Quiz #2 Study Notes

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Psychology 3229A/B
Scott Mac Dougall- Shackleton

Evolution & Human Behaviour Quiz #2 Study notes Karmiloff-Smith • Modularity of the mind  Evidence taken from patients who have lesions in specific brain regions & specific impairments (which leave other modalities relatively unharmed); “double dissociation” logic  Studies first done on adults; later done in children  William’s syndrome (children)  Caused by deletion of 28 genes on one copy of chromosome 7  Proficient with language & face-processing; mean IQ of 58 & severely impaired spatial & numerical cognition  Similar claims made with specific language impairment (SLI), and prosopagnosia (inability to recognize familiar faces)  Suggests that there are no interactions in the brain  Neuroconstructivist approach  Must take into account ontogenetic development; claimed “modularity” that exists in adults doesn’t seem to exist in children • Prosopagnosia: face-processing deficit was ALWAYS accompanied by object-processing deficits; thus the independence of these two modalities seems to develop gradually • SLI: seems to stem from lower-level cognitive impairments and domains once thought to be normal now present with subtle impairments (i.e. even when IQ falls in normal range, it is significantly lower than that of siblings • William’s syndrome: intactness of spared domains challenged on 5 counts: 1. Although they present with standard face-processing scores, the way they achieve their success is radically different 2. Facial & spatial processing both impaired the same way, but the deficit is more salient for spatial stimuli 3. Many studies now challenge the “intactness” of language module (through abnormal brain processing mechanisms)  Late language onset  Rely more on perception than language when identifying objects  Impaired categorization abilities  Atypical pointing/gazing in toddlers  Normal asymmetry between comprehension & production is absent in WS 4. Atypical eye movement planning; these deficits outside the language domain could, through development, lead to the deficits seen in WS • Genetic underpinnings of cognitive modules  Believed that mutations/problems with genes have DIRECT effects on behaviour  KE family  Point mutation on FOXP2 gene (encodes a transcription factor) on one copy of chromosome 7  Mutations to the WS critical region  Mutations to elastin (involved in building of connective tissue; maybe responsible for supravalvular stenoses seen in WS patients) and LIMK1 (protein kinase involved in spatial processing)  Neuroconstructivist approach  People with FOXP2 mutations show other deficits, not just the one in language  Problems with LIMK1 conclusions • Mouse model knocked out 1 gene, but WS involves knockout of 28 genes • LIMK1 expressed throughout the brain, so its function appears to be much more general • Evolutionary underpinnings of cognitive modules  FOXP2 well conserved in primates; only 2 amino acid changes in human lineage compared to the chimps  Change thought to have occurred about 20,000 years ago (just when language is thought to have originated)  Therefore, change of one amino acid responsible for the development of human language  Neuroconstructivist approach  FOXP2 is a transcription factor & affects many other genes  Research on FOXP2 expression in songbirds found that FOXP2 expression was higher when the song was being learned than when it was being produced; suggests that FOXP2 plays a role in vocal plasticity, not language  Evolution produces allelic changes that increase an organism’s plasticity to learning • Direct mappings of genes to cognitive-level outcomes isn’t possible; neonatal brain is highly connected, which discredits the idea of modularity Pinker • Three laws of behavioural genetics; thought to apply most strongly during childhood, when our intellects/personalities are formed 1. All human behavioural traits are heritable  Note that IQ & personality tests have been shown to be quite valid  Heritability: proportion of variance in a trait (for a specific population) that is accounted for by genetic differences • Measured using (I) twin studies, and (II) family studies • Typically range from 0.25 to 0.75  Problems with heritability • Whether measurement error is included in total variance • Additive or interactive effects as well? • Total variance can vary • When the trait is measured during ontogeny • Which population is being studied  Underlying talents & temperaments (i.e. how religious/political you are) that lead to certain behaviours (i.e. being Protestant/Liberal) are heritable  Any study that draws conclusions based on similarities between parents & offspring may be due to genes, not parenting environment  Counterarguments have all been controlled for and did not significantly affect heritability estimates • Perhaps higher similarity in identical twins caused by shared prenatal environment • Measures of how similarly twin
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