Electrophysiological analysis of potassium and sodium movements in crustacean nervous system

1975 ◽  
Vol 63 (1) ◽  
pp. 85-115
Author(s):  
N. J. Abbott ◽  
R. B. Moreton ◽  
Y. Pichon

1. An electrophysiological method was used to estimate the half-times for sodium and potassium entry to, and efflux from, the extra-axonal space in peripheral nerve and central nervous connectives of two species of crustacean. Results from crab (marine) and crayfish (fresh water) were qualitatively similar. 2. Peripheral nerve showed no evidence for diffusion barriers, potassium entry and efflux being rapid, and proceeding at comparable rates. 3. In connective, potassium entry was extremely slow, with a half-time greater than 100 min, while potassium efflux was relatively rapid (T 1/2 = 6 min). Sodium movements were less restricted, but sodium entry was more rapid than sodium efflux. 4. The potassium experiments were compared with the behaviour of a theoretical model system. Evidence is presented for diffusional restriction to potassium at the connective perineurial layer. The mechanism of restriction may involve changes in permeability or activation of an ion pump in the perineurial layer. 5. The physiological significance of these findings is discussed.

1981 ◽  
Vol 61 (3) ◽  
pp. 307-312 ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton

1. The effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes has been studied in vitro. 2. A significant increase in the rate constant for total and ouabain-sensitive sodium efflux was demonstrated at an extracellular potassium concentration of 1 mmol/l as compared with that at either 0 or 2 mmol/l. 3. At potassium concentrations below 3 mmol/l ouabain-sensitive sodium influx was observed suggesting sodium-sodium exchange catalysed by the sodium pump. 4. Both total and ouabain-insensitive potassium efflux rose with external potassium. A small ouabain-sensitive potassium efflux was observed at all levels of external potassium studied. 5. Total and ouabain-insensitive potassium influx increased with external potassium, but did not appear to saturate. Ouabain-sensitive potassium influx reached a maximum at an external potassium concentration of 2 mmol/l then decreased with increasing external potassium.


1973 ◽  
Vol 44 (5) ◽  
pp. 439-445 ◽  
Author(s):  
P. J. Hilton ◽  
J. Patrick

1. Sodium and potassium efflux and influx rates were studied in normal human leucocytes in an artificial extracellular fluid using radioactive isotopes. 2. The rate constant for sodium efflux was 4.2 h−1 corresponding to a sodium efflux rate of 487 mmol kg cell dry weight−1 h−1. Approximately three-quarters of this flux was ouabain sensitive. 3. Potassium influx was 346 mmol kg cell dry weight−1 h−1. Approximately two-thirds of the potassium influx was ouabain insensitive.


1975 ◽  
Vol 49 (5) ◽  
pp. 385-390
Author(s):  
P. J. Hilton ◽  
R. P. S. Edmondson ◽  
R. D. Thomas ◽  
J. Patrick

1. Sodium and potassium transport rates in human leucocytes were measured in vitro at different external potassium concentrations. 2. At nominally zero external potassium concentrations, the ouabain-sensitive sodium efflux was reduced to less than 20% of its maximum value. There was evidence that under these conditions a ouabain-sensitive sodium-sodium exchange occurs. 3. Both total and ouabain-insensitive potassium influx increased with increasing external potassium concentration. The ouabain-sensitive potassium influx showed saturation. 4. Ouabain-insensitive potassium efflux was also stimulated by increasing the external potassium concentration, suggesting significant potassium-potassium exchange at physiological external potassium concentrations.


2019 ◽  
Vol 20 (1) ◽  
pp. 33-37 ◽  
Author(s):  
Marzia Malcangio

AbstractBackgroundAcute pain is a warning mechanism that exists to prevent tissue damage, however pain can outlast its protective purpose and persist beyond injury, becoming chronic. Chronic Pain is maladaptive and needs addressing as available medicines are only partially effective and cause severe side effects. There are profound differences between acute and chronic pain. Dramatic changes occur in both peripheral and central pathways resulting in the pain system being sensitised, thereby leading to exaggerated responses to noxious stimuli (hyperalgesia) and responses to non-noxious stimuli (allodynia).Critical role for immune system cells in chronic painPreclinical models of neuropathic pain provide evidence for a critical mechanistic role for immune cells in the chronicity of pain. Importantly, human imaging studies are consistent with preclinical findings, with glial activation evident in the brain of patients experiencing chronic pain. Indeed, immune cells are no longer considered to be passive bystanders in the nervous system; a consensus is emerging that, through their communication with neurons, they can both propagate and maintain disease states, including neuropathic pain. The focus of this review is on the plastic changes that occur under neuropathic pain conditions at the site of nerve injury, the dorsal root ganglia (DRG) and the dorsal horn of the spinal cord. At these sites both endothelial damage and increased neuronal activity result in recruitment of monocytes/macrophages (peripherally) and activation of microglia (centrally), which release mediators that lead to sensitisation of neurons thereby enabling positive feedback that sustains chronic pain.Immune system reactions to peripheral nerve injuriesAt the site of peripheral nerve injury following chemotherapy treatment for cancer for example, the occurrence of endothelial activation results in recruitment of CX3C chemokine receptor 1 (CX3CR1)-expressing monocytes/macrophages, which sensitise nociceptive neurons through the release of reactive oxygen species (ROS) that activate transient receptor potential ankyrin 1 (TRPA1) channels to evoke a pain response. In the DRG, neuro-immune cross talk following peripheral nerve injury is accomplished through the release of extracellular vesicles by neurons, which are engulfed by nearby macrophages. These vesicles deliver several determinants including microRNAs (miRs), with the potential to afford long-term alterations in macrophages that impact pain mechanisms. On one hand the delivery of neuron-derived miR-21 to macrophages for example, polarises these cells towards a pro-inflammatory/pro-nociceptive phenotype; on the other hand, silencing miR-21 expression in sensory neurons prevents both development of neuropathic allodynia and recruitment of macrophages in the DRG.Immune system mechanisms in the central nervous systemIn the dorsal horn of the spinal cord, growing evidence over the last two decades has delineated signalling pathways that mediate neuron-microglia communication such as P2X4/BDNF/GABAA, P2X7/Cathepsin S/Fractalkine/CX3CR1, and CSF-1/CSF-1R/DAP12 pathway-dependent mechanisms.Conclusions and implicationsDefinition of the modalities by which neuron and immune cells communicate at different locations of the pain pathway under neuropathic pain states constitutes innovative biology that takes the pain field in a different direction and provides opportunities for novel approaches for the treatment of chronic pain.


