Week 2 - Neurobiology Flashcards
Models of addictive behaviour - drug use models
- disease model
- physical dependence model
- positive reinforcement model
Definition of addictive behaviour
Compulsive (impaired control over use of the drug) & self-destructive (harmful consequences to user)
What year was addiction added to the DSM?
1987
Strengths of the disease model
- 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
Limitations of the disease model
- what is the disease?
- may reduce individual responsibility for behaviour
Physical dependence model
the state in which the discontinuation or reduction of a drug would cause withdrawal symptoms
Drug administration and withdrawal effects
- repeated drug administration - body learns to adjust to drug-induced changes
- drug removes - body readjusts again (withdrawal)
- withdrawal symptoms are usually opposite symptoms incurred by drug
How can withdrawal symptoms be stopped?
by re-administering the drug, or a similar drug (cross-dependence)
Strengths of physical dependence model
compatible with disease model; plausible explanation for addiction to drugs with withdrawal effects
Limitations of physical dependence model
cannot account for:
- individual differences as well as the disease model can
- substances of addiction that show little to no withdrawal sickness
- voluntary withdrawal (despite symptoms)
How does the psychological dependence model attempt to refine the physical dependence model?
- circular reasoning
- difficult to assess outward manifestations
Positive reinforcement model
- drugs are self-administered because they act as a positive reinforcer (operant conditioning)
- drugs that are self-administered by animals even in the absence of physical dependence/withdrawal
What is a positive reinforcer?
any stimulus that increases the frequency of a behaviour it is contingent on
Limitations of positive reinforcement model
- can the positive consequences of behaviour outweigh the costs?
- circularity: drug is a positive reinforcer because of increased drug taking behaviour; then positive reinforcement cannot explain drug taking
Strengths of the positive reinforcement model
- accounts for drug-taking behaviour in absence of dependence/withdrawal
- compatible with disease/physical dependence model
- compatible with general model of reinforcement
How does classical & operant conditioning apply to drug taking?
- Reinforcing effects of drugs can be paired with other stimuli through conditioning
- an extinction phase can be demonstrated
- Responses to operant reinforcement schedules can be elicited as predicted
- 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
why do positive reinforcers activate motivational circuits?
because it may increase likelihood of behaviour repeating
What does the motivational circuit rely on?
activity of neurotransmitters
Incentive salience
A strong motivation for rewarding stimuli (natural and acquired)
neuroanatomy of motivation & reinforcement
- ‘wanting’ vs ‘liking’ in reinforcement
- ‘pleasure centres’
- drugs as reinforcers
- stress & reinforcement
- addiction
- drugs alter the functioning of the motivation system & behaviour
- increase dopamine in mesolimbic dopamine system
Incentive Sensitisation Theory
with repeated administration of a drug, the reinforcing effects (incentive value) and related stimuli become sensitised.
- increased sensitisation of the dopamine response in mesolimbic dopamine system & motivation circuitry, leads to;
- increased intensive salience being acquired of the drug and associated stimuli
Drug craving
desire/urge to experience the effect(s) of a previously experienced psychoactive substance (wanting)
Strengths of the Incentive Sensitisation Theory?
- accounts for the development of addiction over time/use
- explain craving triggers (associated stimuli that have acquired incentive salience) & priming effects
Hendonic dysregulation & adaptation (HD&A) is the modern version of which model?
the physical dependence model
Allostatic process of HD&A
- repeated use &/or cessation of use, there’s an opposite compensatory response (depression) - disrupted neurotransmitter functioning & neuroadaptation
- contrast to homeostasis (changing/lowered set point in brain)
- increases tolerance to pleasurable (liking) effect of drug & increases insensitivity to pleasure
Dysphoria
withdrawal mechanism of psychological dependence - can explain relapse long after physical withdrawal symptoms are gone
Disruption of brain control circuits
A dysfunction in information processing and integration amongst multiple brain regions
circuits that regulate
- reward/saliency - (nucleus accumbens & ventral tegmental area)
- motivation/drive (orbitofrontal cortex & motor cortex)
- memory/conditioning - (amygdala & hippocampus)
- inhibitory control/executive function - (dorsolateral prefrontal cortex & anterior cingulate gyrus)
- all interconnected circuits; receive input from dopamine neurons
neurons
responsible for receiving sensory information, integrating & storing information & controlling muscles & glands.
- connected to each other via synapses
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
chemical messengers that operate between synapses
- NTs released at synaptic vesicles into synaptic clefts & occupy receptor sites on post-synaptic neuron
- receptor site may depolarize or hyperpolarize post-synaptic cell
Stimulation of the axon
- action potential (AP)
- the breakdown & restoration of the restin potential (firing; all or non law)
- Depolarization (EPSP)
- Moves toward zero and 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
Action at a synapse
- neurotransmitters - effects depend on receptor site and binds to;
- receptors - ionotropic vs metabotropic
- second messengers
Types of neurotransmitters
- Acetylcholine (ACh)
- Monoamines:
- Catecholamines (CA)
- Epinephrine (E)
- Norepinephrine (NE)
- Dopamine (DA)
- Serotoninc or 5-Hydroxytryptamine (5-HT)
- Adenosine
- Endocannabinoids
- Amino Acides
- Opiod 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 neurotransmitters & occupying their receptor sites
- decreasing activity of enzymes that create or destroy neurotransmitters
- althering neutrotransmitter reuptake
- altering the activity of a second messenger
- interfering with ion channels
- changing the amount of neurotransmitter released
How do drugs have an effect on 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 and neurophysiology
CNS is not static - changes may take place in the CNS in response to drug taking
such plasticity may account for another aspect of drug taking - tolerance
Tolerance
decreased effectivence (or potency) of a dryg usually resulting from repeated administrations; necessity of increased dose to maintain its effect
cross-tolerance
tolerance to one drug diminishes the effect of another drug
what is acute tolerance and tachyphlaxsis
tolerance after one drug administration
how does tolerance work?
- tolerance develops and dissipates to different effect of drugs, at different rates
- tolerance will only develop in a circumstance where a drug places a demand on the homeostatic mechanisms
Metabolic tolerance
pharmacokinetic tolerance
rate of metabolism increases, usually due to increase in enxyme used to break down the drug (enzyme induction)
physiological tolerance
pharmacodynamic tolerance
homeostasis is mechanism by which the body maintains a constant internal environment; can result in tolerance
behavioural tolerance
through experience with a drug, organisms can learn to decrease behavioural effect of the drug (through classical and operant conditioning)
conditioned drug tolerance
environment drug is adminstered in can be a stimulus for the body’s effort to resist a drug leads to eliciting phys. compansatory conditioned responses that decrease effect of drug/increase tolerance
sensitisation (reverse tolerance)
less common than tolerance, refers to increase effects of a drug usually following repear administrations
- cross-sensitisation to other drugs
Diagnostic criteria of identifying people with addictions
- DSM-IV-TR
- DSM-5
- ICD-11
