WEEK 2 Flashcards
What are the Drug use models
- Disease model - addiction as a disease
- Physical dependence model
– Hedonic dysregulation - Positive reinforcement model
– e.g.Incentive sensitization theory
What is the disease model?
- one of first models of addiction
- disease model says that addiction is compulsive and beyond the individuals ability to control use
- thought of as an illness or a disease
What are the disease models strengths?
- may make accessing treatment easier
- rules that usually govern behaviour may not apply to drug taking, since this behaviour is abnormal
- can account for individual differences in response to drugs
What are the disease models limitations
- “what is the disease?” (but, to what extent do we need to be able to identify the disease?)
- May reduce individual responsibility for behaviour
Definitions of addictive behaviour
Compulsive (impaired control over use of the drug) & self-destructive (harmful consequences to user)
What is the physical dependence model?
physical dependence is “The state in which the discontinuation or reduction of a drug would cause withdrawal symptoms”
the model says its the desire to avoid withdrawal symptoms that lead us to seek out that drug.
What are withdrawal effects?
- Repeated drug administration → body learns to adjust to drug-induced changes
- Drug removed → body readjusts again (withdrawal)
- Withdrawal symptoms: usually opposite symptoms incurred by drug
–> Can be stopped by re-administering the drug, or a similar drug (cross- dependence).
–> drug may be re-administered to counteract withdrawal effects
What are the Physical dependence model strengths?
compatible with disease model; plausible explanation for addiction to drugs with withdrawal effects
What are the Physical dependence model limitations
- individual differences as well as the disease model can;
- substances of addiction that show little to no withdrawal sickness;
- voluntary withdrawal (despite symptoms)
What is the Positive Reinforcement Model
- Drugs are self-administered because they act as positive
reinforcers (operant conditioning) - Positive reinforcer: “any stimulus that increases the frequency of a behaviour it is contingent on”
- Drugs that are self-administered by animals even in the
absence of physical dependence/withdrawal (intragastric,
intracranial, intraventricular, inhalation & oral routes)
What is the Positive Reinforcement Model’s limitations
- Can the positive consequences of behaviour outweigh the costs (positive reinforcement paradox)?
- Circularity: drug is positive reinforcer because ↑ drug taking
behaviour; then positive reinforcement cannot explain drug taking* Can the positive consequences of behaviour outweigh the costs (positive reinforcement paradox)? - Circularity: drug is positive reinforcer because ↑ drug taking
behaviour; then positive reinforcement cannot explain drug taking
What is the Positive Reinforcement Model’s strengths
- accounts for drug-taking behaviour in absence of
dependence/withdrawal; - compatible with disease/physical dependence model;
- compatible with general models of reinforcement…(see next slide).
How does controlled conditioning
(classical & operant) apply to drug taking.
- Reinforcing effects of drugs can be paired with other stimuli through conditioning –> other stimuli becomes reinforces (smell of coffee can illicit positive effects that are normally associated with actual caffeine intake)
- An extinction phase can be demonstrated
- Responses to operant reinforcement schedules can be elicitedas predicted _.variable rates vs fixed rates of reinforcement.
- Responses can be elicited following priming
- Response patterns to substances that act as aversive stimuli are consistent with avoidance behaviours
- A conditioned compensatory response can be demonstrated –> sometimes a person experiences the opposite effect of a drug when they are presented with the conditioned stimuli (e.g. for heroin users - when they strap on equipment its a signal to the brain they are about to be hit of heroin so the brain engages in a antcipatory response which helps ready the body –> sometimes leads to overdoses as you already have a response)
Positive reinforcement & neurobiology
- Positive reinforcers activate motivational circuits
–> it is that action which may increase likelihood of behaviour repeating - “Reinforcement centre”/ motivational circuit
(neuroanatomy) - Motivational circuit relies on activity of neurotransmitters
(NTs) - Incentive salience (natural salience & acquired salience)
Neuroanatomy of Motivation & Reinforcement
- “Wanting” vs. “Liking” in reinforcement
–> “Pleasure centres”
–> drug use is due to wanting rather than liking - Drugs as reinforcers –> increase rate of us engaging in drug use via dopamine pathway.
- Stress (both present & past) & reinforcement
- Addiction
–> Drugs alter (“hijack”) the functioning of the motivation system & behaviour
–> increase dopamine (DA) in mesolimbic dopamine system
What is the Incentive Sensitization Theory (robinson and Berridge)
- Repeated drug administration
–> Increases sensitization of mesolimbic DA response & motivation circuitry
–> increases incentive salience of drug & associated stimuli (craving) - says that with repeated administration of a drug the reinforcing/incentive effect of a drug becomes sensitised
increase in sensitization of the dopamine response leads to increased salience which therefore increases craving.
I. E –> as we use a drug more and more it increases sensitisation and our dopamine response gets stronger so more cravings.
