The protective effect of the endocannabinoid system in neurotoxin-induced damage to hippocampal neurons: a focus on light and electron microscopy

Dysregulation of glutamatergic transmission in the brain causes hyperactivation and oxidative stress, which underlie neurodegenerative diseases such as temporal lobe epilepsy (TLE) and Alzheimer’s disease (AD). One of the main targets for the action of neurotoxins in the brain, leading to the development of these diseases, is the hippocampus, a key structure in memory processes. Cytological analysis of the cellular components of the protein-synthesizing and catabolic systems is of key importance in the study of neuronal degeneration, their survival and recovery, particularly, under the influence of neuroprotective agents. The mechanism that controls the excitability of neurons and regulates neurotransmission and neuroplasticity is the activation of the endocannabinoid system. The duration of action of endocannabinoids in the intercellular space is short. To prolong the time of their activity and increase their level in the brain, in particular, the endocannabinoid reuptake inhibitor AM404 and enzyme of the endocannabinoid anandamide degradation, URB597, are used. The review analyzes studies in which prolonged action of eCBs reduced the level of neuronal hyperactivation, as well as their damages and death caused by neurotoxic effects.