Effects of ouabain on intracellular ion activities of sensory neurons of the leech central nervous system

1991 ◽  
Vol 65 (3) ◽  
pp. 736-746 ◽  
Author(s):  
W. R. Schlue
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Membrane Potential Change ◽  
Intracellular Na Activity ◽  
Order Of Magnitude ◽  
Intracellular Ion Activities ◽  
Ion Activities ◽  
K Concentration

1. The intracellular K+, Na+, and Ca2+ of mechanosensory neurons in the central nervous system of the leech Hirudo medicinalis was measured using double-barreled ion-sensitive microelectrodes. 2. After inhibition of the Na(+)-K+ pump with 5 x 10(-4) M ouabain, the intracellular K+ activity (aKi) decreased, while the intracellular Na+ activity (aNai) increased. The input resistance decreased in the presence of ouabain. The intracellular Ca2+ increased more than one order of magnitude after ouabain addition. All changes in intracellular ion activities and membrane resistance were fully reversible. 3. When extracellular Na+ concentration ([Na+]o) was removed [replaced by tris(hydroxymethyl)aminomethane (Tris)], aNai decreased. In the absence of [Na+]o, aKi and aNai remained unchanged after inhibition of the Na(+)-K+ pump by reducing the extracellular K+ concentration ([K+]o) to 0.2 mM. The membrane resistance increased under these conditions. 4. The intracellular Ca2+ decreased or remained constant after removal of [Na+]o. Addition of ouabain in the absence of [Na+]o did not change intracellular Ca2+, which only increased after readdition of [Na+]o. 5. The relative K+ permeability (PK) measured as membrane potential change during a brief increase of the [K+]o from 4 to 10 mM, increased manyfold after addition of ouabain but only little if [Na+]o had been removed before adding ouabain. 6. The results suggest that the intracellular Na+ increase after inhibition of the Na(+)-K+ pump affects the intracellular Ca2+ level by stimulating a Nai(+)-Ca2+ exchange mechanism. The subsequent intracellular Ca2+ activity (aCai) rise may result in an increase of the membrane permeability to K+ ions.

Potassium distribution and membrane potential of sensory neurons in the leech nervous system

1984 ◽  
Vol 51 (4) ◽  
pp. 689-704 ◽  
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Sensory Neurons ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Bathing Medium ◽  
Membrane Hyperpolarization ◽  
K Concentration ◽  
Intracellular K Activity ◽  
K Activity

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Cerebrospinal fluid ceftazidime kinetics in patients with external ventriculostomies.

1996 ◽  
Vol 40 (3) ◽  
pp. 763-766 ◽  
Author(s):  
R Nau ◽  
H W Prange ◽  
M Kinzig ◽  
A Frank ◽  
A Dressel ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
High Performance ◽  
Elimination Half ◽  
Daily Dose ◽  
Order Of Magnitude ◽  
The Central Nervous System ◽  
Occlusive Hydrocephalus ◽  
A Minor

Ceftazidime has proven to be effective for the treatment of bacterial meningitis caused by multiresistant gram-negative bacteria. Since nosocomial central nervous system infections are often accompanied by only a minor dysfunction of the blood-cerebrospinal fluid (CSF) barrier, patients with noninflammatory occlusive hydrocephalus who had undergone external ventriculostomy were studied (n = 8). Serum and CSF were drawn repeatedly after the administration of the first dose of ceftazidime (3 g over 30 min intravenously), and concentrations were determined by high-performance liquid chromatography by using UV detection. The concentrations of ceftazidime in CSF were maximal at 1 to 13 h (median, 5.5 h) after the end of the infusion and ranged from 0.73 to 2.80 mg/liter (median, 1.56 mg/liter). The elimination half-lives were 3.13 to 18.1 h (median, 10.7 h) in CSF compared with 2.02 to 5.24 h (median, 3.74 h) in serum. The ratios of the areas under the concentration-time curves in CSF and serum (AUCCSF/AUCS) ranged from 0.027 to 0.123 (median, 0.054). After the administration of a single dose of 3 g, the maximum concentrations of ceftazidime in CSF were approximately four times higher than those after the administration of 2-g intravenous doses of cefotaxime (median, 0.44 mg/liter) and ceftriaxone (median, 0.43 mg/liter) (R. Nau, H. W. Prange, P. Muth, G. Mahr, S. Menck, H. Kolenda, and F. Sörgel, Antimicrob. Agents Chemother. 37:1518-1524, 1993). The median AUCCSF/AUCS ratio of ceftazidime was slightly below that of cefotaxime (0.12), but it was 1 order of magnitude above the median AUCCSF/AUCS of ceftriaxone (0.007) (Nau et al., Antimicrob. Agents Chemother. 37:1518-1524, 1993). The concentrations of ceftazidime observed in CSF were above the MICs for most Pseudomonas aeruginosa strains. However, they are probably not high enough to be rapidly bactericidal. For this reason, the daily dose should be increased to 12 g in cases of P. aeruginosa infections of the central nervous system when the blood-CSF barrier is minimally impaired.

