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how can the disease model of addiction be described?
a chronic, relapsing disorder, seeking out drugs despite their harmful consequences.
what was addiction originally thought to be caused by?
lack of willpower & moral failing
what caused the shift of thinking for addiciton?
AA movement - alcoholism = disease
E.M.Jellinek published “the disease concept of alcoholism”.
WHO declared alcoholism as a disease (1951)
AMA (1953)
other substances were also considered in the late 20th century.
how has the disease model of addiction been adopted by neuroscientists?
the use of fMRI and PET scans show how drugs alter brain function (reward, motivation, control)
addictive substances are said to hijack the brains reward system
what is the evidence in support of the brain disease model?
neurological brain changes promote drug-seeking behaviour, inhibit PFC
disease model reduces stigma, not a moral failing rather a health issue.
chronic use of drugs decrease dopamine receptors
what is the evidence against of the brain disease model?
the assumption that brain changes equals addiction does not account for those who use but aren’t addicts.
assumes users should not be able to stop but they can & do.
brain changes from drugs are reversible
other factors cause addiction (environment, society, psychological)
brain reward system can also be activated by food & exercise
addiction is complex & manifests differently across individuals.
what is behavioural pharmacology
studies of the effects of drugs on behaviour combining pharmacology, psychology. interactions between drugs and behaviour.
what were the early views of drugs effects on the body?
drugs were studied for the physical effects on the body, and pharmacological properties.
how did behavioural pharmacology develop?
physiological research in mid 20th century were understanding drugs effects on the brains pathways, understanding how drugs influence behaviour.
behavioural psychologists e.g., John B Watson suggested science should study observable behaviours rather than subjective experience.
B.F Skinner developed operant conditioning
Pavolv developed classical conditioning (modifying behaviour through learned association).
what were the large contributors to behavioural pharmacology?
chlorpromazine
operant analysis of drug effects (drugs as reinforcers, punishment)
what were seminal experimental findings of behavioural pharmacology?
self-administration studies (Peter Milner, B.F. Skinner) indicating drugs reinforcing properties.
major societal events leading to behavioural pharmacology?
drug epidemics
anti-drug laws
more public awareness
when was behavioural pharmacology established as separate disciplines?
in late 70s, early 80s these two disciplines converged forming a separate field. it focused on pharmacokinetics of drugs and their the complex interactions on behaviour, cognition
what did Peter Milner discover?
rats in a controlled environment could be trained to self administer a drug by pressing a lever. rats would repeatedly press the level to receive a drug indicating the reinforcing effects of the drug.
what did B.F Skinners framework elaborate?
after developing the operant conditioning paradigm. this laid groundwork for further studies like the “skinner box” to allow for a controlled environment where animals could press a lever to receive a reward,
what did the conditioned place preference study show?
placing animals in two-chambered box, giving the animal a dose of a drug in one chamber. the preference for drug-associated environment indicated drug has reinforcing properties.
classical conditioning
occurs when a neutral stimulus becomes associated with an unconditioned stimulus (drug). overtime the neutral stimulus can elicit a conditioned response similar to the drugs effects, in the absence of a drug.
an example of context and drugs on behaviour
Conditioned Place Preference (CPP). animals receive a drug in one chamber of the two. after repeated exposure the animal shows a preference for the chamber they receive the drug in. drug effects can be context dependent. will return there even if no drug is administered.
physiological response of the body in anticipation
interactions between context, stimuli can create drug-related behaviours in the absence of the drug itself. the body anticipates a drug is coming from previously learnt knowledge which elicits drug like behaviours.
a behavioural response for drugs
looks like engaging in drug seeking behaviours, due to the reinforcing effects
context stimulus causing anticipatory response
Pavlov’s learning theory suggests repeated experience of a reward is learnt to be associated with context and or stimuli. with repeated exposure to a reward, and environmental cues, the context can inflict drug like behaviours in anticipation for a drug. conditioned stimuli overtime may elicit a response in the absence of the drug.
what are the steps of neurotransmission?
synthesis
storage (in vesicles)
release: action potential = vesicles fuse with presynaptic membrane
binding - NT diffuse across synaptic cleft & bind to postsynaptic receptor
response - binding leads to changes in postsynaptic neuron (EPSP, IPSP)
termination (deactivated wither by reuptake or enzymatic degradation)
why is dopamine as the pleasure signal an incorrect statement?
oversimplifed and does not represent the role of dopamine
dopamine plays a role in the brain circuitry involved in reward processing & motivation towards goal-directed behaviours.
dopamine does not directly cause pleasure
surge of dopamine can create the euphoric feeling of a “high” strengthens associations between drug and reward.
chronic drug use can bring about tolerance, and reduce dopamine induction
dopamine is a motivator for addiction but does not cause addiction!
what are some examples of opioids?
heroin, morphine and painkillers (codiene)
what are opioids taken for?
when taken orally have an analgesic effect (painkillers), if injected can create euphoric feelings by increasing dopamine. act on the mu-opioid receptors.
