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  • 1st generation : more likely to bind to D2 receptors
  • 2nd generation : more likely to bind to D4 receptors

That's why we get less extra-pyramidal side effects with 2nd generation (because extra-pyramidal side effects are mediated mainly through D2 receptors).

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Q: What is the difference between first and second generations of antipyschotic in relation to dopamine receptors?
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How does nicotine influence dopamine receptors in the brain?

Increasing release of dopamine


What is the mechanism of action of haldol on dopamine?

it blocks D2 receptors to inhibit the production of dopamine.


What parts of brain do the neurolyptics effect?

The theory behind why individuals develop 'psychotic' symptoms is based upon the idea that there are elevated levels of dopamine in the brain. Dopamine is a neurotransmitter, a molecule that passes messages between neurons. For example, when a nerve impulse arrives at a dopaminergic neuron (also known as a pre-synaptic neuron), dopamine is released from the cell and diffuses through a space between two neurons, called the synaptic cleft. Dopamine then binds to specific dopamine receptors on a different neuron (post-synaptic neuron) producing a specific signal, impulse or effect. Dopamine is then released from its receptors and 're-absorbed' into the pre-synaptic neuron, or degraded by enzymes in the synaptic cleft. The neuroleptics block dopamine receptors thereby inhibiting the ability of dopamine to attach to these receptors and generate signals. However, unlike the typical neuroleptics, the atypicals merely transiently block the receptors therefore allowing some dopamine to bind to the receptors and generate signals. The atypical neuroleptics are also able to block serotonin receptors located on dopaminergic neurons. When serotonin binds to these receptors it inhibits dopamine release. However as these receptors are blocked by atypical neuroleptics, the dopamine secretion is increased. The transient rather than permanent blocking of dopamine receptors and the blocking of serotonin receptors and subsequent increases in dopamine, it is for these reasons that the atypicals are thought to produce fewer adverse effects than the typical neuroleptics. However, the atypical drugs differ in their 'stickyess' when binding to dopamine receptors and also in the ratio of which dopamine ad serotonin receptors are affected. This may result in some atypicals producing higher levels of specific adverse effects than others. The atypicals may also bind to other receptor types, producing further adverse effects (see side effects of atypicals section).


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Does anti psychotic medication affect the human body?

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Why is pcp more addictive than LSD?

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Why do you have delayed response to pain and anger after smoking cannabis indica?

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