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Plasticity of Inhibition; GABA/glycine System

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Molecular Pain

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Abstract

Several conditions of pathological pain involve plastic changes in GABA/glycine-mediated inhibition in the CNS which can (i) alter the gain of the response to nociceptive input (hyperalgesia), but also(ii) allow cross talk between non-nociceptive and nociceptive pathways as a substrate for aberrant pain perception to normally innocuous input (allodynia). While plasticity of the GABA/glycine system had been traditionally overlooked and poorly studied, especially in the context of the pain system, recent findings highlight a richness of mechanisms by which inhibition is modulated that open several avenues for innovative therapeutic treatment for the prevention, as well as the reversal of pathological pain. These findings include (i) evidence of highly plastic GABA/glycine co-synapses, (ii) modulation of specific receptor subclasses by endogenous agents traditionally thought to act mainly in the periphery, but which also act centrally (e.g., neurosteroids and prostaglandins) and (iii) active regulation of anion homeostasis as a means to modulate both the strength and the sign of GABA/glycine action (i.e., excitatory vs.inhibitory).

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Authors and Affiliations

  1. Department of Psychiatry, Centre de recherche Université Laval Robert-Giffard (CRULRG), 2601, Chemin de la Canardière Bureau F-5579, Beauport, Quebec, G1J 2G3, Canada

    Yves De Koninck PhD (Professor and Director)

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  1. Yves De Koninck PhD
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  1. Department of Physiology, University of Toronto, Medical Sciences Bldg, Rm 3342 1 King’s College Circle, Toronto, Ontario, Canada, M5S 1A8

    Min Zhuo

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De Koninck, Y. (2007). Plasticity of Inhibition; GABA/glycine System. In: Zhuo, M. (eds) Molecular Pain. Springer, New York, NY. https://doi.org/10.1007/978-0-387-75269-3_14

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  • DOI: https://doi.org/10.1007/978-0-387-75269-3_14

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-0-387-75268-6

  • Online ISBN: 978-0-387-75269-3

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