Psychology: Clinical – Content (AJW)



Describe one contemporary study of schizophrenia: Carlsson et al (2000)an up-to-date review of the status of the dopamine hypothesisraising awareness of the potential role of other neurotransmitters, e.g. glutamate, serotonin and GABA.excess dopamine may be a by-product of dysfunction of another neurotransmitterexcess in one area may be compensating for a deficiency in another.more research needed in order to improve drug treatments for the wide range of people with schizophrenia, many of whom are “treatment resistant” or who live with the extreme side effects of anti-psychotics (e.g. extra-pyramidal dysfunction)describes evidence for the dopamine hypothesis, e.g. PET scans using radio-labelled dopa that show that people with schizophrenia given amphetamines (dopamine agonists) showed higher levels of dopamine release in the basal ganglia than age-matched controls and were more likely to exhibit schizophrenic symptoms.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 activitydopamine levels may be controlled by serotonin levels, so if serotonin levels are too high, this could be linked to increased dopamine levelslow levels of another neurotransmitter, glutamate, may in turn allow both serotonin and consequently dopamine levels to become too high.glutamatergic failure in the cerebral cortex may lead to negative symptoms, whereas glutamatergic failure in the 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 activity however if this goes wrong and glutamate levels fall too low, the accelerator does not work and dopamine levels drop leading to negative symptomsHowever, glutamate also acts as a brake in the meso-limbic pathways, here glutamate signals to GABA neurons to inhibit dopamine production, however if the brake does not work because the glutamate levels are too low, this can results in low levels of GABA, thus dopamine release is not inhibited and levels become too high, resulting in positive symptoms.concludes by saying that serotonin antagonists and glutamate agonists could provide future treatments for schizophrenia as differing symptoms may be the result of differing neurochemical aetiologies requiring differing treatments. Evaluate one contemporary study of the schizophrenia: Carlsson et al (2000)One strength of Carlsson’s assertion 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, a 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.This is further supported by the studies studies using SPECT imaging that revealed that the NMDA antagonist ketamine enhances amphetamine-induced dopamine release in humans. These findings have also been replicated with rats under more greater controlled conditions.So, on the one hand, the evidence for hypoglutamatergic activity seems compelling, yet competing evidence suggests that some NMDA antagonists in fact inhibit dopamine release leading to the conclusion that decreases in glutamate may bring about schizophrenic symptoms via some route other than increased dopamine release. ................
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