Arachidonic acid and its metabolites increase Cai in cultured rat oligodendrocytes

Fluorescence measurements of intracellular calcium (Cai) were made on cultured rat spinal cord oligodendrocytes (OLGs) using the dye fura-2. Exposure of OLGs to arachidonic acid (AA) (5-50 microM) elicited a concentration-dependent increase in Cai that was derived mainly from extracellular Ca2+. AA at 50 microM also released Ca2+ from intracellular stores. The response to AA was not decreased by nifedipine or by inhibition of Na(+)-Ca2+ exchange. AA-induced Ca2+ influx pathway was permeable to Mn2+ and Co2+ but not to Ba2+ and was not markedly influenced by depolarization, suggesting that AA activates a voltage-independent, not strictly selective, Ca2+ channel. The Cai response to AA was partially attenuated in the presence of indomethacin, indicating that the Cai response was mediated in part by cyclooxygenase products of AA. However, the AA-induced Cai response far exceeded that induced by prostaglandins and was mimicked by linoleic acid. We conclude that AA modulates Cai of OLGs via two mechanisms: 1) indirectly via cyclooxygenase pathway and 2) directly via membrane lipid-protein interaction.

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Urotensin-II regulates intracellular calcium in dissociated rat spinal cord neurons

Journal of Neurochemistry ◽

10.1046/j.1471-4159.2002.01196.x ◽

2002 ◽

Vol 83 (4) ◽

pp. 879-884 ◽

Cited By ~ 38

Author(s):

Catalin M. Filipeanu ◽

Eugen Brailoiu ◽

Siok Le Dun ◽

Nae J. Dun

Keyword(s):

Spinal Cord ◽

Intracellular Calcium ◽

Urotensin Ii ◽

Rat Spinal Cord ◽

Spinal Cord Neurons

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The dopamine D1–D2DR complex in the rat spinal cord promotes neuropathic pain by increasing neuronal excitability after chronic constriction injury

Experimental & Molecular Medicine ◽

10.1038/s12276-021-00563-5 ◽

2021 ◽

Author(s):

Yi-Ni Bao ◽

Wen-Ling Dai ◽

Ji-Fa Fan ◽

Bin Ma ◽

Shan-Shan Li ◽

...

Keyword(s):

Spinal Cord ◽

Neuropathic Pain ◽

Intracellular Calcium ◽

Calcium Concentration ◽

Neuronal Excitability ◽

Chronic Constriction Injury ◽

Pain Modulation ◽

Intracellular Calcium Concentration ◽

Rat Spinal Cord ◽

Spinal Neurons

AbstractDopamine D1 receptor (D1DR) and D2 receptor (D2DR) are closely associated with pain modulation, but their exact effects on neuropathic pain and the underlying mechanisms remain to be identified. Our research revealed that intrathecal administration of D1DR and D2DR antagonists inhibited D1–D2DR complex formation and ameliorated mechanical and thermal hypersensitivity in chronic constriction injury (CCI) rats. The D1–D2DR complex was formed in the rat spinal cord, and the antinociceptive effects of D1DR and D2DR antagonists could be reversed by D1DR, D2DR, and D1–D2DR agonists. Gαq, PLC, and IP3 inhibitors also alleviated CCI-induced neuropathic pain. D1DR, D2DR, and D1–D2DR complex agonists all increased the intracellular calcium concentration in primary cultured spinal neurons, and this increase could be reversed by D1DR, D2DR antagonists and Gαq, IP3, PLC inhibitors. D1DR and D2DR antagonists significantly reduced the expression of p-PKC γ, p-CaMKII, p-CREB, and p-MAPKs. Levo-corydalmine (l-CDL), a monomeric compound in Corydalis yanhusuo W.T. Wang, was found to obviously suppress the formation of the spinal D1–D2DR complex to alleviate neuropathic pain in CCI rats and to decrease the intracellular calcium concentration in spinal neurons. l-CDL-induced inhibition of p-PKC γ, p-MAPKs, p-CREB, and p-CaMKII was also reversed by D1DR, D2DR, and D1–D2DR complex agonists. In conclusion, these results indicate that D1DR and D2DR form a complex and in turn couple with the Gαq protein to increase neuronal excitability via PKC γ, CaMKII, MAPK, and CREB signaling in the spinal cords of CCI rats; thus, they may serve as potential drug targets for neuropathic pain therapy.

