Addictive Behaviours Notes
Lecture 1: Introduction to Addictive Behaviours
Substance Use in the UK:
NHS information & National drug treatment monitoring service data for latest figures.
Women consume less alcohol than men (around half the amount); 45 – 64 year old male
drinks an average of 16 units a week
Cannabis is the most widely used drug in the UK; particularly in the 16-24 year old category.
Is used around 3x’s more than powdered cocaine.
Opiate use is making up 48% of people being treated for drug use. Opiates and crack make
up 32%.
For young people (12-18) = alcohol and cannabis are the most sort out for treatment.
The idea of a gateway drug is not as academically supported as before. This concept suggests a less
effective drug becoming an influence to start heavier drugs, e.g. cannabis as a movement onto
cocaine.
Defining Addiction:
A chronic relapsing condition characterised by compulsive drug seeking and abuse and by
long lasting chemical changes in the brain (www.medterms.com).
A syndrome in which a reward-seeking behaviour has become out of control (West, 2006).
An excessive appetite: An attachment to an appetitive activity, so strong that a person finds
it difficult to moderate the activity despite the fact that it is causing harm (Orford, 2001).
Physical or psychological harm to oneself or others
Cravings which lead to impaired control
Neglecting other activities/responsibilities (comorbidity with depression)
Persistent attempts to cease substance abuse (relapse).
Can also be addicted to non-drug substances; such as internet use, and gambling.
,Lecture 2: Neurobiology of Addiction
Dopamine and Reward: Olds & Milner (1954): Found rats will increase level presses when electric
stimulation is delivered to septal areas of the brain. Electrical stimulation occurs when lever is
pressed. The rat went ‘crazy’ & repeatedly pressed the lever when electrode stimulated the septal
areas. Made something unpleasurable become pleasurable = created an addict. This study
encouraged the concept of a ‘reward centre’.
Brain Regions & Neuronal Pathways:
Neurons connect areas via pathways, and send and integrate information; neurons can be
long or short.
For example, the thalamus receives information about pain, this is then sent to the sensory
cortex. The reward pathway is activated when the individual receives or sees the possibility
of positive reinforcement.
Brain Transmission: Action potential (electrical impulse) travels down the axon towards the
terminal. The terminal makes a connection (synapse) with dendrite of neighbouring neuron, where it
transmits a neurochemical signal.
Synaptic Transmission:
Vesicles contain neurotransmitters, they bond with terminal membrane, released into
synaptic cleft, NT binds to specific receptor (lock & key) on membrane of a neighbouring
neuron
Neighbouring neurons release compounds called neuromodulators; which enhance or inhibit
the effects of NT’s, such as dopamine.
Neuromodulator example = endorphin. This binds to opiate receptors on the post synaptic
cell & thereby alter the effect of dopamine. Neighbouring neurons as neuromodulators are
ones surrounding the 2 involved in the neurotransmission. Endorphins are broken down by
enzymes (specialised protein).
Dopamine: DA may play a role in many different processes that are relevant in this case =
anhedonia, prediction error, salience/attention, cost/benefit computation, uncertainty processing,
incentive salience, energising/motivating behaviour – these are what dopamine rich brain areas
focus on.
So, DA is more concentrated in some brain areas than others; where they are concentrated, causes
previously mentioned behavioural manifestation.
The reward pathway: VTA (Ventral tegmental area) to the Nucleus accumbens onto the PFC.
Addictive stimulants e.g. alcohol & sex, electrically stimulate the VTA (this is where the
reward pathway begins). As the PFC I involved in reward, we know that all of these
outcomes will have higher functions in the brain.
Manufactured drugs impact this pathway they act as modulators of DA neurotransmission.
Heroin is converted into morphine by enzymes; which binds to opiate receptors including
parts e.g. thalamus.
, Effect reward pathway and pain pathway which results in analgesia (reduction in detection
of pain).
Morphine binds to opiate receptors on neuron A; causing it to decrease the release of GABA
(this inhibits DA release by neuron B). In consequence, neuron B now releases more DA than
normal. Morphine is a neuromodulator. Heroin affects large numbers of brain areas.
The Action of Cocaine: There are two forms of Cocaine:
Powdered (hydrochloride salt); which is snorted, takes a relatively slow route.
Freebase form (crack); which is smoked, takes a more rapid route.
