Agonism, Antagonism, and Re-uptake Pumps

Discussion in 'Pharmacology' started by Benzeneringz, Aug 3, 2006.

  1. Benzeneringz

    Benzeneringz Titanium Member

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    May 18, 2006
    from U.S.A.
    There are many ways a drug can act in the brain to create an alteration in biological function. A drug can bind to receptors and mimic the action of neurotransmitters. This process is known as agonism. A drug is considered to be a receptor agonist if it works through agonism of neuronal receptors. An example of a receptor agonist is the opioid morphine. Morphine binds to mu-opioid receptors in the brain and spinal cord, mimicking the action of enkephalin and endorphin. The opposite of agonism is known as antagonism. It occurs when a drug binds to a receptor and prevents neurotransmitters from acting there. The opioid antagonist naloxone is a prime example of antagonism. Like morphine, naloxone binds to mu-opioid receptors. But instead of activating the receptor, naloxone prevents it from being activated. A simple way to explain it: an antagonist does not activate the receptor is binds to while an agonist does.

    Another potential action that a drug can take involves a part of the neuron known as the re-uptake pump. This pump acts like a vaccum, removing neurotransmitters from the synaptic cleft and recycling them back into the axon terminal. A drug can block the flow of the pump, causing neurotransmitters to remain in the synaptic cleft thus increasing their duration of action. Drugs which turn the re-uptake pump off are known as re-uptake inhibitors. Cocaine is a dopamine re-uptake inhibitor. By blocking the re-uptake pump, cocaine increases dopamine's duration of action. Another way the re-uptake pump can be affected by a drug involves the flow of neurotransmitters through the pump. A drug can turn the vaccum into a pump, causing neurotransmitters to be sucked out of the axon terminal and into the synaptic cleft. Not only does this prevent the re-uptake of neurotransmitters, it increases the amount of neurotransmitters in the synaptic cleft. Both the duration and intensity of the neurotransmitter is increased. Methylenedioxymethamphetamine (MDMA) is an example of this method of action. MDMA causes serotonin to flow out of the re-uptake pump, resulting in a surge of serotonin to be released into the synaptic cleft.