Electromagnetic approaches to medical treatment are only lightly explored in comparison to pharmacology, but it is possible that some could turn out to be as effective as the results of the average drug development program. The example here involves the use of electrical stimulation to increase neurogenesis in rats. Neurogenesis is the generation of new neurons in the brain by neural stem cell populations, followed by the integration of these neurons into neural circuits. This is essential for the function of memory, among other cognitive functions, as well as the ongoing maintenance and repair of brain tissue. Greater levels of neurogenesis appear to be beneficial across the board, and it seems worthwhile to keep an eye on progress in the various approaches aimed at achieving that goal.
The major aim of stroke therapies is to stimulate brain repair and to improve behavioral recuperation after cerebral ischemia. Despite remarkable advances in cell therapy for stroke, stem cell-based tissue replacement has not been achieved yet, stimulating the search for alternative strategies for brain self-repair using the neurogenic zones of the brain, the dentate gyrus and the subventricular zone (SVZ). However, during aging, the potential of the hippocampus and the SVZ to generate new neuronal precursors, declines. We hypothesized that electrically stimulation of endogenous neurogenesis in aged rats could increase the odds of brain self-repair and improve behavioral recuperation after focal ischemia.
Following stroke in aged animals, the rats were subjected to two sessions of electrical non-convulsive stimulation using ear-clip electrodes, at 7- and 24 days after injury. Animal were sacrificed after 48 days. We report that electrical stimulation (ES) stimulation of post-stroke aged rats led to an improved functional recovery of spatial long-term memory (T-maze), but not on the rotating pole or the inclined plane, both tests requiring complex sensorimotor skills. Surprisingly, ES had a detrimental effect on the asymmetric sensorimotor deficit.
Histologically, there was a robust increase in the number of doublecortin-positive cells in the dentate gyrus and SVZ of the infarcted hemisphere and the presence of a considerable number of neurons expressing tubulin beta III in the infarcted area. Among the genes that were unique to ES, we noted increases in the expression of seizure related 6 homolog like, which is one of the physiological substrate of the β-secretase BACE1 involved in the pathophysiology of Alzheimer’s disease, and Igfbp3 and BDNF receptor mRNAs which has been shown to have a neuroprotective effect after cerebral ischemia. However, ES was associated with a long-term down regulation of cortical gene expression after stroke in aged rats suggesting that gene expression in the peri-infarcted cortical area may not be related to electrical stimulation induced-neurogenesis in the subventricular zone and hippocampus.