Abstract
Hypoxic-ischemic encephalopathy (HIE), often caused by hypoxia-ischemia (HI), can lead to neurological damage in newborns, and often even to death. HI causes energy shortage, a waterfall of biochemical reactions and massive cell death, among others. Therefore, in recent years, the aim has been to develop mechanisms that compensate for that loss of cells, as well as mechanisms that promote lower cell death, such as 2-arachidonoylglycerol (2-AG). Several research has shown that endocannabinoids can reduce neuro-inflammation, minimize damage from oxidative stress and reduce glutamate-related excitotoxicity. Hence, we examined those effects on the two neurogenic niches known so far: the subventricular zone (SVZ) of the lateral brain ventricles and the subgranular zone of the dentate gyrus (SGZ). It is believed that by promoting cell proliferation, the damage caused by hypoxia-ischemia could be compensated, so the cellularity and area of these niches were measured after hypoxia-ischemia and after the application of 2-AG. The results showed that the area of the ipsilateral hemispheres changed in the affected animals, decreasing in SGZ and increasing in SVZ. In addition, HI reduced cellularity in SGZ, but not in SVZ. However, 2-AG helped to restore morphology and cellularity in SGZ.