what does opioid withdrawal consist of?
not life-threatening but uncomfortable
suppress ANS system so when stopped heighten the sensitivity
increased HR, BP, sweating
increases norepinephrine associated with arousal & stress response causing anxiety.
reduction in dopamine release can cause mood disturbances and depression
neurological adaptations means there are some deficiencies (endorphins)
anxiety, restlessness, insomnia, muscle aches
GI distress, tremors, nausea/vomiting
a lack of opioids creates a hyperactive state
how does alcohol withdrawal occur?
heavily drinking for a period of time followed by a sudden halt can induce alcohol withdrawal ranging from mild to life-threatening. alcohol enhances the activity of GABA which is the primary inhibitory NT. reducing alcohol consumption leads to decreases in GABA activity, creating hyperactivity of the CNS.
symptoms of alcohol withdrawal
reduction in dopamine release
anxiety, tremors, nausea, sweating
irritability, agitation, hypertension
delirium tremens, seizures, alcohol poisoning
risk of mortality
what is the dislocation model?
addiction is a response to being dislocated. this may result in someone experiencing the loss of meaning or purpose in life.
factors of the dislocation model:
capitalism - leading to the industrial revolution Britain and other European colonies accumulated large amounts of wealth. leading to events of colonialism, slavery and enclosure.
enclosures - formerly owned land became privately owned
imperialism - extension of a countries power/influence through colonialism
colonialism effects - dispossession of ownership
post-industrialised revolution
lifestyle factors that result in dislocation
economic instability, social isolation = drug use as a coping mechanism
what effect did the post-industrialised evolution have?
caused job losses, economic hardship, social isolation. these correlated to an increase in substance use.
how does social support effect drug use?
better social support has been shown to reduce drug use
what is the evidence that contradicts the dislocation model?
there is a biological basis of addiction, not solely social factors. not all that are disadvantaged develop addiction. we can not causally say that dislocation causes addiction as there are other factors.
addiction is a multifaceted issue (social, environmental factors)
how does chemical neurotransmission work?
transfers information between neurons
the resting membrane (-70mV), a stimulus acting on the brain can cause depolarisation whereby sodium channels open and Na+ ions enter the cell.
at the threshold of (-55mV) triggers an action potential
action potential travels from axon hillock down axon to presynaptic membrane
voltage-gated channels open and calcium ions enter presynaptic neuron
influx of calcium triggers vesicles holding NT’s to fuse with presynaptic membrane
release of NTs into synaptic cleft
NTs diffuse across the synaptic cleft and bind to ligand-gated channels on postsynaptic membrane.
what to consider when designing a study using mice and a new psychoactive drug?
define specific intended effects (analgesic, antidepressant, stimulant)
create a hypothesis using existing literature
RCT - assigning mice to either control or experimental condition
blind study so there is no bias
determine a range of doses and an appropriate route of administration
monitor the observed behavioural effects, physiological effects and mechanisms of action
use an established model (plus maze, open field) and or behavioural tests.
neuroimaging techniques (PET) to see brain activity
compare new drug with already established drug see if it works better.
consider the ethics, and if effects on mice can be translated to humans.
13 National Institute of Drug Abuse
no single treatment works for all individuals
treatment needs to be readily available
individual treatment plans must be assessed regularly modified if necessary cater to individualistic needs.
effective treatment would attend to multiple needs of the individual not just drug use.
remaining in treatment for an adequate period of time is critical for effectiveness.
individual/group counselling and other behavioural therapies are critical components of effective treatments for addiction.
medications are an important element of treatment, especially when combined with counselling & other behavioural therapies
addicted or drug abusing individuals with co-existing mental disorders should integrate treatments for all aspects.
medical detoxification is the first stage of treatment, by itself does little to change long-term drug use.
treatment does not need to be voluntary to be effective
possible use of drugs during treatment should be continuously monitored.
provide assessments for HIV/AIDS and other infectious diseases, providing counselling to modify these behaviours.
long-term process that may require multiple episodes of treatment
what are the main imaging techniques?
PET, SPECT, MRI, fMRI
PET (Poistron Emission Tomography)
is non-invasive and uses radioactive tracer to measure blood flow and or NTs activity. can be used to detect abnormalities providing info about tissue function.
it allows researchers to directly measure brain distributions of various drugs and local concentration of drugs.
does not show anatomical or structural detail. difficulties distinguishing between small structures. limited spatial resolution.
radiotracers decay quickly so must be made on site.
SPECT (Single Photon Emission Compute Tomography)
similar to PET uses radiotracers, but with a longer half life. cheaper.
lower resolution and sensitivity, more prone to artifacts
MRI
studies brain anatomy, is non-invasive and shows clear detailed images.
expensive, can not accommodate to all patients
fMRI
studies brain function, non-invasive, taking lots of images in a short period of time to map brain activity.
is susceptible to artifacts and distortion
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