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Alkalinization-Induced Changes in Intracellular Calcium in Rat Spinal Cord Neurons

Neurochemical Research ◽

10.1023/b:nere.0000035800.65411.3e ◽

2004 ◽

Vol 29 (9) ◽

pp. 1659-1665 ◽

Cited By ~ 6

Author(s):

E. Potapenko ◽

E. Kostyuk ◽

N. Voitenko ◽

P. Kostyuk

Keyword(s):

Spinal Cord ◽

Intracellular Calcium ◽

Rat Spinal Cord ◽

Spinal Cord Neurons ◽

Induced Changes

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An Early Developmental Marker for Radial Glia in Rat Spinal Cord

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100162648 ◽

1996 ◽

Vol 54 ◽

pp. 36-37

Author(s):

V. Kriho ◽

H.-Y. Yang ◽

C.-M. Lue ◽

N. Lieska ◽

G. D. Pappas

Keyword(s):

Spinal Cord ◽

Intermediate Filament ◽

Radial Glia ◽

Rat Spinal Cord ◽

Future Studies ◽

Spinal Cord Development ◽

Median Septum ◽

Differentiation Marker ◽

Early Developmental ◽

Developing Rat

Radial glia have been classically defined as those early glial cells that radially span their thin processes from the ventricular to the pial surfaces in the developing central nervous system. These radial glia constitute a transient cell population, disappearing, for the most part, by the end of the period of neuronal migration. Traditionally, it has been difficult to definitively identify these cells because the principal criteria available were morphologic only.Using immunofluorescence microscopy, we have previously defined a phenotype for radial glia in rat spinal cord based upon the sequential expression of vimentin, glial fibrillary acidic protein and an intermediate filament-associated protein, IFAP-70/280kD. We report here the application of another intermediate filament-associated protein, IFAP-300kD, originally identified in BHK-21 cells, to the immunofluorescence study of radial glia in the developing rat spinal cord.Results showed that IFAP-300kD appeared very early in rat spinal cord development. In fact by embryonic day 13, IFAP-300kD immunoreactivity was already at its peak and was observed in most of the radial glia which span the spinal cord from the ventricular to the subpial surfaces (Fig. 1). Interestingly, from this time, IFAP-300kD immunoreactivity diminished rapidly in a dorsal to ventral manner, so that by embryonic day 16 it was detectable only in the maturing macroglial cells in the marginal zone of the spinal cord and the dorsal median septum (Fig. 2). By birth, the spinal cord was essentially immuno-negative for this IFAP. Thus, IFAP-300kD appears to be another differentiation marker available for future studies of gliogenesis, especially for the early stages of radial glia differentiation.

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Erratum to 'A simple technique for flat osmicating and flat embedding of immunolabelled vibratome sections of the rat spinal cord for light and electron microscopy' [J. Neurosci. Methods 65 (1996) 51â54]

Journal of Neuroscience Methods ◽

10.1016/s0165-0270(96)00078-7 ◽

1996 ◽

Vol 68 (2) ◽

pp. 309-310

Author(s):

K Nguyen

Keyword(s):

Electron Microscopy ◽

Spinal Cord ◽

Simple Technique ◽

Light And Electron Microscopy ◽

Rat Spinal Cord ◽

Flat Embedding

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Increased Aggregation and Secretion Responses of Human Platelets when Loaded with the Calcium Fluorescent Probes Quin2 and Fura-2

Thrombosis and Haemostasis ◽

10.1055/s-0038-1645981 ◽

1987 ◽

Vol 58 (02) ◽

pp. 737-743 ◽

Cited By ~ 12

Author(s):

Frarnçois Lanza ◽

Alain Beretz ◽

Martial Kubina ◽

Jean-Pierre Cazenave

Keyword(s):

Intracellular Calcium ◽

Shape Change ◽

Calcium Ionophore ◽

Human Platelets ◽

Arachidonic Acid Metabolism ◽

Free Calcium ◽

Membrane Bilayer ◽

Fluorescent Indicators ◽

Fura 2 ◽

Low Concentrations

SummaryIncorporation into human platelets of the calcium fluorescent indicators quin2 or fura-2 at low concentrations used to measure intracellular free calcium leads to the potentiation of the effects of agonists on platelets. This was shown by increased aggregatory and secretory responses of quin2 or fura-2 loaded platelets after stimulation with ADP, PAP and with low concentrations of thrombin, collagen, the endoperoxide analog U-46619 and the calcium ionophore A 23187. Quin2 and fura-2 mediated platelet sensitisation could be due to altered arachidonic acid metabolism since it was inhibited by prior treatment with the cydooxygenase inhibitor acetylsalicylate. In contrast, platelets loaded with higher concentrations of calcium chelators exhibited diminished aggregation responses to all aggregating agents. This latter effect was accompanied by increased fluidity of the platelet plasma membrane bilayer and by the exposure of a new pool of membranes to the outer surface of platelets, as monitored with trimethylammonium- diphenylhexatriene (TMA-DPH) in platelets loaded with the non-fluorescent calcium probe analog MAPT. In contrast, low concentrations of quin2 did not potentiate shape change of platelets activated with ADP. Thus, shape change and aggregation can be influenced separately by intracellular Ca2+ chelators. We conclude that platelet responses are altered by the incorporation of intracellular calcium chelators at concentrations used to monitor intracellular calcium changes.

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