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Active participation of dopamine in the cause of schizophrenia has been an area of interest to researchers. Different versions of the postulated hypothesis have evolved as a result of this.
The cortical configuration of the neurotransmitter is classified into the mesocortical, nigrostriatal, and mesolimbic. Any atypicality in the configuration could cause dopamine dysfunction in the secretory areas located within the skull.
Schizophrenia disease typically commences in early adulthood (ages 15 and 25) and earlier in men than women. Women notably above the age of 30 have been discovered to develop a mental disorder. It is also less frequent in teenage below 10 years and adults already above 40 years without any noticeable onset signs.
The early gimmick of dopamine role in schizophrenia summarizes the relationship to mean when the brain is copiously dopamine enriched, the neuro region becomes hyperactive and schizophrenic signs (sometimes called dementia praecox) could be observed. The Swedish neuropharmacologist Arvid Carlsson presented an inept affirmation concerning a proposition of the bonds of psychotic medicines gravitation of the neurotransmitter’s hike in the neuro-organ. These antipsychotic drugs feature most recreational drugs such as cocaine. Their neural effect could mimic schizophrenia feelings.
However, the enigma most researchers seek an answer is a factual link between the two. Substantial explanation of this puzzle is presumed could help develop a dopamine theory of schizophrenia.
Considering intellectual battles and time of presentation, this is in three versions ― version I, II and III. Prior to the version I proposition, dopamine was not recognized to be a neurotransmitter but instead a norepinephrine precursor.
- Dopamine hypothesis ― version I
The version I dopamine hypothesis schizophrenia postulated schizophrenia is caused by the spike in dopamine receptors present in the brain. This was noted to be prevalent following the administration of the psychotic drugs. Therefore, the strength of antipsychotic drugs schizophrenia assuage is directly linked to its ability to dissipate psychoactive chemicals at the dopamine receptors as much as possible. However, if dopamine is displaced beyond normal leading to hyposecretion, such may result in associated psychiatric problems like Parkinson’s.
- Dopamine hypothesis ― version II
In furtherance of discovering actual linkage of schizophrenia and dopamine, the version II dopamine hypothesis of schizophrenia was premised. Although it contends the explosion of the neurotransmitter (i.e. subjected to the concerned area). It also opined schizophrenia symptoms are not solely caused by dopamine soar but also could be due to low dopamine level depending on the cortical area examined. Prefrontal hypodopaminergia and subcortical hyperdopaminergia regions of the cerebral matter identified to be related to schizophrenia without neglecting the signified differential schizophrenia dopamine levels.
- Dopamine hypothesis ― version III
Technology and research have advanced beyond the state they were when the previous two versions were proposed. Thus, this version combines the old versions postulations and observed changes ever since to analyze contributing and observed factors of schizophrenia ― provide a parsimonious brief of the association between dopamine and schizophrenia. It hypothesizes environmental and genetic risks could cause schizophrenia through a final common pathway. The pathway is guesstimated to be through the presynaptic striatal hyperdopaminergia.
Dopamine and schizophrenia
Experts denouement concur with the postulation that too much dopamine schizophrenia exerts the lethargic denouement on the encephalon. Thus, patients are prescribed medications which debar dopamine receptors D2 to allay symptoms.
Schizophrenic sufferers would experience an interpolation of the neurotransmitter in the thalamus and striatum, inducing irregular measures of D2 receptor possibility of binding.
The augmented subcortical production which invariably causes D2 receptor activation is blamed for dopamine psychology which may include hallucinations and delusions. This is a hypothesized sequel of stir-ups in the cortical pathway through the nucleus accumbens. Other schizophrenia portents married to dopamine increase in the brain include anhedonia, loss of motivation, speech deficiency, and paranoia. The speech deficiency and D1 receptor trigger cooperate. It is worthy to note that the D1 abundance supersedes that of other dopamine receptors.
Dopamine chemical structure
Dopamine is a monoamine (catecholamine) neurotransmitter that has a benzene ring, two hydroxyl side groups at carbons 1 and 2 and a side chain amine. Its chemical name is 4-(2-aminoethyl) benzene-1,2-diol and structural formula (C6H3(OH)2-CH2-CH2-NH2). Chemical structure of dopamine is facile compared to the catecholamine family. Other members of the family include norepinephrine and epinephrine. It can also be classified as a phenethylamine compound considering its possession of a benzene ring. It shares the phenethylamine membership with most psychoactive drugs.
The “jocund hormone” is found naturally in special brain cells and some external cells. Of all the locations, the medulla and adrenal glands (found at the apex of the kidney bean) are the main production sites. Physiologically, the amino acid, tyrosine is used as a precursor for dopamine in the body. Tyrosine is mainly derived from diets and sometimes from hydroxylation of phenylalanine with the assistance of an enzyme in the liver dubbed phenylalanine hydroxylase.
The amino acid is converted to dopamine, thanks to tyrosine hydroxylase (TH) and l-amino acid decarboxylase (AADC) named dihydroxyphenylalanine (DOPA) decarboxylase (DDC).
Aside from the TH and AADC enzymes, there are two other dopamine producing enzymes needed and accretion of another three coenzymes. These enzymes include THFA which is responsible for converting L-tyrosine to L-dopa; pyridoxal phosphate which is concerned with turning L-dopa to dopamine; and nicotinamide adenine dinucleotide (NADH) tasked with tetrahydrofolic acid (THFA) forming THFA and pyridoxal phosphate.
In summary, dopamine synthesis progressed from amino acid tyrosine to form L-dopa and finally dopamine. More important to note, L-dopa is formed by hydroxyl group annexation to the third carbon of the aromatic ring of tyrosine and it can also cross the blood-brain barrier while dopamine cannot.
Psychology of dopamine schizophrenia
The psychological effects of dopamine schizophrenia are classified as negative and positive symptoms. The positive symptoms are brain psychology related to exaggeration of situations and the inability to differentiate between real and imitated occurrence. Psychological positive symptoms include trouble concentrating, hallucinations, and confused thoughts. Negative symptoms are brain psychology associated with psychological dysfunction such as lack of pleasure and withdrawal.