Introduction Chronic intake, delayed onset of action, drug resistance and numerous side effects of current antidepressants have forced researchers to look for new and safer drugs (1, 2) with rapid onset and longer acting times. Results obtained in recent years have been encouraging, especially with ketamine a global NMDAR antagonist. The antidepressant-like activity of ketamine has been shown in many preclinical studies (1–7). A single non-anesthetic dose of ketamine reversed the symptoms of clinical major depression (MDD) (8). The antidepressant effects of ketamine were also observed in patients who suffered from treatment-resistant depression or suicidal ideations (9–12). Despite successful clinical trials with ketamine, its use on a …show more content…
Because Ca2+ is the focal point to all the processes mentioned above, we have focused our study on hyperforin a Ca2+-modulator. Hyperforin is the natural and biologically active compound extracted from Hypericum perforatum (St John’s Wort) (26). Both St John’s Wort and hyperforin attenuated symptoms of mild to moderate depression in a few clinical trials and displayed antidepressant-like activity in preclinical studies (27, 28). From a molecular perspective, hyperforin has a multi-directional mechanism of action. It acts on ligand-gated (GABA, NMDA, and AMPA receptors) (29, 30) and voltage-gated channels (Ca2+, K+, and Na+) (29, 31). In contrast to blockade of ion transport through the plasma membrane, hyperforin can increase inward Ca2+ currents. These processes are dose-dependent and may involve different cellular events. In vitro studies have shown that hyperforin increases intracellular Ca2+ levels by the activation of the non-selective canonical transient receptor potential 6 channel (TRPC6) or by releasing Ca2+ from the mitochondria (32–34). As has been previously shown, hyperforin activates intracellular signaling pathways leading to changes in intracellular Ca2+ levels. Leuner et al. showed that hyperforin increased the
A case report showed Dextromethorphan was effective in a middle-aged man with Major Depressive Disorder. A 51-year–old Caucasian male with DSM-V Major Depressive Disorder, recurrent, severe, non-psychotic and Generalized Anxiety Disorder was treated with 600 mg/day of CYP2D6 inhibitor bupropion XL (a common antidepressant drug) and a 60 mg BID oral dose of Dextromethorphan. The patient showed improvement in major depressive disorder without side effects. This case study was the first to show the fast acting effect of Dextromethorphan in major depressive disorder in humans. This adds to the building literature on the antidepressant effects observed in Dextromethorphan. The report suggested the administration of other common antidepressants with Dextromethorphan, such as lithium might prolong the duration of the rapid-antidepressant effect [19].
Individuals all over the world suffer with clinical depression, which affect their quality of life. Depression usually affects a person’s emotions, thoughts, behaviors and overall physical health. Symptoms include sadness, guilt, moodiness, loss of interest, with drawling from people, changes in sleep, decrease in sex drive, and thoughts of self-harm or suicide. The common antidepressants take at least a two-week period to take effect; that two-week period is a critical time where a patient can increase their symptoms and experience suicidal depression. The party drug, known as ketamine has recently made a big impression for neuroscientists trying to formulate a medication to help those who suffer from clinical depression in a rapid time frame. A key element in the advancement for faster medications is realizing how and why, ketamine works so quickly, in comparison to the other generic drugs that are prescribed. According to Newport, a dose of the nonselective N-methyl-D-aspartate receptor antagonist ketamine can produce a constant antidepressant effect within hours. With the amount of experiments being conducted to expand the knowledge of ketamine, the objective is to find a solution that can be used to relieve the patients who experience serious symptoms in the fastest time possible.
Description: Ketamine is a nonbarbiturate, sedative hypnotic used parenterally to provide anesthesia for short diagnostic and surgical procedures. It is also used as an inducing agent, as an adjunct to supplement low-potency anesthetics such as nitrous oxide, and as a supplement to local and regional anesthesia. Ketamine can be used concomitantly with muscle relaxants without complication because it does not provide muscle relaxation of its own. It is a fairly short-acting agent that provides a profound, rapid, dissociative state and a short recovery time.
In the article “Club Drug Ketamine gains traction as a treatment for depression,” Jon Hamilton describes how Ketamine has a better effect on depression than most drugs or therapy methods available. Although ketamine is not approved by the FDA now, it was approved as an anesthetic back in the 1970 when it was discovered. Ketamine has been tested on patients with even the toughest depression and has shown results. In 2006, the National Institute of Mental Health conducted an experiment on patients with depression with a single intravenous dose of Ketamine and started seeing rapid antidepressant effects within a couple of hours. Dr. Feifel is one of many doctors that believe the future of psychiatry is going to include Ketamine or a derivation
Ionescu et al. (2015) examined the use of ketamine to treat bipolar depression. Ketamine is an anesthetic drug. Lately, there has been a lot of research into possible treatment of several psychological disorders using sub-anesthetic levels of ketamine. Recent research has shown ketamine to be effective at treating depression in patients with treatment resistant bipolar I and bipolar II. Ionescu et al. (2015) examined if the antidepressant effects of ketamine in bipolar patients, was lessened if they had comorbid anxiety. This study was part of a larger, double blind, placebo controlled study, which examined the safety of using ketamine with mood stabilizers. The participants in this study were split into two groups, those with comorbid anxiety, and those without. All participants received
Child-resistant blister pack: (i) 250µm white rigid PVC (ii) 9µm soft aluminium / 35g/m2 glassine paper. Compliant with BS8404.
