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Flashcards in Neuropharmacology of Addiction Deck (12)
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What are the 2 types of dependence?

Psychological --> Craving, compulsive use, loss of control


Physical --> When stopping a drug causes a withdrawal syndrome (physical symptoms)

This can be caused by some non-rewarding drugs also


What do Kappa agonists do to dopamine levels?

Decrease cause dysphoria


How does ethanol decrease hyperpolarization?

Acts as a K+ channel blocker


How is it proposed that alcohol increases the chance of opitate ODs?

Reverses opioid tolerence by reversing mu-opioid receptor desensitisation


Also possible for gabapentin to do the same


What are the 3 current categories of drug treatment for addiciton?

Substitution therapy --> NRT and OST


Aversion Therapy --> Use of disulfiram to prevent ethanol ingestion. This causes a build up of acetaldehyde....but complaince is a huge issue!


Antagonists/Antibodies --> Naltrexone/Buprenorphine are currently used, but several downsides

Antibodies are a devloping field...but a vaccine-like treatment could be possible!


What are the 3 major stimuli for relapse in humans?

Taking a small dose of the drug




Being presented with a cue that's associated with taking the drug (eg, going to the pub)


What is the role of dynorphin in withdrawal?

Dynorphin --> A kappa causes dysphoria


Dopamine binds to D1 receptors that are Gs coupled, causing an upregulation of certain factors like dynorphin. These cause GABA to inhibit dopaminergic neurones, whilst the dynorphin binds, causing a decrease in dopamine release


Why is there a link between D2 receptors and addiction?

Lower levels of D2 receptors = More dopamine needed for a euphoric effect

This can occur due to an SNP in a specific gene


Drug abuse can also cause a reduction in D2 receptors


Why are D2 antagonists not the answer to drug abuse?

As they would compete with dopamine, causing less to addicts would just use more illict drugs to overcome the block!


How could we try to make addicts forget that they are addicted?

By inhibiting synaptic plasticity during re-consilidation of a memory


So exposing the person to the memory (eg, the pub), and giving a drug (like propranolol) to weaken the memory


An ethical nightmare! And it isn't very selective....


What are the following drugs?


Buproprion (Zyban)


Buproprion (Zyban) --> A DNRI that has a role in addicition treatment purley because of its antidepressent properties


Bromocriptine --> A D2 partial agonist

Only seems to work in those with lower levels of D2 receptors




Name two drugs that could help prevent stress related relapse

Antalarmin --> CRH-1 receptor antagonists


Mifepristone (Morning-after-pill) --> Glucocorticoid receptor antagonists