The faster the drug affects the brain, the more addictive the substance. Time between taking
the drug & experiencing the rewarding effects.
Cocaine reaches all areas of the brain but only binds to specific areas these are = VTA &
nucleus accumbens & caudate nucleus.
So, cocaine & heroin have different effects on the brain, yet are both highly addictive. This also
explains why they have different effects on the body. Cocaine binds to reuptake pumps, preventing
them from reuptaking DA. Therefore DA remains within the synaptic cleft; so there is more DA in the
system for longer.
Both Heroin & cocaine cause DA to stay in the system even longer; but heroin acts on the
neuromodulators and cocaine acts of the reuptakers.
Framework for Addiction
1. Binge Intoxication: Start taking or using in larger and larger quantities. This stage is thought
as the feel good stage; it is typically focused on positive reinforcing effects of drugs,
mediated by dopaminergic pathways in the medial forebrain. This stage involves serotonin;
opioid peptides and GABA. The change in dose is caused by a change in threshold; more
drugs needed to get the same effect.
2. Withdrawal/Negative Effect: This is thought of as the ‘dark side of addiction’. It involves the
hypoactivation of DA pathways, increased brain reward thresholds during acute withdrawal
(within – system adaptation). Then, there is a recruitment of ‘anti-reward’ brain systems in
amygdala involves corticotrophin releasing factor (CRF), dynorphin & norepinephrine. This is
thought of as a between systems adaptation.
Systems are visually involved in stress responses & activate to restore balance in the
chronic presence. This stage adds brain areas that make you feel bad in the absence
of the drug
3. Preoccupation/Anticipation: Negative feelings triggered by withdrawal = adaptational
changes in brain function via chronic drug use which allows for sensitivity to relapse & rapid
re-addiction. May be centred in deficits that develop in PFC (attention, memory, inhibition).
This stage is involved in change.
Positive Reinforcement Negative Reinforcement (withdrawal) Change in Cognitive Function
Key Neuroanatomical Structures in Addiction:
, 1. Nucleus Accumbens & Central Nucleus of Amygdala: Involved in reward. Forebrain
structures involved in the rewarding effects of drugs of abuse and drives the binge
intoxication stage of addiction. Contains key reward neurotransmitters: dopamine and
opioid peptides
2. Extended Amygdala: involved in anti-reward system. Composed of central nucleus of the
amygdala, bed nucleus of the stria terminalis, and a transition zone in the medial part of the
nucleus accumbens. Contains “brain stress” neurotransmitter, CRF that controls hormonal,
sympathetic, and behavioral responses to stressors, and is involved in the anti-reward
effects of drug dependence
3. Medial Prefrontal Cortex: neurobiological substrate for executive functions that are
compromised in drug dependence and play a key role in facilitating relapse. Contains major
glutamatergic projection to nucleus accumbens and amygdala.
Allostatic Model of Drug Addiction (Koob & Le Moal)
Allostatic: Maintenance of stability outside the normal homeostatic range. An allostatic load is the
force the body has to cope with when these chronic resets occur.
This model was developed on the basis of opponent – process models; in this model system
parameters are continually reset across time in response to chronic demands on the body e.g.
getting used to reduced food intake.
After the first few experiences, the high isn’t as impacting anymore, and the low is more influential.
Allostatic load involves dealing with this; eventually in a position where the drug isn’t making you
feel good, only more low, people take more drugs to reach a normal level, not the high anymore
(addiction).
1. Initial positive reinforcing effects of drugs in brain rewards regions
2. Chronic use leading to down regulation of dopaminergic and hypo activity in brain reward
regions (within system adaptations)
3. Recruitment of opponent processes based around HPA stress systems and CRF in
hypothalamus (between system adaptation)
Volkow et al 2003: Decreased dopaminergic activity the longer the use of the drug (cocaine in this
case)
Recruitment of opponent processes:
Dark side of chronic drug use; release of CRF in the central nucleus of the amygdala during
withdrawal.
Anxiety like responses and subsequent drug intake blocked by CRF antagonists (Work in the
opposite way to CRF).
There is evidence for a role of norepinephrine, particularly with alcohol withdrawal.
Increases in dynorphin in the amygdala and Nacc – this is associated with negative emotional
states.
Chronic decreases in anti-stress system e.g. Neuropeptide Y
