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Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression

Overview of attention for article published in Brain, Behavior & Immunity, November 2014
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Minocycline modulates neuropathic pain behaviour and cortical M1–M2 microglial gene expression in a rat model of depression
Published in
Brain, Behavior & Immunity, November 2014
DOI 10.1016/j.bbi.2014.06.015
Pubmed ID

Nikita N. Burke, Daniel M. Kerr, Orla Moriarty, David P. Finn, Michelle Roche


There is a paucity of data on the role of microglia and neuroinflammatory processes in the association between chronic pain and depression. The current study examined the effect of the microglial inhibitor minocycline on depressive-like behaviour, spinal nerve ligation (SNL)-induced mechanical and cold allodynia and associated changes in the expression of genes encoding microglial markers (M1 vs. M2 polarisation) and inflammatory mediators in the prefrontal cortex in the olfactory bulbectomised (OB) rat model of depression. Acute minocycline administration did not alter OB-induced depressive-like behaviour but prevented SNL-induced mechanical allodynia in both OB and sham rats. In comparison, chronic minocycline attenuated OB-induced depressive-like behaviour and prevented the development of SNL-induced mechanical allodynia in OB, but not sham, rats. Further analysis revealed that SNL-induced mechanical allodynia in OB rats was attenuated by chronic minocycline at almost all time-points over a 2week testing period, an effect observed only from day 10 post-SNL in sham rats. Chronic administration of minocycline reduced the expression of CD11b, a marker of microglial activation, and the M1 pro-inflammatory cytokine IL-1β, in the prefrontal cortex of sham-SNL animals. In comparison, the expression of the M2 microglia marker (MRC2) and anti-inflammatory cytokine IL-10 was increased, as were IL-1β, IL-6 and SOCS3, in the prefrontal cortex of OB-SNL animals following chronic minocycline. Thus, chronic minocycline attenuates neuropathic pain behaviour and modulates microglial activation and the central expression of inflammatory mediators in a manner dependent on the presence or absence of a depressive-like phenotype.

Mendeley readers

The data shown below were compiled from readership statistics for 116 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 116 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 30 26%
Student > Master 20 17%
Student > Bachelor 16 14%
Researcher 14 12%
Student > Doctoral Student 8 7%
Other 17 15%
Unknown 11 9%
Readers by discipline Count As %
Neuroscience 30 26%
Agricultural and Biological Sciences 20 17%
Medicine and Dentistry 19 16%
Psychology 9 8%
Biochemistry, Genetics and Molecular Biology 5 4%
Other 16 14%
Unknown 17 15%