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      Botulinum Neurotoxin for Pain Management: Insights from Animal Models

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          Abstract

          The action of botulinum neurotoxins (BoNTs) at the neuromuscular junction has been extensively investigated and knowledge gained in this field laid the foundation for the use of BoNTs in human pathologies characterized by excessive muscle contractions. Although much more is known about the action of BoNTs on the peripheral system, growing evidence has demonstrated several effects also at the central level. Pain conditions, with special regard to neuropathic and intractable pain, are some of the pathological states that have been recently treated with BoNTs with beneficial effects. The knowledge of the action and potentiality of BoNTs utilization against pain, with emphasis for its possible use in modulation and alleviation of chronic pain, still represents an outstanding challenge for experimental research. This review highlights recent findings on the effects of BoNTs in animal pain models.

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          A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man.

          Gary Bennett, Y. Xie (1988)
          A peripheral mononeuropathy was produced in adult rats by placing loosely constrictive ligatures around the common sciatic nerve. The postoperative behavior of these rats indicated that hyperalgesia, allodynia and, possibly, spontaneous pain (or dysesthesia) were produced. Hyperalgesic responses to noxious radiant heat were evident on the second postoperative day and lasted for over 2 months. Hyperalgesic responses to chemogenic pain were also present. The presence of allodynia was inferred from the nocifensive responses evoked by standing on an innocuous, chilled metal floor or by innocuous mechanical stimulation, and by the rats' persistence in holding the hind paw in a guarded position. The presence of spontaneous pain was suggested by a suppression of appetite and by the frequent occurrence of apparently spontaneous nocifensive responses. The affected hind paw was abnormally warm or cool in about one-third of the rats. About one-half of the rats developed grossly overgrown claws on the affected side. Experiments with this animal model may advance our understanding of the neural mechanisms of neuropathic pain disorders in humans.
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            The origin and development of glial cells in peripheral nerves.

            Kristjan Jessen, Rhona Mirsky (2005)
            During the development of peripheral nerves, neural crest cells generate myelinating and non-myelinating glial cells in a process that parallels gliogenesis from the germinal layers of the CNS. Unlike central gliogenesis, neural crest development involves a protracted embryonic phase devoted to the generation of, first, the Schwann cell precursor and then the immature Schwann cell, a cell whose fate as a myelinating or non-myelinating cell has yet to be determined. Embryonic nerves therefore offer a particular opportunity to analyse the early steps of gliogenesis from transient multipotent stem cells, and to understand how this process is integrated with organogenesis of peripheral nerves.
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              An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat.

              Paul Chung, K. Fan Chung, H. Kim (1992)
              We attempted to develop an experimental animal model for peripheral neuropathic pain. Under sodium pentobarbital anesthesia, both the L5 and L6 spinal nerves (group 1) or the L5 spinal nerve alone (group 2) of one side of the rat were tightly ligated. For comparison, a parallel study was conducted with another group of rats (group 3) which received a partial tight sciatic nerve ligation, a paradigm developed previously as a neuropathy model. Withdrawal latencies to application of radiant heat to the foot were tested for the next 16 weeks in all 3 groups. Sensitivity of the hind paw to mechanical stimulation was tested with von Frey filaments. The general behavior of each rat was noted during the entire test period. Results suggested that the surgical procedure in all 3 groups produced a long-lasting hyperalgesia to noxious heat (at least 5 weeks) and mechanical allodynia (at least 10 weeks) of the affected foot. In addition, there were behavioral signs of the presence of spontaneous pain in the affected foot. Therefore, we believe we have developed an experimental animal model for peripheral neuropathy using tight ligations of spinal nerves. The model manifests the symptoms of human patients with causalgia and is compatible with a previously developed neuropathy model. The present model has two unique features. First, the surgical procedure is stereotyped. Second, the levels of injured and intact spinal segments are completely separated, allowing independent experimental manipulations of the injured and intact spinal segments in future experiments to answer questions regarding mechanisms underlying causalgia.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Toxins (Basel)
                Journal ID (publisher-id): toxins
                Title: Toxins
                Publisher: MDPI
                ISSN (Electronic): 2072-6651
                Publication date (Electronic): 21 December 2010
                Publication date Collection: December 2010
                Volume: 2
                Issue: 12
                Pages: 2890-2913
                Affiliations
                CNR, Institute of Neuroscience-Roma, via del Fosso di Fiorano 64, I-00143 Roma, Italy; Email: siro.luvisetto@ 123456cnr.it
                Author notes
                [* ] Author to whom correspondence should be addressed; Email: flaminia.pavone@ 123456cnr.it ; Tel.: +39-06-501703272; Fax: +39-06-501703304.
                Article
                Publisher ID: toxins-02-02890
                DOI: 10.3390/toxins2122890
                PMC ID: 3153188
                PubMed ID: 22069581
                SO-VID: 0ff81ffb-5ae2-44e9-a073-5a72bdf49060
                Copyright © © 2010 by the authors; licensee MDPI, Basel, Switzerland
                License:

                This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/3.0/).

                History
                Date received : 18 November 2010
                Date revision received : 17 December 2010
                Date accepted : 20 December 2010
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: botulinum toxin,snare,pain,animal model,analgesia,inflammatory pain,chronic pain,peripheral sensitization,central sensitization,retrograde axonal transport
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: botulinum toxin, snare, pain, animal model, analgesia, inflammatory pain, chronic pain, peripheral sensitization, central sensitization, retrograde axonal transport

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