1. Principles
1.1. 1.There are biological correlates of behaviour
1.1.1. Physiological origins of behaviour: -neurotransmitters -hormones -specialized brain areas -genes
1.1.2. Newcomer et. al (1999)
1.1.2.1. Aim: Role of stress hormone (cortisol) on verbal declarity memeory
1.1.2.2. Prodecure: 51 participants (18-30 y/o) Gr.1 high dose cortisol (160mg for 4 days equivalent to stressful event) Gr.2 low dose cortisol (40mg for 4 days equivalent to minor stressful event) Gr.3 control group (placebo tablets)
1.1.2.3. Results: Gr.1 did worse on verbal declaritive memory test than Gr.2, below Gr.3 from day1. Gr.2 no memory decrease
1.1.2.4. Limitations: Labratory experiment (controlled) Ethical issues tho' negative effect of cortisol reversible
1.2. 2. Animal research can provide insight into human behaviour
1.2.1. Study physiological processes assumed most biological processes is the same
1.2.2. Rosenzweig and Bennet (1972)
1.2.2.1. Aim: Enviormental factors', e.g. rich or impoverished enviorment, effect on neuron development in cerebral cortex
1.2.2.2. Procedure: EC - rats in enriched environment (10-12 rats w/ stimulating objects to explore and play, maze traning) IC - rats in impoverished environment (solo cage w/ no stimulation) 30-60 days in cage before killed to study brain anatomy
1.2.2.3. Results: Difference between EC & IC EC increased thickness and higher wight of cortex, developed more acetyolcholine receptors in cerebral cortex (important for memory and learning)
1.2.2.4. Limitations: Lab study Not neccessarily same with humans Ethical issues w/ use of animals
1.3. 3. Human behaviour is, to some extent, genetically based
1.3.1. Behaviour explained by genetic inheritance
1.3.2. Bouchard et. al (1990) (Minnesota Twin Study)
1.3.2.1. Aim: Genetic inheritance in intelligence
1.3.2.2. Procedure: Cross-cultural & longitudinal. mean age = 41 y/o Monozygotic Twins (MZ) together (MZT) and apart(MZA) Dizygotic Twins (DZ/fraternal) together (DZT) Same person twice Ca. 50 hours of testing and interviews
1.3.2.3. Results: Same person 87% MZT 86% MZA 76% DZT 55% Siblings together 47%
1.3.2.4. Limitations: Relied media to recruit participants Ethical issues the way twins reunited Twin contact prior not controlled 'Equal environment assumption' -ZT may not have same environment
2. Neurotransmission affect human behaviour
2.1. Neurotransmitters:
2.1.1. Chemical messenger allows communication between nerve cells
2.1.2. Receptor sites only take in specific electrochemical
2.1.3. Pre-Synaptic neuron->Synapses->Post-Synaptic neuron
2.1.4. Examples
2.2. Martinez and Kesner (1991) Mouse Maze Study
2.2.1. Aim: Role of acetylcholine in memory formation
2.2.2. Procedure: Gr.1 Rats injected w/ scopolamine (blocks acetylcholine receptors on the neurons -decreasing available acetylcholine) Gr.2 Rats injected w/ physostigmine (blocks clean up process of cholinesterase - responsible for the clean up of acetylcholine from the receptors) Gr.3 Rat control group
2.2.3. Results: Gr.2 complete maze quicker than other rats Gr.1 slowest Gr.3 average pace
2.2.4. Limitations: Lab study Animal study
3. Hormones affect human behaviour
3.1. Hormones
3.1.1. Chemical messengers transfers info to cells to coordinate functions of body
3.1.2. Examples
3.2. Baumgartner et al. (2008)
3.2.1. Aim: Role of oxytocin after trust breach in trust game
3.2.2. Procedure: Trust game. fMRI 41 participants Gr.1 Oxytocin via nasal spray Gr.2 Placebo via nasal spray P1 "investigator" get money - keep or share? P2 "trustee" afterwards decide share(trust) or keep (distrust) if shared money tripled changed Trustees changes or pc. Half the time distrust
3.2.3. Results: Gr.2 less trust when betrayed. invest less. Gr.1 no change when betrayed. invest same. fMRI show decrease amygdala and caudate nucleus response. Amygdala involved emotional processing, many oxytocin receptors. Caudate nucleus learning and memory and reward-related responses and learning to trust
