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What is the central problem of psychology?

Measurability of psychological phenomena


What is materialism?

The idea that psychological phenomena = CNS. Therefore, measuring CNS is a good way to measure mental states, and manipulating CNS would manipulate mental states.


What is objectivism?

A rejection of introspection. Psychology should focus on physical stimuli and overt behaviour, as opposed to mental states, which cannot be measured.


What is behaviourism?

The study of psychology based on observable behaviours. Behaviour can be predicted and controlled from understanding or manipulating discriminative stimuli and consequences of behaviour.


What is psychophysics?

Investigates the relationship between physical stimuli and the perceptions they affect. Involves measuring detection and discrimination thresholds of conscious perception.BUT: poor relationship between nervous activity and perception, as well as physical stimuli and perception. Eg. Fechner


What are Aristotle's four causes, and how do they relate to psychology?

The material cause: “that out of which”, e.g., the bronze of a statue.

The formal cause: “the form”, “the account of what-it-is-to-be”, e.g., the shape of a statue. (Mathematical, parts and their interactions)

The efficient cause: “the primary source of the change or rest”, e.g., the artisan, the art of bronze-casting the statue, the man who gives advice, the father of the child. (Events in sequence, Behavioural approach)

The final cause: “the end, that for the sake of which a thing is done”, e.g., health is the end of walking, losing weight, purging, drugs, and surgical tools. (Function of system and psychological phenomena)


How do drugs enter the body and brain? What factors affect their ability to do so?

Range of ways - oral, intravenous etc.

Factors affecting their ability to do so are:

- Speed of onset/offset
- bioavailability
- compliance


What are the major ways that drugs can affect neural activity?

1. Directly stimulating: by either a) stimulating activity by imitating an NT at a receptor site (agonist) or b) by blocking the receptor (antagonist).
2. Affecting synthesis of drug
3. Acting as a precursor: L-Dopa is a precursor for dopamine. L-Dopa crosses the blood-brain barrier, which dopamine cannot. Thus is used to increase dopamine concentrations in brain.
4. Affecting release of NT: amphetamines pumps more noradrenaline into the synapse
5. Affects rate at which NT is degraded: MAO inhibitors
6. Affecting reuptake of NT: Eg. Cocaine blocks dopamine transporter, preventing reuptake.


What are the effects of repeated drug administration?

1, Tolerance – effect of drug is reduced with repeated treatment. More drug is needed. Can change number of, or sensitivity of, receptors.
2. Withdrawal – generally opposite of effect of drug itself.
Eg. Opiates – effects = reward, analgesia, sedation… ; withdrawal = craving, dysphoria, pain, anxiety; heart rate


What produces differences in the efficacy of different drugs?

- Site of action eg. many different types of pain, and individual differences in response. Also, for Prozac vs Paxil – different 5-HT receptors around the brain in different parts – almost everywhere, so different results in different parts. A drug can be developed that affects only one subtype of receptor.

- Repeated drug use can change efficacy of treatment. As tolerance to drug increases, higher doses are needed to produce desired effect. This can lead to greater side effects – as these do not necessarily have same tolerance profile.


What is the evidence that dopamine mediates reinforcement?

ICSS - more dopamine means more self-stimulation


What are some other possible roles for dopamine?

1. Exertion of effort. Response vigour - progressive ratio experiments - rats give up responding faster if DA receptors blocked

2. Anticipation of reward. Electrophysiology shows evidence that responding of DA neurons shifts over time from the reward itself to a cue that predicts a reward.

3. Assigning salience to environmental stimuli. Response to the cue is exaggerated when rats given DA agonist amphetamine.

4. DA is critical for motor control and contributes to psychosis - more than just reward signal!


What are some potential strategies for the
treatment of addiction?

Exposure therapy (extinction) - seems to work for alcohol

Stimulus control (avoid risky situations)
- effective, but most limiting on lifestyle

Contingency management interventions - giving positive reinforcement (eg. token system) for adherence to treatment plan

Replacement therapies - nicotine patches; methadone. These can be:

Full agonists - methadone, nicotine patches

Partial agonists - drugs that bind to receptor but stimulate them weakly, and also block ability of natural NT to stimulate receptor Eg. buprenorphine for opiates, aripiprazole for stimulants


What are the major features of addiction?

Loss of control
Little concern for consequences


What learning mechanisms contribute to addiction?

Pavlovlian Instrumental Transfer Paradigm
That reward-related cues increase responding to get reward. Environmental stimuli can trigger reward-seeking behaviour – and their ability to do so increases with training.

Learning through positive and negative reinforcement

Insensitivity to devaluation


What neuropathology accompanies addiction?

In meth addicts, less DA transporters, almost as few as Parkinson's patient

In cocaine users, less activation of various brain areas – cerebellum, orbitofrontal and prefrontal cortex, occipital cortex and thalamus - when presented with natural rewards such as food

In cocaine users, decreased volume of grey matter in prefrontal cortex. Addicts less able to control behaviour.

1. DA receptors are downregulated
2. Response to natural rewards is blunted
3. Inhibitory brain areas, such as prefrontal cortex, are less active (although this may not be an effect of drugs - addicts may just have smaller PFCs to begin with)


What behavioural functions do GABA and glutamate neurotransmitters control?

Glutamate is involved in:
Involved in learning, neural plasticity, memory and dark exposure. Also involved in excitotoxicity following stroke or ischemia.

GABA turns stuff off or down:

Brain wouldn't work if everything was active all the time. Must turn things off to get clear signal. Like muscles - antagonist pairs, must relax one muscle to tense other. If you tense all -> no action.