OTC Painkillers and Marijuana-Induced Memory Loss

Δ⁹-THC-Caused Synaptic and Memory Impairments Are Mediated through COX-2 Signaling

• Rongqing Chen^1, 4, 
• Jian Zhang^1, 4, 
• Ni Fan^1, 4, 
• Zhao-qian Teng^1, 4, 
• Yan Wu^1, 4, 
• Hongwei Yang¹, 
• Ya-ping Tang³, 
• Hao Sun¹, 
• Yunping Song¹, 
• Chu Chen^1, 2, , 

• ¹ Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA
• ² Department of Otorhinolaryngology, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA
• ³ Department of Cell Biology and Anatomy, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA

I just read this pretty interesting study about the use of ibuprofen to counteract some of the negative memory-related effects caused by smoking marijuana. THC (one of the psychoactive chemicals in cannibis) has the side effect of impairing memory by affecting the COX-2 enzyme through the CB1 receptor (the main receptor that cannabinoids from marijuana interact with). Scientists believe that it is through this enzyme that acute side effects with short term memory, as well as chronic effects of memory deficits, arise. These side-effects significantly detriment the use of marijuana as medicine, as many are concerned about the side effects that come with the drug. However, a recent study by Chen et al suggests that the use of ibuprofen, which inhibits the COX-2 enzyme, could block these effects. It is an interesting paper, and although it is inconclusive and needs to be studied more, this could really help make the medical marijuana a safe alternative drug.

Summary:
"Marijuana has been used for thousands of years as a treatment for medical conditions. However, untoward side effects limit its medical value. Here, we show that synaptic and cognitive impairments following repeated exposure to Δ⁹-tetrahydrocannabinol (Δ⁹-THC) are associated with the induction of cyclooxygenase-2 (COX-2), an inducible enzyme that converts arachidonic acid to prostanoids in the brain. COX-2 induction by Δ⁹-THC is mediated via CB1 receptor-coupled G protein βγ subunits. Pharmacological or genetic inhibition of COX-2 blocks downregulation and internalization of glutamate receptor subunits and alterations of the dendritic spine density of hippocampal neurons induced by repeated Δ⁹-THC exposures. Ablation of COX-2 also eliminates Δ⁹-THC-impaired hippocampal long-term synaptic plasticity, working, and fear memories. Importantly, the beneficial effects of decreasing β-amyloid plaques and neurodegeneration by Δ⁹-THC in Alzheimer’s disease animals are retained in the presence of COX-2 inhibition. These results suggest that the applicability of medical marijuana would be broadened by concurrent inhibition of COX-2."

Read the rest here:
http://www.sciencedirect.com/science/article/pii/S0092867413013603#