Effects of Cannabidiol on Locomotor Activity

Abstract

Cannabidiol (CBD) is the second cannabinoid, in order of importance after Δ9-tetrahydrocannabinol (THC), from Cannabis sativa. Unlike THC, CBD does not cause psychotomimetic effects, and although these compounds have the same chemical formula, their pharmacological characteristics are not equivalent. Preclinical studies suggest that CBD has anti-inflammatory, analgesic, anxiolytic, antiemetic, anticonvulsant, and antipsychotic properties and influences the sleep-wake cycle. The evaluation of effects on spontaneous motor activity is crucial in experimental pharmacology, and the careful measurement of laboratory animal movement is an established method to recognize the effects of stimulant and depressant drugs. The potential influence of CBD on locomotor activity has been investigated through numerous in vivo experiments. However, there is no clear picture of the impact of CBD on these issues, even though it is administered alone for medical uses and sold with THC as a drug for pain caused by muscle spasms in multiple sclerosis, and it was recently licensed as a drug for severe forms of infantile epilepsy. On this basis, with the aim of developing deeper knowledge of this issue, scientific data on CBD's influence on locomotor activity are discussed here. We conducted research using PubMed, Scopus, Google Scholar, and a search engine for literature between January 2009 and December 2021 on life sciences and biomedical topics using the keywords "motor activity", "locomotor activity", and "locomotion" in combination with "cannabidiol". In this article, we discuss findings describing the effects on locomotor activity of the CBD precursor cannabidiolic acid and of CBD alone or in combination with THC, together with the effects of CBD on locomotor modifications induced by diseases and on locomotor changes induced by other substances.

Keywords: cannabidiol; cannabis; locomotion; locomotor activity; motor activity.

Figure 1

Chemical structure of cannabidiol.

Figure 2

Pharmacological targets potentially involved in cannabidiol effects. 5-HT_1A = serotonin 1A receptor; PPAR-γ = peroxisome proliferator-activated receptor gamma; TRPV-1 = transient receptor potential cation channel subfamily V member 1; TRPM8 = transient receptor potential cation channel subfamily M (melastatin) member 8; FAAH = fatty acid amide hydrolase; GPR55 = G protein-coupled receptor 55; GPR3 = G protein-coupled receptor 3; GPR6 = G protein-coupled receptor 6; GPR12 = G protein-coupled receptor 12; GPR18 = G protein-coupled receptor 18; CB1 = cannabinoid receptor type 1; CB2 = cannabinoid receptor type 2.