The endocannabinoid system and its protective role in ischemic and cytotoxic injuries of brain neurons

Хаспеков, Л. Г.; Bobrov, M. Yu.

doi:10.1134/s1819712407020018

Cited by 2 publications

(1 citation statement)

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“…Moreover, the levels of endocannabinoids, which are normally found at low concentrations in the brain, dramatically increase upon neuronal injury (Berger et al, 2004; Hansen et al, 2001; Panikashvili et al, 2001), suggesting that endocannabinoids provide an endogenous neuroprotective system (van der Stelt and Di Marzo, 2005). The effects of ECS are crucial for restoring normal functioning of CNS synapses and maintaining the viability of neurons during pathological processes associated with impaired regulation of their neurotransmitter function (Khaspekov and Bobrov, 2006). ECS is emerging as a potential target for therapy after neonatal hypoxia.…”

Section: Introductionmentioning

confidence: 99%

Early‐life N‐arachidonoyl‐dopamine exposure increases antioxidant capacity of the brain tissues and reduces functional deficits after neonatal hypoxia in rats

Sukhanova

Sebentsova

Khukhareva

et al. 2019

Intl J of Devlp Neuroscience

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Perinatal hypoxia‐ischemia is one of the most common causes of perinatal brain injury and subsequent neurological disorders in children. The aim of this work was to evaluate the potential antioxidant and neuroprotective effects of N‐arachidonoyl‐dopamine (NADA) in the model of acute neonatal hypoxia (ANH) in rat pups. Male and female Wistar rats were exposed to a hypoxic condition (8% oxygen for 120 min) at postnatal day 2 (P2). Transcription factor HIF1‐α and glutathione peroxidases GPx2 and GPx4 gene expression was increased in rat brains in the hypoxic group compared to control 1.5 h but not 4 days after ANH. There were no post‐hypoxic changes in reduced (GSH) and oxidised (GSSG) glutathione levels in the brain of rat pups 1.5 h and 4 d after hypoxia. Hypoxic rats displayed retarded performance in the righting reflex and the negative geotaxis tests. ANH resulted in increased ambulation in Open field test and impaired retention in the Barnes maze task under stressful conditions as compared with the control group. Treatment with NADA significantly attenuated the delayed development of sensorimotor reflexes and stress‐evoked disruption of memory retention in hypoxic rats but had no effect on the hypoxia‐induced hyperactivity. In rats exposed to hypoxia, treatment with NADA decreased GPx2 gene expression and increased GSH/GSSG ratio in whole brains 1.5 h after ANH. These results suggest that the long‐lasting beneficial effects of NADA on hypoxia‐induced neurobehavioural deficits are mediated, at least in part, by its antioxidant properties.

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