3.2.4. Limitations: Scanner research not definite what it means Not reflect natural physiological processes (oxytocin too complex)
4. Environmental effect physiological processes
4.1. Effect 1: Environmental effects on dendritic branching (brain plasticity)
4.1.1. Environmental stimulation: - Social interaction - Learning opportunities
4.1.2. Experiences processed in brain's nervous system stimulation increasesnumbers of synapses (brain plasticity)
4.1.3. Case studies neglected children i.e. little to no interaction, language, and touch with others Neglected children's brains often smaller and scientific evidence of altered brain function (e.g. emotions and IQ)
4.1.4. Rosenzweig, Bennet, & Diamond (1972)
4.1.4.1. Aim: Enviormental factors', e.g. rich or impoverished enviorment, effect on neuron development in cerebral cortex
4.1.4.2. Procedure: EC - rats in enriched environment (10-12 rats w/ stimulating objects to explore and play, maze traning) IC - rats in impoverished environment (solo cage w/ no stimulation) 30-60 days in cage before killed to study brain anatomy
4.1.4.3. Results: Difference between EC & IC EC increased thickness and higher wight of cortex, developed more acetyolcholine receptors in cerebral cortex (important for memory and learning)
4.1.4.4. Limitations: Lab study Not neccessarily same with humans Ethical issues w/ use of animals
4.2. Effect 2: Environmental stressors and hippocampal damage in PTSD patients
4.2.1. Stressor: Event threathens disrupting body's normal balance Stress response - secretion of stress hormones & activate 'fear sensor' in brain (amygdala)
4.2.2. Acute stressor (e.g. assualt, accident) Chronic stressor (e.g. anticipating violence/worry)
4.2.3. Flight or Fight response (coping mechanism)
4.2.4. Trauma & PTSD
4.2.4.1. Traumatic episodes(no escape) produce intense fear in 5% population can lead to PTSD
4.2.4.2. Veterans and child sexual abuse w/ PTSD have stress related problems (forgetfulness,difficulty learning) In patients stress-related physiological change in brain (hippocampus - important in integrating memory when recollection)
4.2.5. Bremnner et al. (2003)
4.2.5.1. Aim: Measure volume hippocampus based on theory (prolonged stress reduce volume hippocampus due increase cortisol level)
4.2.5.2. Procedure: MRI scans and memory test (e.g. remembering story or word list) Participants - veterans/female adults child sexual abuse victims (some PTSD some not)
4.2.5.3. Results: Deficit in short-term memory PTSD - hippocampus smaller than control group Veterans w/ memory problems smallest hippocampus Clear correlation - number years of abuse (trauma test), memory problems, & hippocampal volume
4.2.5.4. Limitations: Small sample - hard to generalize Other reasons e.g. Depression
5. Genetics influences behaviour
5.1. Caspi et al (2003)
5.1.1. Aim: Role of 5-HTT (influences serotonin) gene in depression after experience stressful event
5.1.2. Procedure: compare participants w/ normal 5-HTT gene & mutation 5-HTT (shorter alleles) Both qute frequent but long allele a bit more (57%)
5.1.3. Results: Mutation 5-HTT gene after stressful event more likely depressed
5.1.4. Limitations: Large portion population have mutated 5-HTT gene - thus not likely major contributor to depression (both become depressed) No cause-effect relationship
5.2. Bouchard et al (1990) Minnesota Twin Study
5.2.1. Aim: Genetic inheritance in intelligence
5.2.2. Procedure: Cross-cultural & longitudinal. mean age = 41 y/o Monozygotic Twins (MZ) together (MZT) and apart (MZA) Dizygotic Twins (DZ/fraternal) together (DZT) Same person twice Ca. 50 hours of testing and interviews
5.2.3. Results: Same person 87% MZA 86% MZT 76% DZT 55% Siblings together 47%
5.2.4. Limitations: Relied media to recruit participants Ethical issues the way twins reunited Twin contact prior not controlled 'Equal environment assumption' -ZT may not have same environment