Rat Model Of Depression : Induced By Daily I.p

Chronic intake, the delayed onset of action, drug resistance and numerous side effects force the researchers to look for the new, safe antidepressant strategies (1, 2) with rapid onset and longer time of action.

Major depressive disorder is one of the most common mental disorders, with a 12-month prevalence of 6.7% of adults in the United States (NIMH). There is no definite etiology of depression, but several risk factors have been identified. Functional and structural changes in the brain have also been explored. The most common treatment for depression is the use of drugs that act on monoamine transmitters, including norepinephrine, dopamine, and serotonin. Decreases in these transmitters, especially serotonin, were hypothesized to play an important role in the cause of depression (Breedlove & Watson, 2013). The serotonin hypothesis led to the development of selective-serotonin reuptake inhibitors (SSRIs), which increase the amount of serotonin in the brain. Further research suggests that the serotonin hypothesis is not entirely accurate and the neurobiology of depression is much more complex. The “chemical imbalance” explanation of depression may not reflect the full range of causes and may be given greater credibility by patients and doctors than is supported by evidence based research.

The body naturally produces these compounds, which are similar to the chemicals in cannabis. Reduction of endocannabinoid production is one reason why chronic stress is a major risk factor in the development of depression. The research team at the university administered marijuana cannabinoids to the rats, finding it to be an effective way to restore endocannabinoid levels in their brains, alleviating some symptoms of depression. In addition, the university that found synthetic cannabinoids activated the part of the brain associated with traumatic memories in rats, preventing the behavioral and physiological symptoms of PTSD. The article notes that depression is such a complex mental disorder as well as alleviating it with cannabis. Because of the lack of testing on the relationship between cannabis and depression, there is no 100% statement claiming that marijuana can help depression in human trials, although there are promising lab tests on rats.

The belief is that antidepressants work by increasing levels of a group of chemicals in the brain called neurotransmitters. Certain neurotransmitters, such as serotonin and noradrenaline, can improve mood and emotion, although we do not yet fully understand this process

In order to be able to treat a person with depression effectively, doctors have to sort out what kind of role the narcotics may play in the depression. If the feelings of depression is simply a part of a withdrawal due to a narcotic and are only something temporary, it is very unlikely that a antidepressant will be of any benefit. Antidepressants take a bare minimum of two to three weeks to begin working. The most effective treatment in such a case would be to try and help the person at hand to get their drug use under control or stop entirely. Both taking drugs and the withdrawal process may produce depressive symptoms themselves, makingit very difficult to know what it is that’s exactly going on, if it even seems that the depression led to taking drugs in the first place. As a result, It’s extremely vital to the treatment of the individual that the problem with narcotics is sorted out so that is will be possible to further judge whether antidepressants or other treatments used for depression will be needed. This, of course, does not mean it’s

Marijuana – interacts with different antidepressants in different ways. With tricyclic antidepressants, it can cause confusion, hallucinations, and chest pain. Marijuana decreases the effectiveness of MAOIs, but interacts very lightly with SSRIs, possibly causing drowsiness.

The patients were involved in the examination of the correlation between the treatment response to rTMS and the regional CBF in the frontal regions, by analyzing their brain scans before the rTMS treatment. The administration of the rTMS was utilized by using a Magstim Super Rapid. There was a total of 12 treatment sessions during a three week period. The study focused on 16 brain regions, which had some correlation with the improvement of depression by rTMS

Drugs that are depressants include Zyprexa, Seroquel and Haldol, are known as major tranquilizers or antipsychotics, they reduce the symptoms of mental illness. Some other depressants, such as Amytal, Numbutal and Seconal, are classed as barbiturate, which are used as sedatives and sleeping pills. Depressants have the effect of feelings of well-being, lowered inhibition, slowed thinking, slowed muscular activity,a distorted view of the world, or hallucinations Depressants act on the brain by affecting the neurotransmitter GABA. By increasing GABA and inhibit brain activity,they produce a drowsy or calming effect beneficial to those suffering from anxiety or sleep

The pertinent findings will be explained, and their implications on future anti-depressants will be addressed.

Depression is a widespread issue in today’s world. It can be caused by abuse, conflict, a sudden change in one’s life, and much more. The number one cause of depression is stress. Cannabis, or marijuana, has been used to treat depression dating back to the year 1621 with doctors in India using it to treat depression in their patients. THC, or tetrahydrocannabinol, was shown to change negative images or emotions in the minds of the patients who smoked marijuana. Many patients stated that it took them to another world, a place where they felt comfortable and the feeling of depression was obsolete. The sad part is that since marijuana is still classified as 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).

(3) While successful drug therapies which act on neurotransmitters in the brain imply that depression is a neurobiological condition (4), the fact that such medications do not help about 20 percent of depression-sufferers seems to show that not all depression is due to such imbalances. Rather, depression is not caused by one single factor; it is most often caused by many different things. Genetics, biochemical factors, medicines and alcohol, developmental and other external factors, and relationships, marriage and children all have effect on the development of clinical depression. (5) The strongest hypotheses on the pathways to depression are in decreases in the activity of specific neurotransmitters, or the overactivity of certain hormonal systems. (3)

As the literature remains inconclusive as to the relation between current major treatment modalities and depressive disorder, and given the extremities of the potential dangers of antidepressant medications, it is apparent that there is a need to develop new interventions, which show greater efficacy, safety, and acceptability.

Antidepressants influence neurotransmitter systems, including norepinephrine, serotonin and dopamine. We know that selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants are classes of antidepressants (Brandon & McKay, 2015). Fluoxetine (FLX) is a well-known and extensively studied SSRI antidepressant. Thus, FLX’s actions include increasing the amount and duration of serotonin availability in the brain by preventing its reuptake (Brandon & McKay, 2015). Few studies have suggested that FLX could work to stabilize weight recovery in AN patients. Klenotich et al. (2012) evaluated the efficacy of FLX in survival, weight gain and food intake in comparison with OLZ and controls in ABA mouse models. ‘Survival’ was a measure of the number of days passed before a mouse lost 25% of its initial body weight. 20 ABA mice were treated with vehicle (VEH—control procedure), 20 were treated with FLX (18 mg/kg/day) and 20 were treated with OLZ (12 mg/kg/day). Results show that between the FLX and OLZ treatments, no effects were found on body weight, but both led to an increase in food intake. Furthermore, FLX had no effect on survival while OLZ increased survival, by prolonging the number of days before the mice lost 25% of their initial weight (see Figure 7). Henceforth, it is demonstrated that FLX doesn’t increase body weight or prolong survival in ABA models.

Many regions of the brain contain cannabinoid receptors, of which anandamide molecules, concerned with regulating mood, appetite and emotions, naturally bind to. Cannabis contains an active ingredient known as ‘delta-9-tetrahydrocannabonic’ (THC), and when smoked or eaten, the THC imitates the activity of anandamide by binding to cannabinoid receptors on nerve cells, and therefore influences