Reward and Addictive Behaviours Flashcards
Limbic System:
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Reward Flowchart:
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Drug Use vs Drug Misuse:
any psychoactive recreational substance use/experimental use
any unsanctioned recreational substance use
Problematic/Hazardous Drug Use:
use of a psychoactive substance at amounts or rates likely to lead to problems
Harmful use of substances must be dependent.
True or False?
False
Dependent Use:
persistent uncontrolled drug use repeatedly leading to multiple harmful consequences
Addicition
a state in which a person engages in a compulsive behaviour, even when aware of potentially negative consequences - behaviour is reinforcing (rewarding or pleasurable)
loss of control in limiting intake
Tolerance:
a state in which a person no longer responds to a drug or substance
a higher dose is required to achieve the same effect
also referred to as the hyposensitisation syndrome
Dependence:
a state in which a person functions normally only in the presence of a drug
manifested as a physical homeostatic disturbance when the drug is removed
Categories of Harm Associated with Substance Abuse Disorders:
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Life Cycle of Addiction:
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What are the series of structures contributing to incentive salience?
The mesocorticolimbic circuit
also implicated in associative learning eg; taking cocaine in a nightclub, nightclubs are associated with craving for cocaine
What structures are used in the mesocorticolimbic circuit?
- mesolimbic system
- mesocortical system
addiction also involves:
- PFC
- amygdala
- hippocampus
When will the mesocorticolimbic system be activated?
in response to many stimuli
dopaminergic response
central to motivation
Pathway for Reward and Reinforcement:
addictive drugs activate this system
Addictive drugs cause more powerful and reliable activation of ——– than natural rewards/
- behaviour activating system
Mesocorticolimbic Circuitry:
- initiates in the ventral tegmental
area - travels along the mesolimbic
pathway to the nucleus
accumbens (linked to emotional
processing) - mesocortical pathway originates
from the ventral tegmental area
and loops up into the prefrontal
cortex and cingulate gyrus - cingulate gyrus is also linked to
emotional processing - nucleus accumbens is the key
structure in secreting the extra-
cellular dopamine
Nucleus Accumbens
- inner core = linked to basal ganglia
and implicated in movement - shell = part of amygdoloid
complex and links into the limbic
system and hence the reward-
addiction pathway and responsible
for the secretion of dopamine
Dopaminergic processing in a normal reaction resulting in a
motivational state
Reward-addiction: More than just Dopamine:
Opiates, cannabinoids and alcohol can act directly act on the nucleus accumbens via non-dopaminergic mechanisms
Functions of the Reinforcement System:
- detect reinforcing stimulus to
recognise something positive has
occurred and learning from
experiences - strengthens neural connections
via synaptic plasticity leading to
long-term potentiation
Dependence:
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Why do craving persist for years?
due to the previous homeostatic changes
the synaptic remodelling
Cocaine and Amphetamines Effects:
- psychosis; evidence of
dopaminergic involvement in the
positive symptoms of psychosis - cellular and molecular changes
that promote dysregulation
can result in hypofrontality, in which there is decreased cerebral blood flow to the pre-frontal cortex
Dopamine enhances Long0Term Potentiation:
- dopamine binds to D1 receptor
- modifies glutamatergic
transmission allowing long term
potentiation - synaptic remodelling: increased
dendritic spine and branches - long term molecular and cellular
changes remain months after
abstinence - memories in these pathways may
trigger relapse years later via
associative learning
Which dopamine receptors is found less in patients suffering with addiction?
D2 receptors
less found due to synaptic remodelling
impacts adversely upon classical conditioning (learning/memory) and motivational status
likely responsible for reduced sensitivity to natural rewards that often develops with addiction
Why do patients who obtain abstinence often have mood disorders/ feel a lack of satisfaction in life?
Decrease in D2 receptors due to synaptic remodelling, which are highly implicated in motivation
the artificial reward triggers more dopamine than the natural reward
What occurs on a molecular level to cause acute withdrawal symptoms in the context of opiate use?
- opiate receptors present in
mesocorticolimbic circuit - locus coeruleus is a noradrenergic
nuclei, which is responsible for
activating the fight or flight
response - acute opiate use = acutely inhibits
the firing of LC neurons - chronic opiate use = LC neurons
return to normal firing rates due
to compensatory mechanisms - in acute withdrawal:
- substantial increase in LC firing
- correlates with the physical
withdrawal symptoms - triggers overactivation of the
ANS
- correlates with the physical
- substantial increase in LC firing
Opiate Dependence: Treatment:
- biopsychosocial interventions
- stepwise process
- needs to motivate patient
- minimise harms related to taking
substance - reduce criminal activity
Alcohol:
- agonist?
- antagonist?
- gaba agonist
- NMDA antagonist
leads to inhibition of functioning of most voltage gated ion channels
alcohol leads to increased dopamine release in nucleus accumbulus and anticipation of alcohol in +ve valence
NMDA antagonism of cortical inputs to ventral tegmental area and inhibits dopaminergic neurons in this area resulting in increased dopamine release in nucleus accumbuls
Alcohol Dependence Syndrome: Criteria:
- strong desire/compulsion to take
substance - difficulty in refraining from
substance - physiological withdrawal state
when substances have either been
stopped or if dosage has been
decreased. Physiological
symptoms can be avoided by
reintroducing the substance - evidence of tolerance
- evidence of a progressive neglect
of alternative pleasures or
interests - persistent use of substance
despite clear evidence of harm
What are the acute effects of alcohol?
- agonist at GABA
- antagonist at NMDa
- prevents influx of NA+, allows
efflux of Cl- - less action potentials fired
What are the molecular effects of chronic alcohol consumption?
- downregulation of GABA receptors
- upregulation of NMDA receptors
- in the presence of alcohol firing
rates return to normal as
compensatory mechanisms allow
the influx and efflux of ions as
normal
Alcohol Withdrawal:
- absence of alcohol
- firing rates increase as more influx
and efflux due to compensation - alcohol not dampening the firing
rates - agitation, tremors, confusion,
seizures
Alcohol Dependence Assessment:
- extent of drinking
- evidence of dependence
- disabilities and co-morbidities
- arrange psychiatric treatment for
any co-morbid mental health
problems - psychoeducation
- motivation for change interview,
self-help materials
Treatment for Alcohol Dependence: Safe Withdrawal:
community based: benzodiazepines and oral thiamine
inpatient: same but management of complications
inpatient is better
Treatment of Alcohol Dependence: Relapse:
- outpatient follow-up
- CBT
- family therapy
- vitamin supplementation
- antidepressants for depression
- assistance with employment,
alcohol and legal issues
