scholarly journals Cell swelling increases the severity of spreading depression in Locusta migratoria

2015 ◽  
Vol 114 (6) ◽  
pp. 3111-3120 ◽  
Author(s):  
Kristin E. Spong ◽  
Brittany Chin ◽  
Kelsey L. M. Witiuk ◽  
R. Meldrum Robertson
Keyword(s):  
Spreading Depression ◽  
Locusta Migratoria ◽  
Cell Swelling ◽  
Extracellular Potassium ◽  
Potassium Ions ◽  
Extracellular Compartment ◽  
Propagating Waves ◽  
The Central Nervous System ◽  
Progressive Accumulation ◽  
Increased Susceptibility

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.

Aminergic Regulation of Anoxic Coma in Locusta migratoria

2016 ◽  
Author(s):  
Tina Hu
Keyword(s):  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Locusta Migratoria ◽  
Control Group ◽  
Extracellular Potassium ◽  
Potassium Ions ◽  
Treatment Groups ◽  
Anoxic Coma ◽  
Cellular Stressors

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.

Central nervous tissue: an excitable medium. A study using the retinal spreading depression as a tool

2007 ◽  
Vol 366 (1864) ◽  
pp. 359-368 ◽  
Author(s):  
Wolfgang Hanke ◽  
Vera Maura Fernandes de Lima
Keyword(s):  
Spreading Depression ◽  
Imaging Techniques ◽  
Optical Signal ◽  
Excitable Medium ◽  
Physical Parameters ◽  
Neuronal Tissue ◽  
Retinal Tissue ◽  
Propagating Waves ◽  
The Central Nervous System ◽  
External Forces

According to its physicochemical properties, neuronal tissue, including the central nervous system (CNS) and thus the human brain, is an excitable medium, which consequently exhibits, among other things, self-organization, pattern formation and propagating waves. Furthermore, such systems can be controlled by weak external forces. The spreading depression (SD), a propagating wave of excitation–depression, is such an event, which is additionally linked to a variety of medically important situations, classical migraine being just one example. Especially in retinal tissue, a true part of the CNS, the SD can be observed very easily with the naked eye and by video imaging techniques due to its big intrinsic optical signal. We have investigated the retinal SD and its control by external physical parameters such as gravity and temperature. Beyond this, especially due to its medical relevance, the control of CNS excitability by pharmacological tools is of specific interest, and we have studied this question in detail using the retinal SD as an experimental tool to collect information about the control of CNS tissue excitability.

Sodium and Potassium Fluxes in the Abdominal Nerve Cord of the Cockroach, Periplaneta Americana L

1961 ◽  
Vol 38 (2) ◽  
pp. 315-322
Author(s):  
J. E. TREHERNE
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nerve Cord ◽  
Periplaneta Americana ◽  
Unit Area ◽  
Potassium Ions ◽  
Sodium Ions ◽  
Nerve Sheath ◽  
The Central Nervous System ◽  
Sodium And Potassium

1. The influx of sodium and potassium ions into the central nervous system of Periplaneta americana has been studied by measuring the increase in radioactivity within the abdominal nerve cord following the injection of 24NA and 42K. into the haemolymph. 2. The calculated influx of sodium ions was approximately 320 mM./l. of nerve cord water/hr. and of potassium ions was 312 mM./l. of nerve cord water/hr. These values are very approximately equivalent to an influx per unit area of nerve cord surface of 13.9 x 10-2 M cm. -2 sec.-1 for sodium and 13.5 x 10-12 M cm. -2 sec.-1 for potassium ions. 3. The relatively rapid influxes of these ions are discussed in relation to the postulated function of the nerve sheath as a diffusion barrier. It is suggested that a dynamic steady state rather than a static impermeability must exist across the sheath surrounding the central nervous system in this insect.

The Neurone and Its Response to Peripheral Nerve Compression

1990 ◽  
Vol 15 (1) ◽  
pp. 5-10
Author(s):  
L. B. DAHLIN ◽  
G. LUNDBORG
Keyword(s):  
Central Nervous System ◽  
Peripheral Nerve ◽  
Peripheral Nerve Injury ◽  
Nerve Cell Body ◽  
Trauma Studies ◽  
Target Tissue ◽  
The Central Nervous System ◽  
Double Crush ◽  
Double Crush Syndrome ◽  
Increased Susceptibility

In all types of peripheral nerve injury, it is important to realize that the lesion affects one extended cell, the neurone, which extends from the central nervous system down to the target tissue in the extremity. Compression of a peripheral nerve can disturb the intraneural transport (axonal transport) of a large variety of substances. This may be followed by morphological and biochemical changes in the nerve cell body. These central changes may effect the axon as a whole and confer on the nerve an increased susceptibility to trauma. Studies concerning the reaction of neurones to compression, relevant when discussing the double crush syndrome, are reviewed.

