Details

Autor(en) / Beteiligte

• Huo, Kang
• Wei, Meng
• Zhang, Meng
• Wang, Zhanqiang
• Pan, Peipei
• Shaligram, Sonali S
• Huang, Jinhao
• Prado, Leandro B Do
• Wong, Julia
• Su, Hua

Titel

Reduction of neuroinflammation alleviated mouse post bone fracture and stroke memory dysfunction

Ist Teil von

• Journal of cerebral blood flow and metabolism, 2021-09, Vol.41 (9), p.2162-2173

Ort / Verlag

London, England: SAGE Publications

Erscheinungsjahr

2021

Quelle

MEDLINE

Beschreibungen/Notizen

• Tibia fracture (BF) enhances stroke injury and post-stroke memory dysfunction in mouse. Reduction of neuroinflammation by activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) reduced acute neuronal injury and sensorimotor dysfunction in mice with BF 1-day after stroke. We hypothesize that reduction of neuroinflammation by activation of α-7 nAchR improves long-term memory function of mice with BF 6-h before stroke. The mice were randomly assigned to saline, PHA-568487 (α-7 nAchR agonist) and methyllycaconitine (antagonist) treatment groups. The sensorimotor function was tested by adhesive removal and corner tests at 3 days, the memory function was tested by Y-maze test weekly for 8 weeks and novel objective recognition test at 8 weeks post-injuries. We found PHA-568487 treatment reduced, methyllycaconitine increased the number of CD68+ cells in the peri-infarct and hippocampal regions, neuronal injury in the infarct region, sensorimotor and long-term memory dysfunctions. PHA-568487 treatment also reduced, while methyllycaconitine treatment increased atrophy of hippocampal granule cell layer and white matter damage in the striatum. In addition, PHA-568487 treatment increased neuron proliferation in granule cell layer. Our data indicated that reduction of neuroinflammation through activation of α-7 nAchR decreased neuronal damage, sensorimotor and long-term memory dysfunction of mice with BF shortly before stroke.