This article is a follow-up to a previous article that I have written about the effects of ketamine on the symptoms of depression. I go into further detail about how ketamine works and the future of using this drug.
When treating depression, doctors typically use trial and error with prescribing the right medication for their patient. There are several medicinal options: tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), selective serotonin reuptake inhibitors (SSRIs), and serotonin and norepinephrine reuptake inhibitors (SNRIs). These medications can improve a person’s symptoms, but may take weeks, even months to have an effect. Naturally, the effects are felt only if the right drug and dose are prescribed; this is where the trial and error comes in.
Researchers at Yale University have found that ketamine may hold the answer to future treatment of depression. It has been discovered that a single intravenous dose of ketamine not only rapidly reduces depression, but last for up to ten days. Furthermore, the scientists have found that the enzyme mTOR, which controls protein synthesis, holds the key to sustaining the effects of ketamine past the ten day period. Scientists are hopeful that this discovery will pave the way for a more accurate and successful treatment of depression in the near future.
The Function of Neurons in the Brain
To fully understand how ketamine works, it must first be understood the basic structure of the brain and its functions. Learning about the brain may seem intimidating; indeed, it is a complex organ. But, it comes down to one “fundamental building block: the neuron” (Knierim, 2010). In simple terms, a neuron is a cell that processes and transmits information. “The human brain has roughly 100 billion neurons, each of them having several thousand connections to other neurons. This comes up to a whopping total of 500-1000 trillion connections within the brain,” says Knierim.
Neurons are responsible for transmitting information throughout the body. Under normal circumstances, a transmission may be sent to provide the necessary coping mechanism that is needed for a stressful situation. For instance, “The behavioral stress response involves multiple brain systems including not only activation of the hypothalamic-pituitary-adrenocortical axis but also initiation of complex cascades of reactions mediated by several neurotransmitters, including release of the excitatory amino acid neurotransmitter glutamate” (Rot, Charney, & Mathew, 2008).
However, when the stress becomes chronic, the neurons become damaged and result in depression or even bipolar disorder. It has been speculated that an extrasynaptic accumulation of glutamate is a direct result of such stress (Rot, Charney, & Mathew, 2008). This could ultimately lead to cell death in the brain. The good news is that it has been learned that “ketamine acts on a pathway that controls the formation of new synaptic links between neurons, encouraging synaptogenesis” (Paddock, 2010).
Studies, Benefits, and the Future of Ketamine
In one clinical study, 17 participants who suffered from moderate to severe depression were analyzed. All participants did not respond to existing pharmaceutical treatments. In week one of the experiment, were given a single intravenous dose of ketamine or a placebo. In week two, the participants that received the placebo now were given the single intravenous dose of ketamine. Those who received the ketamine in week one did not receive the placebo unless they showed no improvement. Preliminary results showed that symptoms of depression improved by 50 percent in 12 out of 17 participants that received ketamine. The effects of the ketamine typically lasted for a week, and up to two weeks (Khamsi, 2006).
The results were somewhat of a surprise to researchers. While they were hopeful and believed that ketamine would indeed have a positive effect, they did not anticipate the long-lasting effect of the drug. They were also pleasantly surprised at how quickly ketamine worked. Ketamine was able to accomplish this by reducing the effects of the neurotransmitter, called glutamate. As mentioned above, the over accumulation of glutamate is caused by extreme stress and may lead to depression disorders and even cell death.
Further research of ketamine and its effectiveness on treating depression is needed in order to fully grasp its potential. Now that the Food and Drug Administration has given its official seal of approval, such research can be realized. Undoubtedly, one of the first things researchers will explore is how to prolong, or sustain the effects of ketamine. Another area to be explored should include alternate ways of administering the drug, as intravenous applications will have to be done in a controlled environment.
Khamsi, R. “Ketamine relieves depression within hours.” NewsScientist. http://www.newscientist.com/article/dn9696-ketamine-relieves-depression-within-hours.html . Accessed 21 Sept. 2010
Knierim, T. “Thinking machine: the human brain.” The Big View. http://www.thebigview.com/mind/neuron.html . Accessed 18 Sept. 2010.
Paddock, C. “New form of ketamine treats depression ‘like magic.'” Medical News Today. http://www.medicalnewstoday.com/articles/198483.php . Accessed 21 Sept. 2010.
Rot, M., D. S. Charney, S. J. Mathew. 2008. “Intravenous ketamine for treatment-resistant major depressive disorder.” Primary Psychiatry, 15(4): 39-47. http://web.ebscohost.com.ezproxy.apollolibrary.com/ehost/pdfviewer/pdfviewer?vid=4&hid=109&sid=ccd8f0c0-7297-4c0c-b2c7-48e9a9de54c8%40sessionmgr114 . Accessed 21 Sept. 2010.