1961 ◽  
Vol 38 (2) ◽  
pp. 315-322
Author(s):  
J. E. TREHERNE

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.


2021 ◽  
Vol 6 (2) ◽  
pp. 253-264
Author(s):  
Amelia Lestari ◽  
Elsa Lisanti ◽  
Rizhal Hendi Ristanto

This study aimed to develop guided discovery learning-based android learning media to improve critical thinking skills. The developed biology learning media was applied to the nervous system material. The discussion of the physiology of the nervous system is one of the difficult biological materials to understand because it includes the organization and structure of neurons and their functions, ion pump mechanisms when neurons are at rest, action potential mechanisms, mechanisms for neurons to communicate with other cells in the synapses, and organization of the nervous system. This study used research and development (RD) with a method developed by Thiagarajan, namely the 4D model with stages: define, design, develop and disseminate. The stages of this study are limited to the development stage. The results showed that the media was feasible with media, language, and a material expert validation of   3.5, 3.8, and 3.3, respectively.


Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 37-37
Author(s):  
Kristin Komnick ◽  
Jennifer May ◽  
Pouneh Kermani ◽  
Sreemanti Basu ◽  
Irene Hernandez ◽  
...  

Blood cell production is regulated by peripheral nerve fibers that innervate the bone marrow. However, little is known about the development or maintenance of hematopoietic innervation. Schwann cells (SCs) are the primary axon 'support cells' of the peripheral nervous system (PNS), and abnormal SC development is sufficient to impair peripheral nerve function. SCs are also the primary repair cell for the PNS which makes them an attractive therapeutic target for normalization of drug or malignancy-induced 'hematopoietic neuropathy'. We hypothesized that neural regulation of hematopoiesis is dependent on SC development. To test this hypothesis, we used the Myelin Protein Zero-Cre (MP0-Cre); Lamc1fl/fl mouse line in which laminin-γ1 expression is deleted from SC precursors and their progeny1. Early SC maturation is dependent on autocrine SC precursor-derived molecules such as laminin-γ1. SC differentiation arrests prior to axon sorting and ensheathment in MP0-Cre; Lamc1fl/fl mice, and causes a global peripheral neuropathy that persists throughout the lifetime of the animal. Preliminary hematopoietic analysis of 'steady state' MP0-Cre; Lamc1fl/fl and littermate control mice has shown the following: (1) MP0-Cre; Lamc1fl/fl bone marrow is innervated, and Cre-mediated gene recombination occurs in cells immunophenotypically consistent with SCs throughout the peripheral nervous system, including those in the bone marrow; (2) MP0-Cre; Lamc1fl/fl mice are lymphopenic but not neutropenic; (3) MP0-Cre; Lamc1fl/fl mice have significantly reduced spleen size and cellularity; and (4) MP0-Cre; Lamc1fl/fl bone marrow has an ~50% reduction in Lin-Sca-1+Kit+(LSK) cells (measured as a percentage of the Lin- compartment of the bone marrow). These results are consistent with earlier work by our groups in which we found that global Lamc1 gene deletion in adult mice induced peripheral blood lymphopenia, reduced spleen size, and a niche-dependent reduction of lymphoid progenitor and precursor cells that was secondary to increased lymphoid precursor cell apoptosis and reduced proliferation (UBC-CreERT2; Lamc1fl/fl mouse line). As with the SC-specific laminin-γ1 deficient mice, myelopoiesis was preserved in the UBC-CreERT2; Lamc1fl/fl mice. Based on results from MP0-Cre; Lamc1fl/fl and UBC-CreERT2; Lamc1fl/fl mice, we conclude that early lymphoid but not myeloid development requires laminin-γ1 expression by MP0-Cre-targetted niche cells, i.e. Schwann Cells. Our results are consistent with reports from other labs that hematopoietic sympathetic neuropathy promotes aberrant myeloid expansion at the expense of lymphopoiesis2. Going forward, we will determine whether lymphopoietic development is dependent on global versus laminin-specific SC-derived cues, and whether these signals are transmitted directly between SCs and lymphoid biased HSPCs or indirectly via other components of the hematopoietic niche. We anticipate that this line of investigation will provide molecular insights and pharmacologic targets for prevention and or normalization of the 'hematopoietic neuropathy' induced by diabetes, aging, neurotoxic chemotherapies and myeloid malignancies. REFERENCES: 1 Yu, W. M., Feltri, M. L., Wrabetz, L., Strickland, S. & Chen, Z. L. Schwann cell-specific ablation of laminin gamma1 causes apoptosis and prevents proliferation. J Neurosci25, 4463-4472, doi:10.1523/JNEUROSCI.5032-04.2005 (2005). 2 Maryanovich, M. et al. Adrenergic nerve degeneration in bone marrow drives aging of the hematopoietic stem cell niche. Nat Med24, 782-791, doi:10.1038/s41591-018-0030-x (2018). Disclosures No relevant conflicts of interest to declare.


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