Psychology: Clinical – Content (AJW)
Let’s Revise: One contemporary study of schizophreniaCarlsson et al (2000)Aim: To provide an up-to-date review of the current status of the dopamine hypothesis To raise awareness of the potential role of other neurotransmitters, e.g. glutamate, serotonin and GABATo present suggestions for future drug treatments for the wide range of people with schizophrenia, many of whom are “treatment resistant” or who live with the extreme side effects (e.g. extra-pyramidal dysfunction)What does Carlsson have to say about the function of neurotransmitters in relation to schizophrenia?excess dopamine may be a by-product of dysfunction of another neurotransmitterexcess in one area of the brain may be a way of compensating for a deficiency in another brain areaWhy is Carlsson convinced that hyperdopaminergia is only part of the answer?some people with schizophrenia show dopamine levels within the normal rangedopaminergic dysfunction may only accounts for symptoms in a sub-group of patientssome people with ‘catatonic’ symptoms have hypodopaminergic activityWhat does he say about other neurotransmitters?dopamine levels may be controlled by serotonin levels, so if serotonin levels are too high, this could be linked to increased dopamine levelslow levels of glutamate, may allow both serotonin and dopamine levels to become too highglutamatergic failure in …the cerebral cortex may lead to negative symptomsthe basal ganglia could be responsible for the positive symptomsglutamate activity provides both “an accelerator and a brake” in different brain regionsIn the meso-cortical pathway…glutamate acts as an accelerator leading to increased dopamine activityif this goes wrong and glutamate levels fall too lowdopamine levels drop leading to negative symptomsin the meso-limbic pathwaysglutamate acts as a brake, signalling to GABA neurons to inhibit dopamine productionif the brake does not work (i.e. glutamate levels are too low) this will lead to low levels of GABA and thus high levels of dopamine resulting in positive symptomsWhat does Carlsson say regarding future drug treatments for schizophrenia? serotonin antagonists – to bring down serotonin levelsglutamate agonists - to increase glutamate levelsdiffering symptoms may be the result of differing neurochemical aetiologies requiring differing treatments Evaluate one contemporary study of the schizophrenia: Carlsson et al (2000)Studies of PCP: Angel Dust (this drug reduces glutamate)One strength of Carlsson’s theory that dopamine levels may be elevated due to low levels of glutamate is that it is supported by experiments with the drug PCP or ‘angel dust’. These studies demonstrate that PCP, an antagonist on the NMDA, glutamate receptor can induce schizophrenic-like symptoms. This is important because it shows that PCP (a drug which decreases glutamate levels) has very similar effects to drugs such as amphetamine which increase dopamine levels, suggesting that schizophrenia may be linked to hypoglutamatergic activity. (well-developed chain of reason)This said, some psychologists argue that PCP research is contradictory and sometimes PCP actually enhances rather than reduces the release of glutamate and this ambiguity casts doubt on hypoglutamatergia as a cause of schizophrenia. (competing argument)Studies with ketamine (this drug also reduces glutamate )A further strength is that SPECT imaging studies show that another glutamate antagonist, ketamine, enhances amphetamine-induced dopamine release in humans.These findings have also been replicated with rats under more controlled conditions.Studies with amphetamines (these drugs elevate dopamine levels)Furthermore, PET scans show that people with schizophrenia given amphetamines show higher levels of dopamine release in the basal ganglia than age-matched controls and are more likely to exhibit schizophrenic symptoms.Post mortem studiesSuggest hyperserotonergic function in people with paranoid schizophreniaCarlsson and Carlsson (1989) mice were given drugs to reduce motor activitymotor activity can be restarted by blocking glutamate receptors with the drug MK801(reduce glutamate, increases serotonin and dopamine) in the nucleus accumbens if you keep on giving the mice MK801 you get highly abnormal behaviour (similar to psychotic behaviour) ................
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