Delta-9-tetrahydrocannabinol (THC) increases brain prostaglandins in the rat

Abstract

Intraperitoneal administration of 9-trans-delta-tetrahydrocannabinol (THC), the major psychoactive component of cannabis, in doses of 0.5, 1.0 and 2.0 mg/kg, produced a dose-related increase in the brain concentrations of prostaglandin (PG) E2 and PGF2 alpha in male rats 4 h after THC administration, as assessed by radioimmunoassay. A time-course investigation indicated that THC (2 mg/kg, IP) induced maximal increases in rat brain concentration of both PGs 2 and 4 h after administration; PG levels declined appreciably by 8 h and were normal by 24 h. A time-course study on the hexobarbitone (100 mg/kg, IP)-induced hypnosis potentiating effect of THC (2.0 mg/kg, IP) in male rats revealed that this pharmacological action of the cannabinoid correlated well with the time-course of the THC-induced increase in rat brain PG concentrations. The present study lends support to earlier reports contending that PGs may mediate some of the central actions of THC.

Decrease in Efficacy and Potency of Nonsteroidal Anti-Inflammatory Drugs by Chronic Δ9-Tetrahydrocannabinol Administration

“…The present study is based upon previous work that indicate that acute administration of cannabinoids stimulates the release of arachadonic acid resulting in elevation of prostaglandins (Burstein and Hunter, 1981;Burstein et al, 1983;Laviolette and Belanger, 1986;Bhattacharya, 1986;Hunter et al, 1991). Furthermore, cannabinoids induce COX-2 expression in the central nervous system (Ramer et al, 2001).…”

R(+)-Methanandamide Induces Cyclooxygenase-2 Expression in Human Neuroglioma Cells via a Non-cannabinoid Receptor-Mediated Mechanism

“…Previous studies suggest that cannabinoids may stimulate arachidonic acid release from cultured astrocytes (24), cortical slices (25) and neuroblastoma cells (26). Additionally, ⌬ 9 -THC has been shown to increase the amount of PGE 2 in the brain (27,28). A possible interference of cannabinoids with the expression of inducible enzymes involved in arachidonic acid metabolism has been recently reported by Chan et al (29) who showed that the PG-dependent hippocampal neuronal toxicity of ⌬ 9 -THC requires de novo synthesis of mRNA and protein.…”

Cannabinoids and pain responses: a possible role for prostaglandins

“…1). Our explanation for this phenomenon is that when THC is given, [20][21][22][23][24][25] s. Indomethacin and the metaholite were each given orally in peanut oil (50 tl) 30 mm before THC. In this experiment, the pain response was measured 10 mm after THC administration.…”