Dopamine is one of the neurotransmitters playing a major role in addiction, Parkinsonism and schizophrenia. It is sometimes called the “spring of happiness” but how does dopamine work? And why is it associated in these disorders? As some would say, too much of something is bad, and too much of nothing is bad too. This is what happens with dopamine. According to Merriam-Webster Medical Dictionary 2006, Dopamine is a monoamine C6-H11-N02 that is a decarboxylated form of dopa and occurs especially as a neurotransmitter in the brain and as an intermediate in the biosynthesis of epinephrine.
Dopamine is similar to adrenaline. It affects brain processes that control movement, emotional response, and ability to experience pleasure and pain. The system of dopamine is drawn in the control of locomotion, cognition, and endocrine function, its relative contribution of the various dopamine-related a component is not well established mainly because drugs that target the dopaminergic system often lack selectivity. According to Joyce LeFever- Kee, In Parkinson’s disease, it is caused by an imbalance of the neurotransmitters dopamine and acetylcholine.
It is marked by degeneration of neurons that originate in the substantia nigra of the midbrain and terminate at the basal ganglia of the extrapyramidal motor tract. By the time early symptoms of Parkinson’s disease appear, 80% of the strial neurons synthesize the dopamine from levodopa and release dopamine as needed. Before the next dose of levodopa, symptoms (e. g. slow walking, loss of dexterity) return or worsen; within 30 to 60 minutes of receiving a dose, the client’s functioning is much improved. By this, it shows that dopamine plays a big part on Parkinsonism. Very low level of dopamine affects a person’s function.
A type of dopaminergic drug that is used to treat Parkinsonism is levodopa. Levodopa is the most effective drug for diminishing the symptoms of Parkinson’s disease. Its major benefit increased mobility. Because dopamine cannot cross the blood-brain barrier, levodopa, a precursor of dopamine that can cross the blood-brain barrier, was developed. The enzyme dopa decarboxylase converts levodopa to dopamine in the brain. However, this enzyme is also found in the peripheral nervous system thereby allowing 99% of levodopa to be converted to dopamine before it reaches the brain.
Therefore about 1% of levodopa is converted to dopamine once it reaches the brain; large doses are needed to achieve a pharmacologic response. Because of these high doses, many side effects occur including nausea, vomiting, dyskinesia, orthostatic hypotension, cardiac dysrrhytmias, and psychoses. Clients who have taken levodopa for 5 years or more may experience “on-off” fluctuations in its effectiveness. During the “on” time, the symptoms of Parkinsonism are diminished or absent; however, symptoms return during the “off” time.
As a result, the levodopa dose may need to be increased or a dopamine agonist or COMT inhibitor may be added to the levodopa regimen. (Joyce LeFever-Kee 2003) With regards to addiction, it is therefore the expression of the excessive control over behaviour acquired by drug-related stimuli as a result of abnormal associative learning following repeated stimulation of dopamine transmission in the nucleus accumbens shell. This is why drug addiction is related to dopamine because the brain is automatically becoming addicted to the drug also.
It yearns for dopamine, which makes us happy, thus resulting into habitual use and eventually, addiction. Neurochemical influences on substance use patterns have been studied primarily in animal research. The ingestion of mood-altering substances stimulates dopamine pathways in the limbic system, which produces pleasant feelings or a “high” that is reinforcing, or positive, experience. Distribution of the substance throughout the brain alters the balance of neurotransmitters that modulate pleasure, pain, and reward responses.
Researchers have proposed that some people have an internal alarm that limits the amount of alcohol consumed to one or two drinks, so that they feel a pleasant sensation but go no further. People without this internal signaling mechanism experience the high initially but continue to drink until central nervous system depression is marked and they are intoxicated. (Joyce LeFever-Kee 2004) To further explain, these effects resemble those of a reward like food except that nicotine-induced release of dopamine does not undergo single-trial, long-lasting habituation.
It is speculated that repeated non-habituating stimulation of dopamine release by nicotine in the nucleus accumbens shell abnormally facilitates associative stimulus-reward learning. Acute effects of nicotine on dopamine transmission undergo acute and chronic tolerance; with repeated, discontinuous exposure, sensitization of nicotine-induced stimulation of dopamine release in the nucleus accumbens core takes place while the response in the shell is reduced. In schizophrenia, previous neurochemical studies have consistently demonstrated alterations in the neurotransmitter system of the brain.
The neuronal networks that transmit information by electrical signals from a nerve cell through its axon and across synapses to postsynaptic receptors on the other nerve cells seem to malfunction. The transmission of the signal across the synapse requires a complex series of biochemical events. Studies have implicated the actions of dopamine, serotonin, norepinephrine, acetylcholine, glutamate, and several neuromodulary peptides. According to Jacob & Silverstone 1986, some of the most obvious evidence for this theory is from the effect of drugs such as amphetamine and cocaine.
The drugs mentioned increases the levels of dopamine in the brain and can cause psychosis, particularly after large doses or prolonged use. This is often referred to as ‘amphetamine psychosis’ or ‘cocaine psychosis’, but may produce experiences virtually indistinguishable from the positive symptoms associated with schizophrenia. However, the acute effects of dopamine stimulants include euphoria, alertness and over-confidence; these symptoms are more reminiscent of mania than schizophrenia.
Plus, more recent experimental studies have shown that amphetamine increases the level and intensity of psychotic symptoms in people who already have, or are liable to psychosis. Some functional neuroimaging studies have also shown that, after taking amphetamine, patients diagnosed with schizophrenia show greater levels of dopamine release (particularly in the striatum) than non-psychotic individual. Concomitantly, those treated with dopamine enhancing Levodopa for Parkinson’s disease can experience psychotic side effects mimicking the symptoms of Schizophrenia.
Genetic evidence has suggested that there may be genes, or specific variants of genes, that code for mechanisms involved in dopamine function, which may be more prevalent in people experiencing psychosis or diagnosed with schizophrenia. It proves that dopamine is a contributing factor in resulting schizophrenia. It plays a huge part in the neurochemicals of our brain. Disturbance of dopamine or other brain imbalances plus other factors like genes, environmental factors and emotional problems will result into schizophrenia.
However, dopamine can also be of good use in patients with schizophrenia. According to O’ Connor, 1998, when a drug blocks the postsynaptic dopamine receptors, the more effective it is in decreasing symptoms of schizophrenia. It shows how the symptoms of schizophrenia can be controlled by controlling the dopamine levels of the brain. Therefore, neurological diseases, even if they are of different signs, symptoms or even etiology, all of this are affected by the dopamine neurotransmitter simply because dopamine is important in maintaining our homeostasis.
If there is a depletion, excess or imbalances in dopamine, either which it could affect our optimum level of functioning. References – Brunner ; Suddarth’s 2004. Textbook of Medical-Surgical Nursing-10th ed; Vol. 2 – Kee, Joyce LeFever 2003. Pharmacology: a nursing process approach/ Joyce LeFever Kee, Evelyn R. Hayes- 4th ed. – Merriam-Webster Medical Dictionary 2006 – O’ Connor, F. L. 1998. The role of serotonin and dopamine in schizophrenia. Journal of the American Psychiatric Nurses Association, 4(4), S30-41. – Videbeck, Shiela 2004. Psychiatric mental health nursing/; 2nd ed.