Mechanism of potassium uptake in neuropile glial cells in the central nervous system of the leech

1990 ◽  
Vol 63 (5) ◽  
pp. 1089-1097 ◽  
Author(s):  
W. A. Wuttke
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Cell Volume ◽  
Normal Saline ◽  
Cell Swelling ◽  
Equilibrium Potential ◽  
K Uptake ◽  
The Central Nervous System ◽  
The Mean ◽  
K Concentration

1. Ion-selective double-barreled microelectrodes (ISME) were used to measure intracellular K+ (aKi), Na+ (aNai), and Cl- (aCli) activities of neuropile glial (NG) cells in the central nervous system of the medicinal leech Hirudo medicinalis. Ion fluxes were induced by an increase in extracellular K+ concentration [( K+]o) and analyzed to elucidate the ionic mechanism of the K+ uptake occurring under such conditions. 2. In addition, the K+ concentration of the extracellular space of the nerve cell body region (NCBR) and the neuropile (N) was measured with neutral carrier K(+)-ISME. In normal saline (4 mM K+), a concentration of 4.2 mM was measured in both extracellular spaces. No differences between the K+ concentration of the bathing fluid and the extracellular spaces were found at higher (i.e., 10 and 40 mM) K+ concentrations. 3. In normal saline, the mean membrane potential (Em) was -68 mV, and the mean aKi, aNai, and aCli were found to be 77, 10, and 7 mM, respectively. The corresponding equilibrium potentials were -81, 56, and -66 mV. The chloride equilibrium potential (ECl) was similar to Em, and it is concluded that chloride is passively distributed across the NG cell membrane. 4. When [K+]o was transiently increased 10-fold (i.e., to 40 mM), aKi and a Cli increased transiently by 22 and 25 mM, respectively, and the membrane depolarized to -28 mV, which was similar to both K+ equilibrium potential (EK) and ECl. The KCl uptake was accompanied by a transient decrease in aNai to 5 mM. 5. After incubation for at least 1 h in Na(+)-free saline, NG cells accumulated K+ in the absence of extracellular Na+ to levels similar to those observed in the presence of Na+. Therefore the uptake of K+ was not dependent on external--and probably also internal--Na+. 6. Changes in cell volume induced by the increase in [K+]o were estimated by loading NG cells with choline and monitoring its intracellular concentration with Corning-K(+)-ISME. In saline containing 40 mM K+, NG cell volume increased to approximately 150% of its volume in normal saline. 7. It is concluded that the mechanism of K+ uptake in NG cells is by passive KCl and water influx, which causes cell swelling.

scholarly journals Effects of ethidium bromide on cells of the cockroach central nervous system

1984 ◽  
Vol 70 (1) ◽  
pp. 17-24
Author(s):  
C.A. Leech
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ethidium Bromide ◽  
Membrane Potentials ◽  
K Concentration ◽  
Nerve Cords

The effects of ethidium bromide were tested on isolated cockroach interganglionic connectives, either with the perineurium intact or desheathed. Intact connectives showed small, reversible depolarizations in response to 25 mM-ethidium. Desheathed connectives showed much larger, concentration-dependent depolarizations and the membrane potentials repolarized only slowly after washing out ethidium. The ethidium-induced depolarization could be blocked by raising the K concentration in the salines and was also shown to be reduced by rubidium, caesium, ammonium and ouabain. These treatments also reduced the degree of staining of nerve cords by ethidium, which was demonstrated to enter the cells.

Selected Contribution: Neuroplasticity in nucleus tractus solitarius neurons after episodic ozone exposure in infant primates

2003 ◽  
Vol 94 (2) ◽  
pp. 819-827 ◽  
Author(s):  
Chao-Yin Chen ◽  
Ann C. Bonham ◽  
Charles G. Plopper ◽  
Jesse P. Joad
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nucleus Tractus Solitarius ◽  
Sensory Nerve ◽  
Membrane Resistance ◽  
Ozone Exposure ◽  
Sensory Transmission ◽  
Shallow Breathing ◽  
The Central Nervous System ◽  
Whole Cell Recordings

Acute ozone exposure evokes adverse respiratory responses, particularly in children. With repeated ozone exposures, however, despite the persistent lung inflammation and increased sensory nerve excitability, the central nervous system reflex responses, i.e., rapid shallow breathing and decreased lung function, adapt, suggesting changes in central nervous system signaling. We determined whether repeated ozone exposures altered the behavior of nucleus tractus solitarius (NTS) neurons where reflex respiratory motor outputs are first coordinated. Whole cell recordings were performed on NTS neurons in brain stem slices from infant monkeys exposed to filtered air or ozone (0.5 ppm, 8 h/day for 5 days every 14 days for 11 episodes). Although episodic ozone exposure depolarized the membrane potential, increased the membrane resistance, and increased neuronal spiking responses to depolarizing current injections ( P < 0.05), it decreased the excitability to vagal sensory fiber activation ( P < 0.05), suggesting a diminished responsiveness to sensory transmission, despite overall increases in excitability. Substance P, implicated in lung and NTS signaling, contributed to the increased responsiveness to current injections but not to the diminished sensory transmission. The finding that NTS neurons undergo plasticity with repeated ozone exposures may help to explain the adaptation of the respiratory motor responses.

