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Addiction (Short) Notes

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Addiction - short notes Example questions:

1. what may be the importance of synaptic plasticity in the brain's response to addictive drugs?

2. To what extent can we understand drug addiction by exploring the function and plasticity of the mesostriatal dopamine axis?
Drug addiction

Addiction is a disease  when drug-seeking becomes compulsive despite negative consequences o E.g. helath risk, physical detriment, inability to sustain normal social interactions, job Alcohol, tobacco and illicit drug use ranked among the top 10 leading risk factors for disease worldwide (1990) (WHO) Availability and consumption of tobacco, alcohol and illicit drugs are increasing worldwide due to changing social, environmental and economic conditions

Drug addiction: pharmacology, physiology, environment and learning?
(n.b. not mutually exclusive)

Acute pharmacological ("physical") effects Rewards… reinforcement Tolerance and escalation Withdrawal Dysregulation of hedonic processes Learning - synaptic adaptations Increased incentive/desirability/wanting Drug-associated environmental cues Cue-induced drug-seeking Cue-drug interactions Drug-seeking habits Diminished executive control Impaired decision making Compulsion

THESE ALL LEAD TO COMPULSIVE DRUG-TAKING = ADDICTION A disease of pathological reinforcement learning and compulsive behaviour Animal models:

Intracranial self-stimulation (ICSS) Olds and Miller (1953) - rats will work for ICSS of mesolimbic pathways - the stimulus is reinforcing. Rats will press a lever at a rate of several thousand times per hour for DAYS to obtain stimulation at the expense food until starvation (compulsive behaviour)

Drug self-administration  pressing of lever results in drug administration into discrete brain region via indwelling cannula (into VTA). Drug has reinforcing properties if lever pressing increases, or animal will work for reward. this pattern of behaviour resembles compulsive or addictive behaviour in humans.

Circuits that may be involved in addiction

Drug effects on reinforcement, actions-outcome learning, stimulus-response habits in NAcb and dorsal striatum - pathological learning of maladaptive behaviour Memory? - processing of conditioned reinforcement by basolateral amygdala and context by hippocampus Drug craving/drive - orbital and anterior cingulate cortex, and temporal love including amygdala "executive control" of decisions about goal-directed actions - PFC-striatum (contingencies, outcomes, value and subjective states including craving) serial interactions via nigrostriatonigral spirals

Transition from PREFRONTAL control to STRITAL control of drug-seeking behaviour

• over-representation of dopaminemodulated processes?
o May depend on neuroplasticity in cortical and striatal structures that is induced by chronic administration of drugs PFC: disrupted function of the PFC leads to a syndrome of impaired response inhibition and salience attribution (iRISA) in addiction

Addictive drugs have a common outcome: increased mesostriatal dopamine Classically, in ventral striatum (NAc) BUT not the whole story
 disinhibition, excitation and/or direct modulation of DA availability Diverse neurobiological targets of addictive drugs

1. drugs that activate GPCRs (Opioids, cannabinoids)

2. drugs that bind to ionotropic receptors (nicotine, alcohol, benzodiazepines)

3. drugs that bind to transporters of biogenic amines (cocaine, amphetamine, ecstasy) Not all psychoactive or abused drugs are addictive e.g. ketamine, LSD the ability to INCREASE DOPAMINE may be a defining characteristic of addictive drugs Can we understand drug addiction if we understand what dopamine neurons do?

Mesostriatal dopamine neurons signal reward prediction error during learning

Discrimination learning task: initially monkey does not know which is rewarded stimulus (lever presses) Action potentials in VTA/SN:

• Neuron activity increases briefly after reward stimulus

• Neuron activity is briefly inhibited after un-rewarded stimulus (error)

• As monkey learns which is rewarded stimulus, both excitatory and inhibitory responses disappear

• Rewardd prediction error - a teaching signal during learning?
 From Hollerman and Schultz 1998 - Dopamine neurons report an error in the temporal prediction of reward during learning
 Dopamine neurons in the SN and VTA are believed to be involved in rewarddependent learning - activated by rewards and because they are activated more strongly by unpredicted than predicted rewards they may play a role in learning. In this experiment, dopamine neurons were activated by rewards during early trials, when errors were frequent and rewards unpredictable, but activation was progressively reduced as performance was consolidate and rewards became more predictable

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