Schizophrenia - Methods Of Modifying Behaviour: Antipsychotic Drugs

Question 1

What are the 3 components to describe

Answer 1

• conventional antipsychotics
• atypical antipsychotics
• differences between Conventional and Atypical

Question 2

Describe conventional antipsycotics

Answer 2

-Developed in the 1950s by Delay and Deniker and it works by blocking the neurotransmitter dopamine
- Chlorpromazine is an antagonist, which means that it is a blocking agent.
- The drug is mainly received at D2 receptor sites and antagonises them
- After the presynaptic neuron releases dopamine into the synapse, the receptor sites are blocked by the chlorpromazine which therefore reduces the activity of that post-synaptic neuron.
- Initially this causes the presynaptic neuron to temporarily increase the amount of dopamine secreted into the synapse.
- Eventually production ends up dropping because it becomes depleted as a result of being broken down by an enzyme.
- This means that you have lower levels of dopamine overall
- This is maintained if you keep taking the drug, leading to a substantial decrease in neural activity which then eventually leads to lowered levels of dopamine
- This is linked to the mesolimbic pathway (The Ventral Tegmental Area → Nucleus accumbens).
- leads to less schizophrenic symptoms - in particular the positive symptoms, such as hallucinations and delusions.
- It also has an impact on 2 serotonin receptor sites → 5-HT1 and 5 HT-2 as well as also blocking D1, 3, 4 and 4 receptor sites (but mainly blocking D2).

Question 3

Describe Atypical antipsychotics

Answer 3

• developed in the 1990s.
• They work like conventional antipsychotics because they’re a dopamine antagonist.
• However the precise mechanism for how they work is unclear.
• We know it blocks dopamine but don’t know what its effect is on serotonin.

Question 4

Describe the differences between conventional and atypical antipsychotic drugs

Answer 4

• Some report that atypical antipsychotics are different from conventional antipsychotics because they are received at fewer dopamine D2 receptor sites and at more D1 and D4 receptor sites.
• Another difference is that most atypical antipsychotics also antagonise the serotonin receptor 5-HT2A, to the same degree as they antagonise the dopamine D2 receptor.
• Another possible difference between atypical and conventional antipsychotics is the actual amount of time they occupy the D2 receptor sites. Philip Seeman (2002) reports on the ‘fast-off” theory; this proposes that atypical antipsychotics bind more loosely to the D2 receptor sites than conventional antipsychotics. This means that, although the blockade has a therapeutic effect, it does not last long enough to also produce the side effects seen in conventional antipsychotics (such as tardive dyskinesia, which involves involuntary writhing or tic-like movements of the tongue, mouth, face or whole body).
• The ‘half-life’ of atypical antipsychotic medication is also thought to be less than conventional antipsychotic medication - with atypical antipsychotics the occupancy of D2 receptors fall off within 24 hours, however with conventional antipsychotics the fall off is longer than 24 hours.