Block of an insect central nervous system GABA receptor by cyclodiene and cyclohexane insecticides

1989 ◽  
Vol 237 (1286) ◽  
pp. 53-61 ◽  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gaba Receptors ◽  
Chloride Channels ◽  
Periplaneta Americana ◽  
Chloride Concentration ◽  
Experimental Conditions ◽  
Order Of Magnitude ◽  
Insect Central Nervous System

The effects of a cyclodiene (endrin) and a cyclohexane (lindane) insecticide have been tested on γ -aminobutyric acid (GABA) receptors in the central nervous system of the cockroach ( Periplaneta americana ), by using electrophysiological methods and an in vitro functional receptor assay. In electrophysiological experiments on an identified motor neuron (D f ), endrin blocked the GABA response with a 50% inhibition concentration of 5.0 x 10 -7 M in a non-competitive manner. The actions of endrin were irreversible under the experimental conditions adopted. Increasing the intracellular chloride concentration reduced the effectiveness of endrin, whereas a change in the potassium concentration failed to influence the block by endrin of GABA responses. Lindane exhibited similar actions to endrin on insect GABA receptors, but was approximately an order of magnitude less effective. In a microsac preparation from cockroach nerve cords, endrin, at a concentration of 1.0 x 10 -5 M, completely blocked GABA-stimulated 36 C1 - uptake, whereas the same concentration of lindane was less potent, only blocking about 40% of uptake under similar conditions. Neither insecticide had any effect on L-glutamate-activated chloride channels. The results demonstrate that endrin and lindane block functional insect neuronal GABA receptors.

scholarly journals Potassium Activity Measurements in the Microenvironment of the Central Nervous System of an Insect

1987 ◽  
Vol 127 (1) ◽  
pp. 211-227
Author(s):  
C. H. HENDY ◽  
M. B. A. DJAMGOZ
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Brain Barrier ◽  
Neuronal Activity ◽  
Brain Barrier ◽  
Second Phase ◽  
Blood Brain ◽  
Activity Measurements ◽  
The Central Nervous System ◽  
K Concentration

The activity of K+ and the control of influx of + into the extracellular space (micro-environment) of the central nervous system of the cockroach, Periplaneta americana, were measured directly with K+-sensitive microelectrodes. Using an in vivo preparation, it was possible to follow the effects of changes in K+ concentration in the medium bathing the nervous system on extracellular K+ and spontaneous and evoked neuronal activity. For bath K+ levels less than 31 mmoll−1, roughly corresponding to maximal haemolymph level in natural physiological conditions, the blood-brain barrier was found to be suitably efficient in restricting the influx of K+ and thereby allowing normal neural activity. At an external K+ concentration of 100 mmoll−1, however, the system was unable to maintain a sufficiently low extracellular K+ concentration and neuronal activity was suppressed. Influx of K+ from the external medium into the micro-environment occurred mainly in two phases. The early phase had a fast time course and probably reflects the physical aspects of the blood-brain barrier. The later, second phase was a slower process possibly corresponding to activation of metabolic ion pumps. The time courses of the functioning of these two systems and their control of the extraaxonal K+ activity are also discussed.

Neurotropic enteroviruses co-opt “fair-weather-friend” commensal gut microbiota to drive host infection and central nervous system disturbances

2019 ◽  
Vol 42 ◽  
Author(s):  
Kevin B. Clark
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gut Bacteria ◽  
Infection Cycle ◽  
Fair Weather ◽  
Host Health ◽  
Microbe Interactions ◽  
Animal Hosts ◽  
Host Infection ◽  
Neuropsychiatric Conditions

Abstract Some neurotropic enteroviruses hijack Trojan horse/raft commensal gut bacteria to render devastating biomimicking cryptic attacks on human/animal hosts. Such virus-microbe interactions manipulate hosts’ gut-brain axes with accompanying infection-cycle-optimizing central nervous system (CNS) disturbances, including severe neurodevelopmental, neuromotor, and neuropsychiatric conditions. Co-opted bacteria thus indirectly influence host health, development, behavior, and mind as possible “fair-weather-friend” symbionts, switching from commensal to context-dependent pathogen-like strategies benefiting gut-bacteria fitness.

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