The binding of IgG1 containing immune complexes to the FcR of allogenically activated T cells induces changes in the membrane potential and the cell surface charge

Hückel, C; Sándor, Mátyás; Jenssen, H. L.; Rychly, Joachim; Brock, Josef; Gergely, J.

doi:10.1016/0161-5890(88)90073-9

Cited by 2 publications

(2 citation statements)

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“…Our data indicate that anti-morphine antibody dose-dependently excited spinal cord dorsal horn neurons, which is consistent with a previous report showing that IgG microperfusion activated inward current at the range of 200 to 800 pA as recorded from human alveolar macrophage using a whole-cell patch-clamp setup [12]. In addition, an IgG-antigen complex also increased the Ca 2+ concentration in DRG neurons [13] and binding of immune complex to the Fc receptor changed membrane potential in activated T cells [11]. If there were interactions between anti-morphine antibody and Fc receptors, 2.4G 2 , an antibody blocking antibody-Fc receptor interaction, would be expected to prevent the effect of anti-morphine antibody on neuronal responses.…”

Section: Discussionsupporting

confidence: 88%

“…Most mammalian species express Fc receptors in immune cells [10]. Moreover, antibody binding to the Fc receptor has been shown to induce electrophysiological changes including prolonged depolarization in activated T cells [11], increased peak inward current in alveolar macrophages [12], and increased [Ca 2+ ] influx in dorsal root ganglion neurons [13]. …”

Section: Introductionmentioning

confidence: 99%

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Anti-morphine antibody contributes to the development of morphine tolerance in rats

Kim¹,

Oh²,

Sung³

et al. 2010

Neuroscience Letters

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Previous studies have shown that tolerance to the antinociceptive effect of morphine develops after a prolonged exposure, but its mechanisms remain unclear. In the present study, we examined whether anti-morphine antibody produced by chronic morphine exposure would contribute to the development of morphine antinociceptive tolerance in rats. Our results showed that anti-morphine antibody was present in rats rendered tolerance to antinociception after intrathecal morphine exposure for seven consecutive days. Superfusion of anti-morphine antibody onto spinal cord slice dose-dependently produced an inward excitatory current in spinal cord dorsal horn neurons using whole cell patch-clamp recording, which surpassed morphine-induced outward inhibiting current. Co-administration of morphine with a monoclonal antibody (2.4 G 2 ) against Fc receptors for seven days significantly attenuated the production of anti-morphine antibody as well as the behavioral manifestation of morphine tolerance in same rats. These results indicate that antimorphine antibody produced by morphine exposure may contribute to the development of morphine tolerance possibly through counteracting the inhibitory morphine effect on spinal cord dorsal horn neurons.

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Section: Discussionsupporting

confidence: 88%