Abstract 152: Neurotrophin Expression Is Increased by Whole Body Periodic Acceleration (pGz) in Mice
Neurotrophins are factors which control signaling pathways and guide synaptic, axonal and neuronal circuits to regulate brain plasticity and neurogenesis. They improve cognitive performance, promote angiogenesis, and cell survival. Brain and Glial Cell Line Derived Neurotrophic Factors (BDNF, GDNF) are two such neurotrophins. Exercise upregulates both neurotrophins in animals and humans. It is difficult to carry out exercise following post global neurological injury such as after cardiac arrest, ischemic or traumatic brain injury. Whole body periodic acceleration (pGz) can be accomplished with a motion platform that rapidly moves the body in a repetitive head to foot motion thereby increasing pulsatile shear stress to the endothelium to stimulate eNOS, a necessary event in the production of BDNF. pGz when performed as a preconditioning strategy in whole body or focal ischemia reperfusion injury models is cardioprotective and neuroprotective. In a rodent model of ischemic stroke, pGz administered after stroke significantly (-82%) decreased infarct volume at one week. We hypothesized that pGz applied daily for 2 weeks would increase expression of the aforementioned proteins in brain. Mice (n=20) where placed in a mice holder and randomized to receive 1 hr per day of pGz for 10 sessions over two weeks (f=480 cpm and Gz 0.3mt/sec2) or rested within the mice holder as controls (CONT). Protein immunoblotting in whole brain is shown below. (Data are mean ±SD, A.O.U=arbitrary optical units, † p <0.001 CONT vs pGz). pGz increased BDNF and GDNF expression by 30% and 26% of CONT values respectively (p < 0.001). pGz is a well tolerated intervention in healthy and diseased humans. Therefore, pGz has potential as a noninvasive strategy to increase neuroprotection with BDNF and GDNF post cardiac arrest or in other global neurological injuries.
- Post cardiac arrest care
- Post cardiac resuscitation
- Cardiopulmonary resuscitation
- Ischemia reperfusion
- © 2011 by American Heart Association, Inc.