 Our seventh presenter is Daniel Suarsky. What my thesis project is about is opioids and finding a cure, possible cure for chronic pain inhibition. So, since the early 1800s, pharmaceutical companies have been trying to develop and isolate the perfect treatment for chronic pain. And this began with the isolation of morphine in the early 1800s, but was soon brought with negative consequences of addiction and other adverse side effects. Shortly thereafter, the pharmaceutical company Bayer decided it was going to create the heroin of all medications and came up with heroin as their treatment for chronic pain. Now, this obviously was not good, and since then we still have a huge problem with opiates and spend over $14 billion a year in prescription opiates. All of these having negative consequences. So, we really need an alternative target to these traditional opiates and one possibility is to target a different protein than the traditional opiates, which is the delta-opiate receptor. Now, in order for these drugs to work, they have to bind to a protein in the cells in our body to cause an effect. And these are called receptors, and the classical opiates bind to the mu-opiate receptor. And they need to be on the surface of neurons to inhibit pain. As you can see here is an example of the mu-opiate receptor. But the delta-opiate receptor is actually expressed in the inside of these neurons, so it doesn't work. And so, what we hypothesized was maybe if we can induce the delta-opiate receptor to the surface, this could be an alternative target for chronic pain, and this might be less addictive because they're expressed in a different population of neurons that don't lead to the same addictive side effects. So what I was able to determine is that through the pathway of making these receptors, the delta-opiate receptor traffics from the endoplasmic reticulum, which is like the factory of proteins, through the Golgi apparatus, which you can think of as the shipping and receiving center, and is stuck in the trans-Golgi network, which is kind of like the UPS of the cell. And it waits here for a trafficking signal. You can think of this as either a red light or a green light to get to the surface. And so I was able to identify the mechanism that held the receptors inside, and then we were able to use different pharmacological agents to drive these receptors to the surface, give them the green light, and influence their surface presence. Now this was able to be done in a mouse model of chronic pain, and by driving these receptors to the surface, we were able to treat the mice with delta-opioid agonists that were previously unaffected and provide pain inhibition. Now this not only provides a mechanism for driving receptors to the surface to treat chronic pain, but shows a new paradigm where by influencing increased expression of these receptors on the surface, we can make agonists that were previously unaffected effective.