http://www.cnr.it/ontology/cnr/individuo/prodotto/ID59298

The effect of botulinum neurotoxin A on sciatic nerve injury-induced neuroimmunological changes in rat dorsal root ganglia and spinal cord (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

The effect of botulinum neurotoxin A on sciatic nerve injury-induced neuroimmunological changes in rat dorsal root ganglia and spinal cord (Articolo in rivista) (literal)

Anno

2011-01-01T00:00:00+01:00 (literal)

Alternative label

Mika J.; Rojewska E.; Makuch W.; Korostynski M.; Luvisetto S.; Marinelli S.; Pavone F.; Przewlocka B. (2011)
The effect of botulinum neurotoxin A on sciatic nerve injury-induced neuroimmunological changes in rat dorsal root ganglia and spinal cord
in Neuroscience
(literal)

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Mika J.; Rojewska E.; Makuch W.; Korostynski M.; Luvisetto S.; Marinelli S.; Pavone F.; Przewlocka B. (literal)

Pagina inizio

358 (literal)

Pagina fine

366 (literal)

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175 (literal)

Rivista

Neuroscience (Rivista)

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(*) L'Unità Operativa di Servizio dell'Istituto di Neuroscienze di Roma, è stata soppressa il 12/1/2011 con provvedimento prot. n. 0002130 ed è confluita nell'IBCN, costituito il 21/12/2010 con provvedimento prot. n. 0091899. (literal)

Note

ISI Web of Science (WOS) (literal)

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a - Department of Pain Pharmacology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343 Krakow, Poland; b - Department of Molecular Neuropharmacology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna Street, 31-343 Krakow, Poland; c - CNR, Institute of Neuroscience, Via del Fosso di Fiorano 64, 00143 Rome, Italy (*) (literal)

Titolo

The effect of botulinum neurotoxin A on sciatic nerve injury-induced neuroimmunological changes in rat dorsal root ganglia and spinal cord (literal)

Abstract

Botulinum neurotoxin serotype A (BoNT/A) acts by cleaving synaptosome-associated-protein-25 (SNAP-25) in nerve terminals to inhibit neuronal release and shows long-lasting antinociceptive action in neuropathic pain. However, its precise mechanism of action remains unclear. Our study aimed to characterize BoNT/A-induced neuroimmunological changes after chronic constriction injury (CCI) of the sciatic nerve. In the ipsilateral lumbar spinal cords of CCI-exposed rats, the mRNA of microglial marker (complement component 1q, C1q), astroglial marker (glial fibrillary acidic protein, GFAP), and prodynorphin were upregulated, as measured by reverse transcription-polymerase chain reaction (RT-PCR). No changes appeared in mRNA for proenkephalin, pronociceptin, or neuronal and inducible nitric oxide synthase (NOS1 and NOS2, respectively). In the dorsal root ganglia (DRG), an ipsilateral upregulation of prodynorphin, pronociceptin, C1q, GFAP, NOS1 and NOS2 mRNA and a downregulation of proenkephalin mRNA were observed. A single intraplantar BoNT/A (75 pg/paw) injection induced long-lasting antinociception in this model. BoNT/A diminished the injury-induced ipsilateral spinal upregulation of C1q mRNA. In the ipsilateral DRG a significant decrease of C1q-positive cell activation and of the upregulation of prodynorphin, pronociceptin and NOS1 mRNA was also observed following BoNT/A admistration. BoNT/A also diminished the injury-induced upregulation of SNAP-25 expression in both structures. We provide evidence that BoNT/A impedes injury-activated neuronal function in structures distant from the injection site, which is demonstrated by its influence on NOS1, prodynorphin and pronociceptin mRNA levels in the DRG. Moreover, the silence of microglia/macrophages after BoNT/A administration could be secondary to the inhibition of neuronal activity, but this decrease in neuroimmune interactions could be the key to the long-lasting BoNT/A effect on neuropathic pain. (literal)

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