Biological explanations: Dopamine hypothesis Flashcards
Biological explanation 1
Dopamine hypotheis
Initial Hypothesis
The initial concept of the dopamine hypothesis was very basic. Individual have too much nt dopamine, so they demonstrated symptoms associated with high levels of dopamines
However, when drugs were administered to individuals, they reduced the positive but no negative symptoms
Modern
In years, dopamine in the limbic system has been the main area of study. Research (Cole et al) has been able to show the impact of anti psychotic drugs on d2 dopamine receptor cites. Found primarily in subcorticol regions. Cole et al administered a conventional anti-psychotic drug to patients so they can block the D2 receptors, 75% were improved.
Mesolimbic and positive symptoms
Dopamine is a major neurotransmitter in the mesolimbic pathway. This pathway carries signals from the ventral tegmental area to the nucleus accumbens
Too much dopamine, either from neyorins fire too often or quickly, cause over stimulation and ultimately positive symptoms of schz, such as hallucinations and delusions.
Negative and mesocortical pathway
Dopamine is a major neurotransmitter in the mesocortical pathway.
Carries signals from the ventral tegmental area to the frontal lobe
To little dopamine in the D1 receptors of the frontal lobe has been known to cause cognitive impairments and negative symptoms of schz
Chlorpromazine
Chlorpromazine is very effective in the treatment of schizophrenia. This antipsychotic drug works by reducing the levels of dopamine inherent an individual. The main cause of poise symptoms in schizophrenia.
Anphetamine
Amphetamine causes the brain to respond as if there is too much dopamine in the brain (although the dopamine levels remain unchanged) High doses of amphetamine produce some symptoms of schizophrenia.
L- dopa
L-dopa is used for parkinsons disease, which increases dopamine levels can produce many of the symptoms of schz
Lavender
lavender said that evidence of whether dopamine is responsible is inconclusive as there is is no consistent difference in dopamine levels between drug-free schizophrenics and non-schizophrenics. Lloyd developed this further by adding that even if dopamine was a causative factor, it may be indirect, e.g. abnormal family circumstances giving rise to high levels of triggering symptoms. Dopamine hypothesis is not reliable if there is no consistent difference between levels of dopamine in drug free schizophrenics and non schizophrenics, therefor dopamine may not be as closely linked to schz as people may suggest
Schizophrenia working group of the psychiatric genomics
in 2014. there was 108 genetic loci associated with schizophrenia. There is also a genetic basis to schz, not just dopamines.
Cause
We don’t know if schz causes abnormal dopamine levels or if abnormal dopamine levels causes schz. Research using PET scans hasn’t yet been able to detect differences in dopamine activity in the brain of individuals with schz and those without. this suggests that it may be some time before we know for certain if dopamine imbalances cause schizophrenia or the other way round.
Biological 2
Genes