Psychology: Clinical – Content (AJW)



The function of neurotransmitters as a theory/explanation of schizophrenia Preparation work: Refresh your memory of the synapse and neurotransmission, revisit your notes from Topic 3 Biological Psychology. You also need to view the PowerPoint about the dopamine hypothesis.What do I need to understand before tackling this explanation of schizophrenia? What is a neurotransmitter? How is this different to a hormone?How many different neurotransmitters are you aware of, what effects do they have on behaviour?Are you able to draw and label a synapse?What are the effects of amphetamines and PCP (angel dust) on the brain and on behaviour?What psychological processes and behaviours are the following brain regions associated with: pre-frontal cortex, the limbic system including the nucleus accumbens There are several neurotransmitters which help to explain schizophrenia and we will consider three of them here: dopamine, serotonin and glutamate. 356425546037500The dopamine hypothesisThe original version of the dopamine hypothesis suggested that an ................... of dopamine activity may be responsible for schizophrenic symptoms, (hyperdominergia) in sub-cortical regions, e.g. the limbic system (Carlsson and Lindqvit, 1963) but an updated version (Davis, 1991) suggested that although there may be an excess of dopaminergic activity in some brain regions, schizophrenia is also associated with hypodominergia, or a ……………of dopaminergic activity in brain regions such as the pre-frontal cortex. Dopamine has many effects on our behaviour, emotions and thinking, including it’s ability to help us to direct and shift ....................., therefore irregularities of dopaminergic activity would account for the cognitive impairment and disordered thinking which characterizes schizophrenia. Also, it has been said that dopaminergic irregularities in the frontal lobes could account for positive symptoms such ………………………. and the characteristic loss of ………….. associated with psychosis. There are many reasons why someone might have excessive dopamine activity. For example, the pre-synaptic cell may release ........................ dopamine molecules (‘upstream’), the post-synaptic cell may be overly ...................... or may have too many ............................ and this would mean that the dopamine molecules are taken up very ..................... and nerve impulses transmitted too readily (downstream). Furthermore, people with schizophrenia may have lower than average levels of the ...................... which breaks down leftover dopamine in the ................................ This would lead to a build-up of dopamine, making transmission easier and easier with each successive ...................... of the presynaptic cell. Part of the rationale for the original hypothesis was the discovery that ......................... drugs such as ......................................., which ........................dopamine receptor sites have the effect of reducing schizophrenic symptoms. The fact the drugs such as LDopa (commonly used to treat ..............................) and amphetamines, which ......................... dopamine activity both induce schizophrenic-type symptoms as side effects further corroborated this line of thought.Serotonin and schizophrenia……………….., (1991) published an updated version of the dopamine hypothesis, following a wave of conflicting data from …………………… and metabolite studies, imaging data, and new insights from ………………. studies. It was becoming increasingly clear that not all people with schizophrenia have an excess of dopamine and the finding that as many as …………….% of people with schizophrenia do not experience relief from dopamine ………………………., or drugs that blocked D2 dopamine receptors, e.g. chlorpromazine, and many who do experience some relief still experience …………………symptoms threw the original hypothesis into question.By this point new drugs were being found to be particularly helpful to those people who did got get any relief from typical antipsychotics (dopamine blockers). These people seemed to respond well to drugs like ………………….. which block both dopamine and serotonin receptors. These drugs seem effective in reducing both positive and negative symptoms and therefore it is possible that negative symptoms are linked to an excess of serotonin. Also, it should be noted that serotonin regulates dopamine levels in areas such as meso-limbic pathway and this demonstrates how important it is to consider how neurotransmitters influence and effect each other.At this time PET scanning had also revealed that many schizophrenics have low blood flow in the frontal lobes, known as ……………………………….., and they also had low levels of metabolites for dopamine in their cerebro-spinal fluid, suggesting low levels of dopamine (hypodominergia) in the frontal regions. Davis hypothesized that schizophrenia was caused by ………………dominergia in the frontal lobes and ………………dominergia in the striatum. Furthermore, he suggested that ……………………. symptoms of schizophrenia are the result of hypodopaminergia in the frontal lobes and meso-cortical pathways, while …………………. symptoms result from hyperdopaminergia in the striatum and mesolimbic pathway.Version 3 of the dopamine hypothesisIn 2009, …………………………………. published what they called “version 3” of the dopamine hypothesis, where they discuss a wide range of genetic and environmental factors that may lead to “dopamine dysregulation” in the striatum region, which they refer to as the …………………… …………………….. to psychosis. They also note that it is presynaptic dopamine levels are responsible for schizophrenic symptoms as opposed to irregularities of D2 receptors as previous versions had highlighted. They also suggest that the dopamine hypothesis should be softened and viewed as an explanation of “psychosis ………………………” not an explanation of schizophrenia, as socio-cultural factors are critical in determining the actual diagnosis. Finally, they indicate that dopamine dysregulation may alter the way a person appraises external stimuli. For example, abnormal firing of dopamine neurons and the abnormal release of dopamine leads the individual to erroneously perceive links between innocuous (unlinked) stimuli. Psychotic symptoms, especially delusions and hallucinations, emerge over time as the individual attempts to explain to him or herself the experience of “…………………… salience”. Psychosis is, therefore, aberrant salience driven by dopamine and filtered through the individual's existing cognitive and sociocultural schemas—thus allowing the same chemical (dopamine) to have different clinical manifestations in different cultures and different individuals. Incentive salience models also provide a plausible explanation for negative symptoms: dopamine dysregulation may increase the “noise in the system” and therefore, “drowning out”, dopaminergic signals linked to stimuli indicating reward. The net result would be reduced motivational drive that would lead over time to negative symptoms, such as social withdrawal, and neglect of interests. They conclude by saying that that as the dopamine hypothesis evolves further, the scientific challenge will be not just to find predisposing ………………… but to articulate how genes and ………………………. interact to lead to dopamine dysfunction.The final neurotransmitter that we are going to study that has been linked to schizophrenia is glutamate. You will learn all about this in our key study of schizophrenia by Carlsson et al (2000). If you are writing about the function of neurotransmitters as an explanation in the exam don’t forget to write about Carlsson et al and glutamate!!Further ReadingDr Sutton’s “Clinical & Criminal Psychology Handout”, 2015 (see .uk schizophrenia web page and google classroom)Gross, (2015) p. 768Howes and Kapur, (2009). ncbi.nlm.pmc/articles/PMC2669582/Abi-Dargham (2012), for/curr/AbiDargham/Pause ..think…write….Assessment questions:Describe ONE neurochemical explanation of schizophrenia (4)Describe the function of neurotransmitters as an explanation of schizophrenia (6)Explain/Apply/Issues and Debates: Psychological knowledge is used to help people in society every day. Read the following extract about how biological explanations of schizophrenia could be helpful to people in everyday life: Zara is mum to 8 year old Maya. Sadly, Zara’s relationship broke down just before Maya’s third birthday and shortly afterwards she was diagnosed with paranoid schizophrenia. Luckily, she has a lot of support from her MZ twin, Elizabeth and Maya’s dad, Joe. Zara has suffered a recent relapse and is being looked after in residential care, following a particularly difficult few weeks. Maya is staying with Auntie Elizabeth and with her mum’s consent, Elizabeth and Joe have decided that they want to try and explain to Maya about her mum’s condition. They have talked it over with Lucy, their community psychiatric nurse and she thinks Maya is old enough to understand; she loves science and so they have decided to help her understand more about how the brain works and the role of neurotransmitters in triggering symptoms of schizophrenia. Imagine you are in Elizabeth and Joe’s position, how would you explain the role of neurotransmitters to Maya? How could you make it easier for her to understand? What questions do you think Maya might ask?Issues and Debates: Wise and Stein have showed that people with schizophrenia who have died in accidents have lower than average levels of beta hydroxylase, an enzyme which breaks down dopamine in the synapse. This has been taken as evidence, by some, to support the neurochemistry as an explanation of schizophrenia. To what extent do you consider this finding to be scientific? How would you design a lab experiment to test neurochemical explanation such as the dopamine hypothesis or the glutamate hypothesis? How might a cross-sectional study differ from a proper lab experiment? What are the problems of doing quasi-experiments to test these hypotheses?Could animal experiments be used to test neurochemical hypotheses regarding schizophrenia? What issues does this present ethically and scientifically?Zara has tried a few different medications to control her psychotic episodes and she is now on clozapine, a drug which blocks dopamine and serotonin receptors. How have advances in neurochemical understanding helped people in the real world (3)Extension/Rich Questions: Fast forward ten years, Maya is now 18. She has started to have some rather odd beliefs including anxiety that she is being watched by a man who she says follows her home sometimes. She also has some peculiar mannerisms and her speech can be very fragmented and hard to follow. People who know about her mum, might say she is showing prodromal symptoms of schizophrenia. The DSM 5 includes a possible future diagnosis called Attenuated Psychosis Syndrome, under the section of “conditions requiring further study”. In the future, people who meet the criteria could be treated early in an attempt to halt the onset of schizophrenia; Should Maya be given drugs to stabilise her dopamine levels? What reason are there for and against starting Maya on some form of medication?We are looking forward here to the possible future of psychiatry but let’s introduce Maya to 4 new people from history: Robert Laing, Thomas Szasz, Frances Farmer and Nellie Bly. If you don’t know who these people are, look them up! What do you think they might have to say about Maya’s situation? Think about how Zara, Elizabeth and Joe and Maya’s friends might feel about all of this, considering arguments for and against. ................
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