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Journal Article

The AMPA receptor subunits GluR-A and GluR-B reciprocally modulate spinal synaptic plasticity and inflammatory pain

MPS-Authors
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Borchardt,  Thilo
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Seeburg,  Peter H.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

External Resource

http://www.sciencedirect.com/science/article/pii/S0896627304006853/pdfft?md5=707e592615dc6e0f313a96f61952ba86&pid=1-s2.0-S0896627304006853-main.pdf
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http://dx.doi.org/10.1016/j.neuron.2004.10.029
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Citation

Hartmann, B., Ahmadi, S., Heppenstall, P. A., Lewin, G., Schott, C., Borchardt, T., et al. (2004). The AMPA receptor subunits GluR-A and GluR-B reciprocally modulate spinal synaptic plasticity and inflammatory pain. Neuron, 44(4), 637-650. doi:10.1016/j.neuron.2004.10.029.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002A-1A0D-0
Abstract
Ca(2+)-permeable AMPA receptors are densely expressed in the spinal dorsal horn, but their functional significance in pain processing is not understood. By disrupting the genes encoding GluR-A or GluR-B, we generated mice exhibiting increased or decreased numbers of Ca(2+)-permeable AMPA receptors, respectively. Here, we demonstrate that AMPA receptors are critical determinants of nociceptive plasticity and inflammatory pain. A reduction in the number of Ca(2+)-permeable AMPA receptors and density of AMPA channel currents in spinal neurons of GluR-A-deficient mice is accompanied by a loss of nociceptive plasticity in vitro and a reduction in acute inflammatory hyperalgesia in vivo. In contrast, an increase in spinal Ca(2+)-permeable AMPA receptors in GluR-B-deficient mice facilitated nociceptive plasticity and enhanced long-lasting inflammatory hyperalgesia. Thus, AMPA receptors are not mere determinants of fast synaptic transmission underlying basal pain sensitivity as previously thought, but are critically involved in activity-dependent changes in synaptic processing of nociceptive inputs.