Studied by 0 people
Eduqas psych component 3
Initial dopamine hypothesis
Initially a basic concept.
Proposed that individuals with SZ had too much dopamine.
They demonstrated symptoms related to high levels of dopamine.
IDH - Griffiths et al (1968)
Induced psychosis in non-schizophrenic volunteers with the administration of dextro-amphetamine (drug that increases amount of dopamine in brain).
Volunteers demonstrated an abrupt onset of paranoid delusions and demonstrated a cold and detached emotional response.
Issue with initial dopamine hypothesis
Too simplistic.
Confirmed by the fact that administering drugs that reduce the levels of dopamine had little to no effect on those individuals who suffered mainly with the neg symptoms of SZ.
Dopamine receptor sites
Situation was also complicated by discovery of several subtypes of dopamine receptor sites, D1-D5, which are widely distributed in the cerebral cortex and also subcortically (underneath the cortex) in the limbic system.
D2 receptor was of particular interest.
Research (e.g. Seeman and Lee, 1975) had shown impact of antipsychotic drugs on this specific type of receptor.
As D2 receptors are found primarily in the subcortical regions, the limbic system became the main focus of the dopamine hypothesis.
Revised dopamine hypothesis - the limbic system
Limbic system consists of a variety of subcortical structures that are engaged in many functions, but most notably emotions, memory formation, and arousal.
Nerve pathways leave from the limbic system to many other subcortical structures and also to the cerebral cortex
Two of the main pathways associated with SZ are the mesolimbic pathway and the mesocortical pathway.
Mesolimbic pathway
Pathway carries signals from the ventral tegmental area to the nucleus accumbens.
Too much dopamine (either from neurons that fire too often or too quickly) cause overstimulation and ultimately positive symptoms of SZ.
Antipsychotic drugs reduce dopaminergic neurotransmission - reducing dopamine activity in pathway, reducing positive symptoms.
Mesocortical pathway
Pathway carries signals from the ventral tegmental area to the frontal lobe.
This nerve pathway is vital in emotional responses, motivation, and cognition.
Davis et al (1991) - noted that too little dopamine (‘hypofunction’) is evident in D1 receptors of the frontal lobe of many individuals with the cognitive impairments and neg symptoms of SZ.
Evaluation: Supporting evidence
Griffiths et al (1968)
Study clearly supports dopamine hypothesis and the concept that increased dopmaine levels are linked to psychotic symptoms.
However, use of non-schizophrenic volunteers reveals very little about actual sufferers - suggests we should question usefulness of this research.
Evaluation: Measuring metabolites (methodological issues)
In order to assess neurotransmitter levels, have to measure the metabolite levels (what neurotransmitters get broken down into) in cerebrospinal fluid.
Dopamine becomes metabolised into HVA or homovallinic acid and this is measured in cerebrospnal fluid, which can only be obtained from a lumbar puncture.
Participant’s diet and drug use may also seriously effect metabolite levels and, even when research is conducted under controlled conditions, the results can be difficult to interpret with HVA levels varying widely between participaints.
Suggests that until we have refined procedures for measuring NTs, should perhaps be cautious in the conclusions we draw from metabolite-based research.
Evaluation: Role of serotonin
Dopamine is not the only neurotransmitter implicated in SZ.
Serotonin also identified as a potential influence.
Conventional antipsychotics - traditionally worked by blockading the D2 receptor sites, however now all those with SZ benefit from these.
Atypical antipsychotics (e.g. clozapine) - block the D2 receptor and also the serotonin receptor 5-HT2A equally.
May not suggest dopamine hypothesis is completely wrong, however does suggests that it cannot explain SZ on its own.
Means that, at best, it is only a partial explanation.
Evaluation: Dopamine - cause or effect?
Although dopamine hypothesis proposes that dopamine imbalances cause SZ, it could also legitimately be proposed that SZ causes the dopamine imbalances.
Are the dopamine discrepancies seen in some people with SZ just another symptom rather than a cause of it?
Hope that as investigative techniques become less invasive, will be able to conduct research that will be able to establish what comes first, dopamine imbalance or SZ.
Research using PET scans (e.g. Copolov and Crook, 2000) hasn’t been able to even detect differences in the dopamine activity of the brains of people with SZ and those without.
Therefore, may be some time before we know for certain the cause-and-effect relationship.
Bio explanation method of modification: Drug treatments
Phenothiazine - earliest type of antipsychotic.
Sedates the person and reduces positive symptoms by binding to dopamine receptors and blocking the build-up of dopamine.
Prior to introduction of phenothiazine, SZ considered to be untreatable.
Previous unsuccessful treatments included insulin shock and ECT - controversial as involve creating an epileptic fit as a means of shocking the brain into change.
Cole et al (1964) - one of first controlled pieces of research investigating effectiveness of phenothiazines.
Reported that 75% of those given the drug were ‘much improved’, compared with only 25% of those receiving a placebo.
in addition, 48% of those in the placebo condition were considered to have gotten worse compared to none in the phenothiazine conditon.
