Minocycline Does Not Reduce the Regenerative Capacity of Peripheral Motor and Sensory Neurons after a Conditioning Injury in Mice
Sánchez Brualla, Irene (Universitat Autònoma de Barcelona. Institut de Neurociències)
Calls, Aina (Universitat Autònoma de Barcelona. Institut de Neurociències)
Udina i Bonet, Esther (Universitat Autònoma de Barcelona. Institut de Neurociències)

Data:	2018
Resum:	Minocycline has been reported to be both beneficial and detrimental for nerve regeneration after peripheral nerve injury. By reducing the inflammatory response, minocycline administration reduces pain and has neuroprotective effects, but it also inhibits Wallerian degeneration in the distal stump, and reduces microglia and macrophages activity on motor and sensory neurons, which could reduce their intrinsic regenerative capacity. The aim of this study was to determine if the administration of minocycline after nerve injury inhibits the regenerative capacity of motoneurons and sensory neurons after a conditioning lesion. We used two groups of mice: a control group and a group treated with minocycline (30 mg kg−1 ip twice daily). We labeled motor and sensory neurons that had regenerated to a distance of 3 mm in a predegenerated graft, after a conditioning lesion. Our results indicate that minocycline administration is not detrimental for nerve regeneration. Indeed, it even promoted a slight, no significant increase 7 days after the nerve graft. These results indicate that minocycline, given at a dose able to reduce pain after peripheral nerve injury, does not interfere with the intrinsic growth capacity of injured peripheral neurons. Anat Rec, 301:1638-1645, 2018. © 2018 Wiley Periodicals, Inc.
Drets:	Tots els drets reservats.
Llengua:	Anglès
Document:	Article ; recerca ; Versió sotmesa a revisió
Matèria:	Conditioning injury ; DRG neurons ; Microglia ; Minocycline ; Motor neurons ; Peripheral nerve ; Regeneration
Publicat a:	The anatomical record (Hoboken), Vol. 301 (2018) , p. 1638-1645, ISSN 1932-8494

DOI: 10.1002/ar.23845
PMID: 29710422

15 p, 2.2 MB

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