Minocycline does not inhibit microglia proliferation or neuronal regeneration in the facial nucleus following crush injury

• Published in: Neuroscience letters 2005-09, Vol.385 (3), p.220-223
• Main Authors: Fendrick, Sarah E., Miller, Kelly R., Streit, Wolfgang J.
• Format: Article
• Language: English
• Subjects: 3H-thymidine; Animals; Biological and medical sciences; Brain - drug effects; Cell Proliferation - drug effects; Facial Nerve Injuries - physiopathology; Fluorogold; Fundamental and applied biological sciences. Psychology; Male; Microglia - drug effects; Microglia - metabolism; Minocycline; Minocycline - pharmacology; Motor Neurons - drug effects; Motor Neurons - metabolism; Nerve Crush; Nerve Regeneration - drug effects; Neuroprotective Agents - pharmacology; Rats; Rats, Sprague-Dawley; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2005.05.047

Minocycline is thought to be neuroprotective by inhibiting neuroinflammation (microglial activation) associated with neurodegenerative diseases. In this study we investigated the effect of minocycline specifically on microglial mitotic activity and neuronal regeneration within the facial nucleus following a nerve crush injury. Proliferation was measured by labeling the dividing microglia with 3H-thymidine and quantifying labeled cells throughout the facial nucleus on days 2, 3 and 4 post-axotomy. Regeneration patterns of the axotomized motoneurons were studied by labeling regenerating neurons with fluorogold at 7, 14 and 21 days post-axotomy. No significant difference was found between minocycline treated and control rats when comparing the 3H-thymidine labeled microglial cells or fluorogold labeled neurons at these post-injury time points. The findings show that microglia maintain the ability to become activated in vivo even in the presence of high levels of minocycline.