Botulinum toxin type a (150 kDa) decreases exaggerated neurotransmitter release from trigeminal ganglion neurons and relieves neuropathy behaviors induced by infraorbital nerve constriction

Kitamura, Yoshihisa; Matsuka, Yoshizo; Spigelman, Igor; Ishihara, Yoshihito; Yamamoto, Yasutake; Sonoyama, Wataru; Kuboki, Takuo; Oguma, Keiji

doi:10.1016/j.neuroscience.2009.01.066

Cited by 75 publications

(55 citation statements)

References 76 publications

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“…For these reasons, we suggest that the stimulus-evoked release of CGRP occurs in a calcium-dependant manner from areas of LDCV exocytosis in a regulated fashion. This is consistent with electron microscopy studies (Alvarez et al, 1993;Hayes and Carlton, 1992) and functional investigations in the literature (Hingtgen and Vasko, 1994a;Kitamura et al, 2009;Matsuka et al, 2007). Because synaptic vesicles and LDCVs share similarities in the core aspects of the machinery involved in transmitter release (Edwards, 1998), our results showing the synaptic localization of CRMP-2 suggests that a CRMP-2-mediated increase in neurosecretion might occur via both classical and non-classical mechanisms.…”

Section: Crmp-2 Modulates Transmitter Releasesupporting

confidence: 91%

Regulation of N-type voltage-gated calcium channels (Cav2.2) and transmitter release by collapsin response mediator protein-2 (CRMP-2) in sensory neurons

Xuan

Schmutzler

Brittain

et al. 2009

Journal of Cell Science

127

157

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Collapsin response mediator proteins (CRMPs) mediate signal transduction of neurite outgrowth and axonal guidance during neuronal development. Voltage-gated Ca2+ channels and interacting proteins are essential in neuronal signaling and synaptic transmission during this period. We recently identified the presynaptic N-type voltage-gated Ca2+ channel (Cav2.2) as a CRMP-2-interacting partner. Here, we investigated the effects of a functional association of CRMP-2 with Cav2.2 in sensory neurons. Cav2.2 colocalized with CRMP-2 at immature synapses and growth cones, in mature synapses and in cell bodies of dorsal root ganglion (DRG) neurons. Co-immunoprecipitation experiments showed that CRMP-2 associates with Cav2.2 from DRG lysates. Overexpression of CRMP-2 fused to enhanced green fluorescent protein (EGFP) in DRG neurons, via nucleofection, resulted in a significant increase in Cav2.2 current density compared with cells expressing EGFP. CRMP-2 manipulation changed the surface levels of Cav2.2. Because CRMP-2 is localized to synaptophysin-positive puncta in dense DRG cultures, we tested whether this CRMP-2-mediated alteration of Ca2+ currents culminated in changes in synaptic transmission. Following a brief high-K+-induced stimulation, these puncta became loaded with FM4-64 dye. In EGFP and neurons expressing CRMP-2–EGFP, similar densities of FM-loaded puncta were observed. Finally, CRMP-2 overexpression in DRG increased release of the immunoreactive neurotransmitter calcitonin gene-related peptide (iCGRP) by ∼70%, whereas siRNA targeting CRMP-2 significantly reduced release of iCGRP by ∼54% compared with control cultures. These findings support a novel role for CRMP-2 in the regulation of N-type Ca2+ channels and in transmitter release.

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Section: Crmp-2 Modulates Transmitter Releasesupporting

confidence: 91%

Regulation of N-type voltage-gated calcium channels (Cav2.2) and transmitter release by collapsin response mediator protein-2 (CRMP-2) in sensory neurons

Xuan

Schmutzler

Brittain

et al. 2009

Journal of Cell Science

127

157

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“…TG neurons ipsilateral to the ION-CCI exhibited a significantly faster onset of FM4-64 release than those contralateral to the ION-CCI (sham surgery) (Fig. 2) [19]. ION-CCI induced long-lasting ipsilateral tactile allodynia, measured as large decreases in the withdrawal thresholds to mechanical and thermal stimulation.…”

Section: Introductionmentioning

confidence: 84%

Basic research and clinical investigations of the neural basis of orofacial pain

Matsuka

Iwata

Terayama

et al. 2015

Journal of Oral Biosciences

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“…In animals BoNT/A reduces nociceptive behavior 24 hours after injection over sensitized nerves suggesting an analgesic effect 9 . Kitamura et al demonstrated that unilateral infraorbital nerve constriction (IoNC) results in long-lasting (superior to 2 weeks) tactile allodynia associated with vesicle secretion of neurotransmitters from trigeminal ganglion 18 . The main neurotransmitters involved in the therapeutic effect of BoNT/A are substance P 19 and CGRP 20,21 .The animals of Kitamura study were treated with intradermal BoNT/A and showed reduced immediate release vesicular of this neurotransmitters with consequent control of allodynia 11 days after treatment 18 .…”

Section: Discussionmentioning

confidence: 99%

Botulinum neurotoxin type-A when utilized in animals with trigeminal sensitization induced a antinociceptive effect

Piovesan

Oshinsky

Silberstein

et al. 2016

Arq. Neuro-Psiquiatr.

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Purpose of the study was evaluate the possible antinociceptive effect of botulinum neurotoxin type-A (BoNT/A) in an experimental model of trigeminal neuralgia. Method Neuropathic pain was induced by surgical constriction of the infraorbital nerve in rats. A control group underwent a sham procedure consisting of surgical exposure of the nerve. Subgroups of each group received either BoNT/A or isotonic saline solution. The clinical response was assessed with the -20°C test. Animals that underwent nerve constriction developed sensitization; the sham group did not. Results The sensitization was reversed by BoNT/A treatment evident 24 hours following application. Pronociceptive effect was observed in the sham group following BoNT/A. Conclusion BoNT/A has an antinociceptive effect in sensitized animals and a pronociceptive effect in non-sensitized animals.

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Botulinum toxin type a (150 kDa) decreases exaggerated neurotransmitter release from trigeminal ganglion neurons and relieves neuropathy behaviors induced by infraorbital nerve constriction

Cited by 75 publications

References 76 publications

Regulation of N-type voltage-gated calcium channels (Cav2.2) and transmitter release by collapsin response mediator protein-2 (CRMP-2) in sensory neurons

Regulation of N-type voltage-gated calcium channels (Cav2.2) and transmitter release by collapsin response mediator protein-2 (CRMP-2) in sensory neurons

Basic research and clinical investigations of the neural basis of orofacial pain

Botulinum neurotoxin type-A when utilized in animals with trigeminal sensitization induced a antinociceptive effect

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