PSYC 241 Lecture Notes - Lecture 2: Neurotransmitter, Dementia, Existentialism

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Lecture 2 Theoretical perspectives
Goals of the theory perspective (a good theory)
- explain etiology (what causes X, why others don’t have X)
- identify maintaining factors (what makes symptoms persist, these factors can be the same OR
different from causal factors)
- predict course of disorder
- design effective treatment (intervention targets factors that cause and or maintain a disorder)
In the past theories were single factor / unidimensional
- this is where the nature versus nurture debate stems from
interactionist theories (today)
- Both nature and nurture influence mental health
models and theories outline
1. biological models
2. psychosocial models
3. integrated theories (both)
biological models (5)
- damage to the brain
o structural damage to the brain leads to disorder
direct head injury
diseases
childhood cancer influences adult brain
dementia, deterioration of cog functioning linked to loss of brain cells
toxins (lead, etc.)
- neurotransmitters
o focus on box 2.1
Know generally how neurotransmitters work? (Na and K involved)
nerve impulses received by dendrites of neighbouring neuron (excite or
inhibition signals)
travels down axons, and excites/inhibits the next neuron
messages travel through synapse
o Neurotransmitter definition: Chemical messengers released from the propagating
neuron and move through the synapse to the postsynaptic neuron
o Research attention on: DA, 5-HT, NE, GABA
o Neurotransmitters act together (ie: DA and 5-HT act together to create balance in brain)
DA = pleasure seeking /exploring
5-HT: constraint and inhibition behaviour
NE: excite neurons/agitate
GABA: gamma aminobutyric acid, relax/inhibit neurons
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o different neurotransmitters are concentrated in different brain areas, and relate to
different functions
o neurotransmitter disturbances (also how drugs work)
(quantity of NT produced) produce too much/too little at synapse
(quantity of receptors) too many/too little Receptors (reabsorption )
(amount of transmitter deactivation) too much or too little deactivation via
enzymes
(quantity of NT in synapse)
(time of reuptake process) too fast or too slow, ie SSRI drugs inhibit reuptake,
make it slower
o Abnormal behaviour can result from any of the 5 things above, (excessive or reduced
activity), ie: schizo happens when too much excitation in dopamine system
o Unlikely single neurotransmitters determine behaviour
o behaviour & neurotransmitter's impact each other (bidirectional relationship)
- PNS (SNS and ANS)
o somatic nervous system: controls muscles (cuz soma = body).
GAD: chronic muscle tension .
o autonomic nervous system: controls automatic body functions (breathing, digestion,
heart rate, etc.) to produce homeostatic (balanced) activity.
sympathetic: fight or flight .
increased HR/breathing, vision acuity, movement, adrenalin, decreased
digestion, salivation, constrict bladder (so easier to run)
individuals defer in duration, intensity, and return to baseline
o quicker/slower f/f response.
o different intensity experienced.
o quicker/slower return to baseline.
the body still activates sympathetic system in face of both true and false
fears (ie, scared of flying, no imminent danger of dying but u still
stressed).
Parasympathetic: rest and digest.
- endocrine system
o chemicals released into blood stream
o hormone imbalance can lead to disrupted behaviour/thoughts/feelings (make sure u
don’t misdiagnose a mood disorder, that is in fact a hormonal disorder)
hypoglycemia: hard for pancreas to regulate blood sugar cuz too much insulin
converting glucose away. (too low sugar),
mimics anxiety, easy to misdiagnose with anxiety if you don’t do
hormonal test
cretinism: dwarf and intellectual deficits (defective thyroid)
o hypothalamus releases (releasing hormones), which travel to dif pituitary, which then
release other hormones that affect our behaviour in adrenals or gonads (tests/ovaries),
HPA and HPG axes.
- genetics
o genetics definition: inherited characteristics/behaviours
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