Neuroscience

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Neuroscience
Late in the nineteenth century when tuberculosis set in, the actual cause of the disease was not known and it was linked to the famous personalities. Later in the mid-twentieth century, it was discovered that the illness was communicable and that a bacteria caused it. Scientists failed to identify the cure of the drug, till when some doctors discovered Iponiazid. They were optimistic that the medicine would cure the illness. However, the administration of the drug only revealed that the patients expressed relief from stress, with some of them dancing in the halls. Contrarily, the mortality rate remained constant. How possibly could a drug prevent depression and post-traumatic stress disorder? (Brachman 00:00:12-00:01:13).
When Iponiazid was discovered, the doctors did not realize its antidepressant properties. Instead, they listed euphoria as a side effect of the drug when managing patients with tuberculosis. Fearing that the symptom might interfere with the ability to cure the illness, they recommended that the drug was only to be administered to patients who were highly emotionally stable and in the extremity of the disease. The consumption of Iponiazid was later discovered to have dire side effects, leading to liver toxicity, suicidal thoughts and rapid weight gain. The other advantageous discovery was that it led to a rise in the levels of serotonin, which is a brain neurotransmitter. Similarly, an antihistamine discovered in the 1950’s had a similar effect.

The study of antidepressants concentrated on serotonin-related drugs. The series of studies led to the development of the selective serotonin reuptake inhibitors (SSRI’s). The earlier drugs had a disadvantage of taking an extended period before working (Brachman 00:01:18-00:06:21).
How possible would it be that the studies concentrated on the wrong neurotransmitter? If that were the case, the discovery of the ultimate antidepressants would be futile. It would similarly be difficult to discover the most appropriate antidepressant if the consumer does not express manic episodes. Calypsol was initially used as an anesthetic in surgery. Its action depended on glutamine, a different neurotransmitter. In the talk, Brachman reveals that the drug needed a keen investigation since it lacked the manic episodes which are present in most antidepressants. In fact, the drug suited the “perfect antidepressants” because of the sure half-life. In their study, mice were used and were tested in both the PTSD model and the psychological model. The results were fruitful (Brachman 00:06:25-00:11:37).
The actual cause of depression remains unknown. However, stress is an initial etiological component in over 80% of the cases. Post-traumatic stress disorder (PTSD) often occurs after traumatic events. They may include the well-known lifetime events such as active combat between individuals, sexual assault, natural disasters, violence or a road accident. Studies indicate that not all the incidences of stress lead to depression. Stress resilience, which is the inability of developing PTSD among people who are exposed to the triggering factors of strain, is also characteristic among some individuals. Unlike other antidepressants, Calypsol acts as though it enhances resilience. Furthermore, a small dose functions for a long duration. The unique roles are similar to those which immune vaccines portray, earning them the title para vaccines. However, not all antidepressants are para vaccines (Brachman 00:11:37-00:14:59).
To conclude, there are various groups in the society that might require an antidepressant para vaccine who compose of all those with predictable episodes of stress. The categories include prisoners, firefighters, rapid responders and soldiers. According to Yehiuda and LeDoux, some independent resilience-related traits decrease the susceptibility of one developing depression after being stressed (28). Since the field of neuroscience allowed fear-provoking to be used, the experiment with mice indicated success in the antidepressant (Yehiuda & LeDoux 28). The properties of para vaccines prove that indeed, a drug can prevent depression and PTSD by preventing the stress that causes depression and post-traumatic stress disorder.
Work Cited
Brachman, Rebecca “Could a drug prevent depression and PTSD?” Ted www.ted.com/talks/rebecca_brachman_could_a_drug_prevent_depression_and_ptsdYehuda1Rachel & LeDoux Joseph. “Response Variation following Trauma: A Translational Neuroscience Approach to Understanding PTSD.” Neuron Review. 56. 2007. Pp. 19-38. DOI 10.1016/j.neuron.2007.09.006