2021/01/14 by Ryuji Terayama, Kenta Uchibe
Biochemistry, Genetics and Molecular Biology · Medicine · #Botulinum Toxin and Related Neurological Disorders #Ion channel regulation and function #Pain Mechanisms and Treatments
paper · doi:10.1080/00207454.2021.1873980
openalex publication_date 2021/01/14 · crossref created 2021/01/14 · crossref issued 2021/01/18 · crossref published 2021/01/18 · crossref published-online 2021/01/18 · crossref deposited 2022/11/12 · crossref published-print 2022/12/02 · openalex created_date 2025/10/10 · crossref indexed 2026/07/30 · openalex updated_date 2026/07/31
Peripheral nerve injuries produce a variety of negative structural and functional changes in the central terminal sites of damaged axons, as well as the injured primary afferents. Such changes have been shown to be involved in the development of neuropathic pain, which includes abnormal pain sensations such as allodynia and hyperalgesia. Since the spinal dorsal horn is the first central site where signals from peripheral sensory nerves are transmitted and shows a variety of changes after peripheral nerve injury or chronic inflammation of peripheral tissues, it is one of the most important sites contributing to the mechanisms underlying the development of neuropathic pain. The functional disruption of inhibitory interneurons and glial activation in the spinal dorsal horn after peripheral nerve injury cause reorganization of neuronal circuits and changes in the excitability of second-order neurons. These events are involved in the development or maintenance of neuropathic pain. Here, we describe the interactions of primary afferents, interneurons, and glial cells that may cause reorganization of synaptic inputs to spinal dorsal horn neurons after peripheral nerve injury.