders: a history in which Balanchine was not the driving force, but rather the outcome.


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