Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

(Endo)Cannabinoids and Cognitive Functions in Animals: Healthy and Pathological Brain

Version 1 : Received: 10 April 2023 / Approved: 11 April 2023 / Online: 11 April 2023 (10:56:55 CEST)

How to cite: Kitchigina, V. (Endo)Cannabinoids and Cognitive Functions in Animals: Healthy and Pathological Brain. Preprints 2023, 2023040224. https://doi.org/10.20944/preprints202304.0224.v1 Kitchigina, V. (Endo)Cannabinoids and Cognitive Functions in Animals: Healthy and Pathological Brain. Preprints 2023, 2023040224. https://doi.org/10.20944/preprints202304.0224.v1

Abstract

Cognitive functions are based on neuronal plasticity, which is provided by various mechanisms involving numerous bioactive molecules, the most important of which are endocannabinoids (eCBs). Over the past three decades, a lot of data have been accumulated on the involvement of eCBs in the mechanisms of memory and other cognitive functions. These functions are impaired in neurodegenerative diseases such as Alzheimer's disease (AD) and temporal lobe epilepsy (TLE). The main pathological feature of neurons in AD and TLE is increased excitability; therefore, an activation of the endocannabinoid system, which controls cellular excitation, may be a promising approach in their therapy. The available information about the effect of (endo)cannabinoids on cognitive functions is contradictory, which may depend on the drugs used, their dose, and the experimental conditions. There is an extensive literature indicating a protective effect of cannabinoids in the treatment of neurodegenerative diseases in humans and in animal models of cognitive deficits. This review, focusing on the recent researches, is devoted to the analysis of the effects of endocannabinoid system activation on cognitive functions in norm and in the brain with neurodegeneration that occurs in AD and TLE diseases. Possible reasons for inconsistencies in the available data are discussed.

Keywords

endocannabinoid system; cognition; neurotransmitters; CB receptors; endocannabinoid catabolism; Alzheimer's disease; tempral lobe epilepsy; protection

Subject

Biology and Life Sciences, Neuroscience and Neurology

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