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Reviewing the case for compromised spinal inhibition in neuropathic pain

Journal

JOURNAL OF NEURAL TRANSMISSION
Volume 127, Issue 4, Pages 481-503

Publisher

SPRINGER WIEN
DOI: 10.1007/s00702-019-02090-0

Keywords

Presynaptic inhibition; Inhibitory interneuron; Spinal cord; Sensory; Gaba; Glycine

Funding

  1. National Health and Medical Research Council (NHMRC) of Australia [631000, 1043933, 1144638]
  2. Hunter Medical Research Institute
  3. National Health and Medical Research Council of Australia [1144638] Funding Source: NHMRC

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A striking and debilitating property of the nervous system is that damage to this tissue can cause chronic intractable pain, which persists long after resolution of the initial insult. This neuropathic form of pain can arise from trauma to peripheral nerves, the spinal cord, or brain. It can also result from neuropathies associated with disease states such as diabetes, human immunodeficiency virus/AIDS, herpes, multiple sclerosis, cancer, and chemotherapy. Regardless of the origin, treatments for neuropathic pain remain inadequate. This continues to drive research into the underlying mechanisms. While the literature shows that dysfunction in numerous loci throughout the CNS can contribute to chronic pain, the spinal cord and in particular inhibitory signalling in this region have remained major research areas. This review focuses on local spinal inhibition provided by dorsal horn interneurons, and how such inhibition is disrupted during the development and maintenance of neuropathic pain.

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