Brain Respiration and Glycolysis in Cardiazol Convulsions

1940 ◽  
Vol 86 (361) ◽  
pp. 276-280 ◽  
Author(s):  
Leslie Dundonald MacLeod ◽  
Max Reiss
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Direct Action ◽  
Reducing Power ◽  
Liver Glycogen ◽  
Potassium Ions ◽  
Blood Picture ◽  
The Central Nervous System ◽  
Respiratory Centre ◽  
Convulsant Effect

Since Hildebrandt (1926) described the convulsant effect of cardiazol injection, several studies have been carried out on the mechanism of such convulsions. Zung and Tremonti (1931) suggested a direct action on the respiratory centre when cardiazol is used as a stimulant; Kerr and Antaki (1937) found no effect on brain glycogen or phosphocreatine in cardiazol-induced convulsions; Hashimoto (1937) found differences in distribution of calcium and potassium ions in the central nervous system after cardiazol. Goodwin and Lloyd (1938) recorded a direct effect on brain potential changes as shown on oscillographic records. Leibel and Hall (1938) found a large (75 per cent.) diminution of cerebral blood-flow at the onset of cardiazol convulsions. Weigand (1938) found no effect on liver glycogen or vitamin A content, reducing power of suprarenal cortex or blood picture. Denyssen and Watterson (1938) and Watterson and Macdonald (1939) attribute the convulsions to action on the vasomotor centre and note the action of vasodilator drugs in inhibiting convulsions. Wortis (1938) quoted by Quastel (1939) found no effect on brain respiration.

scholarly journals Astrocyte-Selective Volume Increase in Elevated Extracellular Potassium Conditions Is Mediated by the Na+/K+ ATPase and Occurs Independently of Aquaporin 4

ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142096715
Author(s):  
Erin Walch ◽  
Thomas R. Murphy ◽  
Nicholas Cuvelier ◽  
Murad Aldoghmi ◽  
Cristine Morozova ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Water Movement ◽  
Barium Chloride ◽  
Neuronal Firing ◽  
Aquaporin 4 ◽  
Stratum Radiatum ◽  
Cell Swelling ◽  
Extracellular Potassium ◽  
Atpase Inhibitor ◽  
Extracellular Potassium Concentration

Astrocytes and neurons have been shown to swell across a variety of different conditions, including increases in extracellular potassium concentration (^[K+]o). The mechanisms involved in the coupling of K+ influx to water movement into cells leading to cell swelling are not well understood and remain controversial. Here, we set out to determine the effects of ^[K+]o on rapid volume responses of hippocampal CA1 pyramidal neurons and stratum radiatum astrocytes using real-time confocal volume imaging. First, we found that elevating [K+]o within a physiological range (to 6.5 mM and 10.5 mM from a baseline of 2.5 mM), and even up to pathological levels (26 mM), produced dose-dependent increases in astrocyte volume, with absolutely no effect on neuronal volume. In the absence of compensating for addition of KCl by removal of an equal amount of NaCl, neurons actually shrank in ^[K+]o, while astrocytes continued to exhibit rapid volume increases. Astrocyte swelling in ^[K+]o was not dependent on neuronal firing, aquaporin 4, the inwardly rectifying potassium channel Kir 4.1, the sodium bicarbonate cotransporter NBCe1, , or the electroneutral cotransporter, sodium-potassium-chloride cotransporter type 1 (NKCC1), but was significantly attenuated in 1 mM barium chloride (BaCl2) and by the Na+/K+ ATPase inhibitor ouabain. Effects of 1 mM BaCl2 and ouabain applied together were not additive and, together with reports that BaCl2 can inhibit the NKA at high concentrations, suggests a prominent role for the astrocyte NKA in rapid astrocyte volume increases occurring in ^[K+]o. These findings carry important implications for understanding mechanisms of cellular edema, regulation of the brain extracellular space, and brain tissue excitability.

Modulation of Jellyfish Potassium Channels by External Potassium Ions

1999 ◽  
Vol 82 (4) ◽  
pp. 1728-1739 ◽  
Author(s):  
Nikita G. Grigoriev ◽  
J. David Spafford ◽  
Andrew N. Spencer
Keyword(s):  
Potassium Channels ◽  
Motor Neurons ◽  
Fruit Fly ◽  
Site Directed Mutagenesis ◽  
High Threshold ◽  
Extracellular Potassium ◽  
Potassium Ions ◽  
Polyorchis Penicillatus ◽  
State Dependent ◽  
Inactivation Mechanism

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.

Sign in / Sign up

Export Citation Format

Share Document