What is a drug craving
The desire/urge to experience the effect(s) of a
previously experienced psychoactive substance (‘wanting’)
What is the Incentive Sensitization Theory’s strengths
- accounts for the development of addiction over time/use
- explains craving triggers (associated stimuli that have acquired incentive salience) & priming effects
What is Hedonic Dysregulation & Adaptation
- Modern version of physical dependence model (e.g., Koob & le Moal)
- Allostatic process
–> Repeated use &/or cessation of use opponent process or compensatory response (depression) – disrupted Neuro transmitter functioning & neuroadaptation
–> Contrast to homeostasis as it changed and lowers set point further (rather than just returning to normal as in homeostasis)
–> increases tolerance to pleasurable (‘liking’) effect of drug & increases insensitivity to pleasure - increased liking of drug leads to dysphoria (a withdrawal mechanism of dependence). Therfore a strength of the model is that it explains relapse long after physical withdrawal symptoms are gone.
Explanation: So we’re less happy we become less happy about using the drug and more depressed when they stop, because the mood set point keeps lowering and lowering each time they use it.Which motivates the person to take larger doses, seek and take larger doses, decreasing that set point even further and reducing the reinforcing value of other non drug stimuli.
What is Dysphoria
- withdrawal mechanism of psychological dependence
- Can explain relapse long after physical withdrawal symptoms gone
What is Disruption of Brain Control Circuits
A theory proposed byVolkow et al, which says that drug addiction is a dysfunction in information processing & integration amongst multiple brain regions (4 different circuits of brain regions)
What are the Circuits in Volkow’s Brain control circuit theory
- “reward/saliency” (e.g., nucleus accumbens & ventral tegmental area)
- “motivation/drive” (e.g., orbitofrontal cortex & motor cortex)
- “memory/conditioning” (e.g., amygdala & hippocampus)
- “inhibitory control/executive function” (e.g., dorsolateral prefrontal cortex & anterior cingulate gyrus)
- all interconnected circuits; receive input from DA neurons
What are Neurons
Neurons are responsible for receiving sensory
information, integrating & storing information
& controlling muscles & glands
Neurons are connected to each other via synapses
What are the parts of a neuron
Cell body (soma): contains the nucleus
Nucleus: contains genetic information & controls
metabolism of the cell
Membrane: surrounds the cell; semipermeable; filled
with cytoplasm
Dendrites: fibres extending from axon; connect to
other cells
Axon: length of the neuron
Axon hillock: place where axon is attached to cell body
Myelin sheath: fatty substance surrounding the axon
Terminal buttons: swelling at the end of the axon
What are Neurotransmitters (NTs):
- chemical messengers that operate between
synapses - NTs released at synaptic vesicles into synaptic cleft & occupy receptor sites on post-synaptic neuron
- Receptor site may depolarize or hyperpolarize post-synaptic cell
what is resting potential
Is when a nerve is not firing, what the voltage difference is from the outside of the cell membrane to the outside of the cell membrane (about 70milivolts)
Neurophysiology: APs & PSPs
- Stimulation of the axon
- Action Potential (AP) –> The breakdown & restoration of the resting potential
- Firing; all-or-none law
- Depolarization (EPSP) –> Moves toward zero & positive numbers
- Hyperpolarization (IPSP) –> Moves further away (more negative) from zero
- Threshold of excitation
- Voltage gated ion channels
- Stimulation of dendrites & cell body
-> Postsynaptic potentials (PSPs): graded; excitatory (EPSP) vs. inhibitory (IPSP); summation across time & space
Neurophysiology: the synapse
- Action at a synapse
- NTs (“1st messengers”) – effects depend on receptor site
binds to: - Receptors - ionotropic vs. metabotropic
- Second Messengers
–> Special molecule is released into the postsynaptic cell
*–> Multiple mechanisms & durations of effect
Neurophysiology: Neurotransmitters
- Acetylcholine (ACh)
- Monoamines:
- Catecholamines (CA)
- Epinephrine (E)
- Norepinephrine (NE)
- Dopamine (DA)
- Serotonin or 5-Hydroxytryptamine (5-HT)
- Adenosine
- Endocannabinoids (e.g., anandamine)
- Amino Acids: GABA(-), Glycine(-), Glutamate(+)
- Opioid Peptides
- Enkephalines or Endorphins
Neurotransmitter action
- Most drugs work by interfering with the chemical process that occurs at a synapse
How do Drugs alter the synaptic process
- Mimicking NTs & occupying their receptor sites
- decreasing activity of enzymes that create or destroy NTs
- Altering NT reuptake
- Altering the activity of a second messenger
- Interfering with ion channels
- Changing the amount of NT released
Drug effects on NT: an illustration
- Acetylcholine (ACh)
- Acetylcholinesterase (AChE) - enzyme in synapse which normally
breaks down Ach - Drugs may interfere with AChE or with receptor sites
- Insecticides, Nerve Gases
- Cholinergic synapses
- Nicotinic
- Stimulated by nicotine
- Blocked by curare & Botox
- Muscarinic
- Stimulated by muscarine
- Blocked by atrophine & scopolamine
Plasticity of physiology & neurophysiology
- CNS is not static; changes make take place in the CNS in
response to drug taking (e.g., ↑receptor sites, ↑sensitivity
of receptors etc.) - Such plasticity may account for another aspect of drug
taking - tolerance
What is tolerence
decreases effectiveness (or potency) of drug usually
resulting from repeated administrations; necessity of ↑
dose to maintain its effect
What is cross-tolerance:
tolerance to one drug diminishes the effect of
another drug
