Anti depressants such as MAOI’s which increase the available amount of nor adrenaline in the brain, were found to be effective for elevating the symptoms of depression. So when noradrenalin is increased in the brain, symptoms of depression get better, suggests that it is chemicals that are the root cause of depression. This idea is also found in the results of taking reserpine, a drug used to treat high blood pressure. Depression is a unwanted side effect of this drug, as this drug acts by lowering levels of nor adrenaline. So again strongly suggests that low activity noradrenaline, is a factor contributing to the cause of depression.
This has been shown in research done by Noble et Al in which a gene DRD2 responsible for the D2 dopamine receptor, to severe alcoholism. It was found that the A1 variant of this gene was present in more than two-thirds of deceased alcoholics. Although this research does not look at smoking behaviour, it suggests that this gene plays a role in the addictive behaviour and can also be generalised to smoking behaviour. There has also been additional evidence to support the biological model as an explanation for smoking addiction. Research has been done by Silverstein et al in which it was found that biological factors may influence a person’s first positive or negative experience with their first cigarette.
The 1970s saw the publication of the first American Psychiatric Association task force report on electroconvulsive therapy (to be followed by further reports in 1990 and 2001). The report endorsed the use of ECT in the treatment of depression. The decade also saw criticism of ECT. Specifically critics pointed to shortcomings such as noted side effects, the procedure being used as a form of abuse, and uneven application of ECT. The use of ECT declined until the 1980s, "when use began to increase amid growing awareness of its benefits and cost-effectiveness for treating severe depression".
For example, Piggott et al. (1990) used drugs that increased the amount of serotonin in the brain such as the selective serotonin reuptake inhibitor (SSRI) Anafranil, which has been shown to reduce the symptoms of OCD. PET scans show lower serotonin levels in OCD patients than control patients. After treatment with SRRIs, the PET scan of an OCD patient looks more like the scan of a normal
Now the patient is hyperkalemic from the metabolic acidosis causing dysrhythmias leading to cardiac arrest. (Excited Delirium Strikes Without Warning). Dopamine can be a self-induced problem by taking illegal drugs that block the uptake of dopamine or it can be something the body produces too much of on its own. Wesley goes on to say that, “A large number of these patients who suffer from excited delirium have pre-existing psychiatric conditions…” (Excited Delirium Strikes Without
Many prescription drugs have been released onto the market that effectively target the levels of certain hormones which in turn enable one to counteract the symptoms of ADHD (3). Adderall is a cocktail of several active ingredients that include amphetamine salts, an active ingredient in many ADHD medications. These amphetamines are thought to treat ADHD by blocking the reuptake of dopamine from the neural synapses and increasing the uptake into subsequent neurons. The increased dopamine flow in the frontal cortex then allows the brain to carry on its executive functions as a normal brain would, thus counteracting the effects of ADHD(4). So, as a stressed out college student striving to succeed in school and boost my GPA, I sit here wondering how much faster and more efficiently I could have written this paper had I been taking Adderall.
People who think they have taken a drug but really haven’t may display the effects of the drug because they expect to be affected by it. The learned expectations regarding a drugs effect vary from culture to culture. 13.Depressant: reduce the central nervous system activity. Many depressants increase GABA neurotransmitter activity. Effect of alcohol: Alcohol has an impact on the dopamine, serotonin, endorphins, glutamate, and GABA neurotransmitters.
Noninvasive human brain imaging studies have shown alterations in the activity of the dopamine system that are associated with reduced motor skills and impaired verbal learning. Recent studies in chronic methamphetamine abusers have also revealed severe structural and functional changes in areas of the brain associated with emotion and memory which may account for many of the emotional and cognitive problems observed in chronic methamphetamine
Critical Point 3: There is a flaw with one of the key pieces of evidence to support the dopamine hypothesis. The drugs used to treat schizophrenia by blocking the dopamine receptors can actually increases it as neurons struggle to compensate for the sudden deficiency. Haracz, in a review of post-mortem studies of schizophrenics, found that most of those studied who showed elevated dopamine levels had received antipsychotic drugs shortly before death, unlike post-mortem of schizophrenics who hadn’t received medication these results showed that these individuals had normal levels of dopamine. Therefore, this evidence weakens the support for the dopamine
This is described by the dopamine hypothesis which states that schizophrenia is due to a high density and a high level of sensitivity of dopamine receptors. Due to this the neurons that transmit dopamine fire too easily or too often. More specifically Weinberger claims that the illness is due to over-activity in the pathways linking the mid-brain to the limbic system and under-activity linking the mid-brain to the