A problem with this is that it doesn’t state whether it is cause or effect. Significant support for the biological explanation of depression comes from neuroendocrine factors. Cortisol levels are higher in depressed people. A stress reaction leads to the production of Cortisol, a key hormone in arousal. In normal people a mechanism prevents excessive or prolonged arousal in response to a stressor.
When the nicotine in a cigarette is inhaled this activates nicotinic receptors in the brain which leads to a release of dopamine in the NA. This creates a sense of pleasure however this sensation of the nicotine is rapidly broken done by enzymes in the liver and removed from the bloodstream so within hours this pleasure sensation is replaces by low moods and reduced concentration. According to the biological model people with certain genes may find it harder to stop behaviour once it has started. There is no single gene responsible for this, however a number of genes have been linked to playing a role. 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.
So again strongly suggests that low activity noradrenaline, is a factor contributing to the cause of depression. Support for this explanation has also come from research studies. Findings from psychologists , have led to the idea that depression is caused by a depletion of these naimes , especially serotonin and noradrenaline (in which I have discussed), however this idea is too simplistic, when infact its more complex than that. A example of why it is more complex is from the original theory, is that anti depressants do
The fact that both twins wouldn’t always develop schizophrenia means that another factor must be involved, for example family environment. Too much or too little of a particular neurotransmitter may produce psychological disorders. For example, an increased level of dopamine is linked to schizophrenia, and drugs like cocaine, which increase dopamine levels, can lead to schizophrenia like problems. Also, depression can be effectively managed and often treated with drugs that manage serotonin levels in the brain. However, Watson et al found that low serotonin levels may in fact be due to environmental factors.
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.
When serotonin is released by one cell, it enters the next cell through an area of the cell membrane called the receptor. In OCD, some receptors are thought to block serotonin from entering the cell. This leads to a deficiency in the neurotransmitter in key areas of the brain; i.e. people with OCD may have too little serotonin for their nerve cells to communicate effectively.Dopamine activity:40% of OCD patients do not respond to SSRIs, suggesting that, in some at least, other neurotransmitters are involved. Animal studies have shown that high doses of dopamine aginists induce stereotyped movements in animals that resemble the compulsive behaviours found in OCD patients.
Generic name is tramadol. This is a nonopioid analgesic, but it does have weak agonist activity at mu opioid receptors. However, it causes minimal respiratory depression (although the patient should still be monitored for this). Previously was not a controlled substance, but was switched to a schedule IV in 2014. Notable side effect: seizures. Avoid use in clients with or at high risk for seizures.
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
People with bipolar disorder have a genetic predisposition to this disease. This is because neurotransmitters, norepinephrine and serotonin play a part in mood disorders. The structure of the brain can influence a person with bipolar disorder. Research shows people with bipolar disorder have a smaller hippocampus and amygdale. This might be possible because of an excess stress hormone cortisol [ (Sparknotes, 2009) ].
Causes The exact cause of depression is uncertain. A large number of researchers believe it is caused by chemical imbalances in the brain, which may be hereditary or triggered by events in a person's life. Some forms of depression tend to run in families, but depression can also appear in people who have no family