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behavioural tolerance
through experience with a drug, an organism can learn to decrease the effect that the drug is having
classical conditioning
associating a neutral stimulus with a meaningful stimulus
operant conditioning
associating a behaviour with its consequence
what is classical condtioning
a neutral stimulus becomes associated with an unconditioned stimulus, which leads to a conditioned response
NS
neutral stimulus
US
unconditioned stimulus (naturally elicits a response)
UR
unconditioned response (naturally occurs)
CS
conditioned stimulus (formerly neutral stimulus)
CR
conditioned response (learned response)
what is operant conditioning
a behaviour followed by a consqeunce that increases or decreases the likelihood of that behaviour occurring again.
US for drug
effect of the drug on the brainU
UR for drug
compensatory reactions (opposite to drug effect)
CS for drug
novel stimulus paired with the drug
CR for drug
conditioned response (same as UR but to lesser extent)
in a novel environment
the CS is absent, so the CR is not triggered and full drug effect can lead to overdose
SR
spontaneous response
R+
reinforcement (increases behaviour)
R-
punishment (decreases behaviour)
tolerance occurs due to
increased UR
repeated pairings of CS and US
lead to compensatory responses (UR and CR)
the UR happens
when drug is present
the CR happens
even when no drug is present, body still processing as if it is
sudden loss of tolerance to heroin
due to taking heroin in unusual circumstance or environment
operation conditioning of drug effects demonstrated by
Campbell and Seiden 1973 study that used DRL: differential reinforcement of low rates of responding. animal is reinforced only if it waits for 17.5sec between responses
by the end of training in Skinner box
both groups of rats performed comparably - group 1 rats demonstrated tolerance to amphatamine
when group 2 rats given amphetamine prior to Skinner’s box instead of after…
they behaved as though they have never received amphetamine - no tolerance
sensitization also referred to as
reverse tolerance
drug sensitization
a progressive increase in the behavioural or physiological response to a drug after repeated, intermittent exposure - the opposite of tolerance
sensitization is well demonstrated with drugs that
increase activity in the brain’s dopamine reward system, such as stimulants
first exposure to cocaine
increased alertness, energy and locomotor activity
repeated intermittent exposure to cocaine
person takes cocaine on several separate occasions
later exposure to cocaine
same dose produces greater behavioural response - enhanced response is sensitization
drug sensitization occurs because
repeated drug exposure causes long lasting increases in dopamine responsiveness and neural plasticity in reward pathways
reward pathways with sensitization
dopamine/mesolimbic pathways become over-reactive and more easily triggered
long term neural changes occur where
in ventral tegmental area, nucleus accumbens, and prefrontal cortex
sensitization is amplified by
learning - over time just seeing a cue can activate circuits, making the response even stronger and faster
Bingel study
the effect of expectation on painful heat stimulation
conditions of Bingel study
baseline - saline solution
no expectation - drug presented but thought receiving saline
positive expectation - told drug was present
negative expectation - told drug was discontinued to investigate possible increase in pain
pain rating (greatest to smallest)
baseline > negative expectation > no expectation > positive expectation
placebo effect
change in person’s symptoms or physiological state that occurs because they believe or expect that a treatment will have an effect
nocebo effect
a change in persons symptoms or physiological state because they expect or believe that a treatment will have negative effects
summary of placebo
positive expectations can produce beneficial effects
summary of nocebo effect
negative expectations can produce unpleasant effects
what did brain imaging show
brain’s pain networks responded to different extents according to expectations at each stage and matched their reports of pain
brain areas involved in perception of pain
insula, thalamus, somatosensory cortex, anterior cingulate cortex, prefrontal cortex, amygdala, brainstem, cerebellum
pain perception process
nociceptors detect harmful stimuli and send signals via peripheral nerves to spinal cord
thalamus relays signal to multiple brain regions
somatosensory cortex processes the location, intensity and quality of the pain
ACC and insula adds emotional and unpleasantness components
prefrontal cortex provides cognitive evaluation and modulates the response (increase or decrease the perception)
descending pathways
regulate pain perception
the brain can send signals down to the spinal cord
that either decrease or increase transmission of pain signals
descending signals
decreased pain perception when releases serotonin, norepinephrine, or endorphins - increased pain perception when releases substance P and increases excitability