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Lecture 23

PSYC 211 Lecture 23: PSYC211 December 4th

17 Pages

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PSYC 211
Jonathan Britt

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th December 4 Schizophrenia Generally, schizophrenia is the kind of thing where in the late teenage years, people develop a host of symptoms seemingly out of the blue Generally, there are no symptoms in the early childhood years Causes While no single gene has been shown to cause schizophrenia, many gene variants have been found to increase likelihood of this disease Not even a pair of genes Even if you have these genes variants, you still have a very small risk of actually developing schizophrenia An individuals genetic makeup appears to interact with signals from the environment (particularly during embryonic development) to cause the disease. There is an interaction between genes and environmental signals Evidence for abnormal brain development Symptoms of schizophrenia are not normally seen in childhood, however behavioral and anatomical evidence indicates that abnormal prenatal development is associated with schizophrenia Behavioural: Children who go on to develop schizophrenia display less sociability and deficient psychomotor functioning as kids. Anatomical: Minor physical abnormalities can be seen in children who go on to develop schizophrenia, such as partial webbing of the two middle toes and a high-steepled palate. But there is no one tell-tale sign and these things are all generally rare in the population So there is no obvious indicator in a young child There are signs, but no indicators The cascade of events that lead to schizophrenia probably start at a very young age Many studies have found evidence of loss of brain tissue in CT and MRI scans of schizophrenic patients The most likely cause of the enlarged ventricles is loss of brain tissue Although everyone loses some cerebral gray matter as they age, rate of tissue loss is greater in schizophrenic patients, but just during the onset of the disease. Schizophrenia is not a neurodegenerative disease. The loss of brain tissue is not ongoing When these symptoms first emerge, there seems to be a loss of brain tissue It is not progressive, but it appears that around the time where there is an onset of symptoms, there is a sudden reduction in brain volume This graph shows how large are the ventricles among a population of people Many people with schizophrenia have much larger ventricles than the average person This also probably occurs around the onset of symptoms It is not neurodegenerative, because the loss of tissue is not ongoing It happens once but does not keep going for the rest of the persons life Ventricles get larger and there is a decrease in brain tissue There is excessive pruning, probably because there is something that is going on in the rules that determine synaptic plasticity Pharmacology of schizophrenia: the dopamine hypothesis Many drugs have been developed that relieve the positive symptoms of schizophrenia. They are called antipsychotics or neuroleptics, and they all block dopamine receptors, particularly D2 dopamine receptors. We try to give drugs that affect synaptic plasticity because we think this might be a key part of schizophrenia Neuroleptics are good at getting rid of the positive symptoms Some drugs produce some aspects of the positive symptoms of schizophrenia in people who do not have the disorder. These are dopamine agonists, like crystal meth and cocaine. Dopamine hypothesis Suggests that positive symptoms of schizophrenia are caused by over-activity of dopaminergic synapses, particularly in the striatum (nucleus accumbens). Less involved in motor movements and more involved in thought process and cognition Most researchers believe that mesolimbic dopamine pathway, which begins in ventral tegmental area and ends in nucleus accumbens and amygdala, is likely to be involved in the positive symptoms of schizophrenia Indiscriminate activity of dopaminergic synapses in nucleus accumbens makes it difficult for patients to follow an orderly, rational thought sequence Paranoid delusions may be caused by increased activity of dopaminergic input to amygdala Relationship between positive and negative symptoms: role of prefrontal cortex There is some evidence that suggests that the negative/cognitive symptoms of schizophrenia are result of brain abnormalities (developmental or degenerative), particularly in the prefrontal cortex For example, the negative/cognitive symptoms of schizophrenia are similar to those produced by damage to the prefrontal cortex, and schizophrenic patients do poorly on neuropsychological tests that are sensitive to prefrontal damage The negative symptoms of schizophrenia may be caused by hypofrontality, which is decreased activity of the frontal lobesin particular, of dorsolateral prefrontal cortex (dlPFC) Hypofrontality Decreased activity of the prefrontal cortex Believed to be responsible for negative symptoms of schizophrenia The idea is, are there other pills or medications we can use to boost activity in the PFC? In is unclear if the hypofrontality observed in schizophrenic patients is related to the excessive dopamine signaling in other brain areas. Dopamine regulates activity in the prefrontal cortex, and the prefrontal cortex regulates dopamine neuron activity. All the neurons are acting together, so it is difficult to figure things out at a neural level Interestingly, injections of the atypical antipsychotic clozapine into monkeys caused both a decrease in release of dopamine by mesolimbic system and an increase in release of dopamine in prefrontal cortex Atypical antipsychotics means that it has another target besides blocking the dopamine D2 receptor People are trying to control another receptor like serotonin, for example So this drug has effects on other neurotransmitters, not just dopamine The dopamine neurons that project to the PFC are clearly regulated differently and signal different information than dopamine neurons that project elsewhere in the brain. So, it is possible that schizophrenic patients have too little dopamine in the PFC and too much elsewhere.
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