Research reportElectrical stimulation of olfactory bulb downregulates RGMa expression after ischemia/reperfusion injury in rats

Repulsive guidance molecule A (RGMa) is associated with limited axonal growth after cerebral ischemia. This study focused on the effects of electrical stimulation of olfactory bulb (OB) on the expression of RGMa and axonal regeneration after focal cerebral ischemia/reperfusion injury. Sprague-Dawley (SD) rats were randomly divided into sham-operated group, ischemia/reperfusion (I/R) group (48 h, 1 w), stimulation group (48 h, 1 w), and sham-stimulated group (48 h, 1 w). Focal cerebral ischemia/reperfusion was induced by intraluminal middle cerebral artery occlusion. Electrical stimulation was performed via a bipolar electrode implanted in the right OB. The changes in the expression of RGMa were analyzed by reverse transcription polymerase chain reaction (RT-PCR), Western-blot and immunohistochemistry, respectively. Neurofilament protein 200 (NF-200) immunohistochemical staining was used to assess axonal regeneration. Another group of rats were divided into sham-operated group, I/R group, sham-stimulated group and stimulation group. The behavioral test was conducted using the modified neurological severity score (mNSS). The infarct volume was determined by triphenyltetrazolium chloride (TTC) staining. The levels of RGMa were significantly elevated after ischemia/reperfusion injury. Stimulation treatment downregulated the expression of RGMa, reduced infarct volume and improved neurological function. These observations demonstrated that electrical stimulation of OB might promote axonal regeneration and function recovery after ischemic cerebral injury.

► We electrically stimulated OB of rats with cerebral ischemia/reperfusion injury. ► Stimulation down-regulated the expression of RGMa in cortex and hippocampus. ► Stimulation increased the expression of NF-200 in cortex. ► Stimulation diminished infarct area and elevated neurological function. ► OB stimulation may be effective in the treatment of cerebral ischemia.