The Leaf THE LEAF November-December 2017 | Page 8

switch in the intracellular signalling pathway activated. In Huntington’s Disease, there are changes in the expression and function of both CB1 and A2A in the dorsal striatum. The above study also showed that the CB1-A2A heteromer is selectively lost as Huntington’s Disease progresses to later stages. This may cause drugs acting on the cannabinoid or adenosine systems to have different effects early vs. late in the disease. CB1 & Orexin Receptors The orexin OX1 and OX2 receptors bind the neuropeptides orexin-A and orexin-B. These receptors regulate many functions which overlap with cannabinoids, including wakefulness and sleep, appetite, pain, and reward. The CB1 receptor dimerises with both the OX1 receptor and OX2 receptor. The OX1 receptor activation by an agonist was much more potent in the presence of the CB1 receptor. Activation of OX1 causes internalization of the OX1 receptor (this is a method of downregulating the receptor). When the CB1 receptor is expressed in the same cell, CB1 is also internalized through the heteromer, indicating the two receptors can be co-regulated. However, we must await further studies to see how this affects the biological functions listed above. CB2 & Chemokine Receptors Chemokine receptors generate signals that lead to cellular migration and proliferation. Although there are important roles for chemokine receptors in healthy tissues, they also can promote cancer cell development and metastasis. Expression of the chemokine CXCR4 receptor on tumor cells is a negative prognostic factor associated with increased tumor aggressiveness, metastasis, and decreased probability of survival. A 2016 study has shown that the CB2 and CXCR4 receptors can form heterodimers in breast and prostate cancer cells. Simultaneous activation of both receptors led to reduced CXCR4 signalling. Downstream effects of this included reduced cancer cell migration, which is an important step in metastasis. This study shows that receptor dimerization is a new mechanism of how cannabinoids can exert effects on tumours.