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  • Amino acid transmitters  (1)
  • Astrocytes  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Experimental brain research 65 (1987), S. 482-485 
    ISSN: 1432-1106
    Keywords: Electrophysiology ; Dopamine ; Serotonin ; Astrocytes ; Tissue cultures ; Spinal cord ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The actions of dopamine, apomorphine and serotonin on the membrane potential of cultured astrocytes from rat spinal cord and striatum were examined. All three compounds caused a hyperpolarization of the majority of astrocytes tested. A small number of cells was depolarized and on a relatively large number of cells the amines had no effect. The dopamine antagonists cis-flupenthixol and domperidone reversibly blocked the effects of dopamine whereas the action of serotonin was antagonized by ketanserin. It is therefore concluded that the effects of both amines are due to activation of specific dopamine and serotonin receptors, respectively. Our electrophysiological data together with autoradiographic binding studies provide evidence that astrocytes possess receptors for dopamine and serotonin in addition to adrenoceptors and histamine receptors.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1106
    Keywords: Neurone-glia interaction ; Amino acid transmitters ; K+ ; Tissue culture
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The action of inhibitory amino acid transmitters GABA, glycine, β-alanine and taurine has been studied on the membrane potential of cultured astrocytes and on the extracellular K+-concentration ([K+]0) using K+-sensitive microelectrodes. All four amino acids caused a depolarization of glial cells and an increase of [K+]0. The effects produced by GABA were usually more pronounced than those caused by the other amino acids. Simultaneous recordings of the action of GABA and glycine on the glial membrane potential and on [K+]0 usually revealed a good correlation in time course, but often there were differences between the amplitudes of glial depolarizations and the values calculated from the [K+]0 increase. 4-Aminopyridine, which blocks K+-conductance of excitable membranes, reversibly abolished both the glial depolarization and the [K+]0 increase produced by GABA and glycine. From these results it is concluded that unlike neurones, glial cells do not have receptors for these amino acid transmitters and that their action on glial cells is caused by the efflux of K+ from activated neurones.
    Type of Medium: Electronic Resource
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