From molecular perspective, hyperforin has multidirectional mechanisms of action. It acts on ligand-gated (GABA, NMDA and AMPA receptors) (29, 30) and voltage-gated channels (Ca2+, K+, and Na+) (29, 31). In contrast to blockade of ion transport through the plasma membrane, hyperforin can increased an inward Ca2+ current. These processes are dose dependent and probably involved a few different cellular events. In the details, hyperforin in in vitro studies increased the Ca2+ intracellular level by activation of the non-selective canonical transient receptor potential 6 channels (TRPC6) or by the releasing Ca2+ from mitochondria (32–34). As has been previously shown hyperforin activates intracellular
The demand for antidepressants has skyrocketed since the early 1990’s with a majority of users being adults. Appalling to this fact is that about half of those under the prescriptions have in the recent past visited a mental health professional. In addition to this, almost 60 percent of those who use antidepressant do not really need them. I also concur with the fact that our modern lifestyle has contributed so much to augment depression rate.
Pharmaceuticals are a very popular method of curing depression. Although they are popular these drugs show little to no progress in curing depression. In the article, "Taking Anti-Depressant Medication: A Qualitative Examination of Internet Postings,” proves this. The article gives accounts of multiple patients who have taken the medication and recorded their results. One patient states, “It seems like I’m about five times as anxious/depressed as I was pre-Paroxetine”. (353). Research proves that pharmaceuticals do not help individuals with their depression, but in fact cause it to worsen. The studies shows that many individuals receive a
The linkage of serotonin to depression has been known for the past five years. From numerous studies, the most concrete evidence of this connection is the decreased concentration of serotonin metabolites like 5-HIAA (5-hydroxyindole acetic acid) in the cerebrospinal fluid and brain tissues of depressed people. If depression, as suggested, is a result of decreased levels of serotonin in the brain, pharmaceutical agents that can reverse this effect should be helpful in treating depressed patients. Therefore, the primary targets of various antidepressant medications are serotonin transports of the brain. Since serotonin is activated when released by neurons into the synapse, antidepressants function at the synapse to enhance serotonin activity. Normally, serotonin's actions in the synapse are terminated by its being taken back into the neuron then releases it at which point "it is either recycled for reuse as a transmitter or broken down into its metabolic by products and transported out of the brain." As a result, antidepressants work to increase serotonin levels at the synapse by blocking serotonin reuptake (2).
This affects the the brain-derived neurotrophic factor (BDNF)- a crucial factor in the neurobiology of depression. The hippocampus is rich in BDNF, which is related in neuronal growth, survival and maturation, as well as arborization and synaptic plasticity in the adult brain. Stress suppresses BDNF synthesis in the hippocampus showing low concentrations in depressed patients, correlating with the severity of the depression. The use of antidepressant drugs increase its synthesis and signalling in the hippocampus and PFC. In a post-mortem study of depressed patients at the time of death, there were significant differences between the BDNF concentrations in treated and untreated patients. Antidepressants work by balancing neurotransmitters that affect mood and emotion. The use of antidepressants and going to therapy are the most effective ways to treating depression. Weight gain and the feeling of mental numbness is a side effect of antidepressants. Depression can be prevented. Daily exercise, having strong relationships,and watching alcohol intake are ways to prevent depression. Depression is a long term,recurrent condition often taking a chronic course. It is associated with significant morbidity, comorbidity and mortality (suicide and physical illness). In order to achieve and maintain optimum brain function and reduce the risk of recurrence, antidepressant drug treatment full remission is
The pertinent findings will be explained, and their implications on future anti-depressants will be addressed.
The pain spoke meanwhile sadness pierced through skins, however, the drugs was able to silence the beast within. Antidepressant the legal drug of choice is prescribed by doctors to treat a variety of medical conditions. These drugs are often prescribed by themselves or sometimes with others with the intent of having a greater effect on the beast within. Antidepressants come in several classes with each being stronger than the one before. Although antidepressants are often prescribed to treat depression in recent times the distribution of these drugs across the medical field have widened. Since the 1950s, medical personnels have moved from having two antidepressants: iproniazid and monoamine-oxidase inhibitor used to treat tuberculosis to now
In a world where the population struggles with worries of life, many men, women, and children struggle with depression; however, new studies are showing that treating the disorder with antidepressants can do more harm than good. In 1990, millions of people used Prozac, a SSRI (a type of antidepressant defined later) to treat their mental disorders (Kent). Now, with suicide the third leading cause of death among fifteen to twenty-four year olds, the numbers are skyrocketing impossibly more (Williams). Depression percentages in teens are growing at an alarming rate also, in 2012 an amazing 28.5 percent of them claiming to be depressed. Even more worrying, not only depression numbers have increased. In the
Antidepressants have been widely used and accepted to treat depression and its related disorders. Sadly, many people commit suicide in America because they are depressed and it is one of the leading causes of death taking over 41,000 lives each year (United States). This is astonishing considering that one in ten Americans is currently taking an antidepressant that is supposed to reduce suicidal thoughts and actions (Rabin). Most doctors and psychiatrists swear by antidepressants claiming that the benefits and effectiveness of them outweigh the risks and side effects, but researchers have started to uncover that this medication may not deliver as promised (Satel). New research has discovered that, “whilst antidepressants offer benefits in both