Ketamine has been studied more than a few times recently for it’s use as a treatment for depression. The most recent research from Penn State University will be published in September 2016 and reveals much more about the biology behind depression, what happens in certain brain receptors and how the mechanism of certain drugs can offer new hope for those who suffer from depression. This research demonstrates the effectiveness of ketamine to treat depression.
The research is being led by Bernhard Lüscher, professor of biology and of biochemistry and molecular biology at Penn State University who said that about 17% of Americans will be treated at some point for depression, but about 1/3 of those patients will not respond to available treatments. In addition, many people who have symptoms do not seek treatment because they believe it will not work.
Lüscher and the team at Penn State genetically altered lab mice to show symptoms of depression by introducing a mutation into a gene that codes for one of the subunits of a receptor for GABA -- the second most abundant chemical used by nerve cells in the brain to communicate. GABA functions mainly to reduce the activity of nerve cells. The receptor mutation results in a reduction in GABA signaling of about 15 to 20 percent. Patients who have depression very often have poor GABA signaling and reduced receptor activity. The mice in the study that were altered to have the mutation exhibited classic behaviors associated with depression, such as reduced pleasure seeking and interaction with others and these behaviors were eliminated following treatment with antidepressant medications.
In a press release Lüscher said, "You can think of GABA as acting like the brakes of a car -- its function is to slow activity in nerve cells. Its counterpart is glutamate, another signaling chemical in the brain that acts as the accelerator of nerve-cell activity. When we reduced the function of GABA in our mice, we were surprised to see that the level of glutamate was also reduced. This result suggests that the brain has mechanisms that maintain a balance between the brakes and the accelerator to prevent brain activity from going out of control, a state we refer to as homeostasis."
The researchers treated the mice with low doses of ketamine. Currently it is being tested as a possible antidepressant, but is mostly used in anesthesia, providing pain relief, a trance-like state and memory loss. It’s often referred to as Special K when sold and used as a street drug. The chemistry of ketamine results in the blockage of glutamate receptors in nerve cells. In the study at PSU, when ketamine was used, glutamate receptor activity was brought back up to functional levels and GABA function was also improved. Lüscher believes the results show that two hypotheses about the mechanism of depression(GABA signaling and glutamate deficits) are likely a significant part of the cause of it. Ketamine as it exists now is not completely safe to use in humans but the team hopes to do further research to develop a form of the drug that is not addictive and does not carry the risk of inducing psychosis. The video below explains more about the study.
Source:
Penn Statue University,
PsyPost
