Drug Interactions on Synapse

Homework on Drug Mechanisms 1. Release and degradation of the neurotransmitter inside the axon terminal. Drug: Reserpine Pharmacology: Most often used to treat mild to moderate hypertension. Mode of action: Reserpine inhibits the ATP/MG2+ pump responsible for packaging neurotransmitters into vesicles in the presynaptic neuron. This causes the free neurotransmitters to be degraded by MAO, leading to a reduction in catecholamines. 2. Increased neurotransmitter release into the synapse. Drug: Black Widow Venom Pharmacology: Neurotoxin. Mode of action: Alpha-latrotoxin (a-LTX) is the three-dimensional protein toxin unique to widow spiders.

This protein has a high affinity for receptors that are specific for neuronal and endocrine cells of vertebrates. a-LTX will assemble into homotetrameric complexes which embed in the plasma membrane of the presynaptic synapse. a-LTX will then bind to a receptor on the plasma membrane and form cation-permeable channels (specifically Ca 2+, although Na +, K +, Mg 2+, etc. can enter the membrane too), allowing a massive influx of Ca 2+ into the axon terminal and cause massive release of any and all neurotransmitter in the terminal. A swollen terminal bouton is left in its wake. 3.

Prevention of neurotransmitter release into the synapse. Drug: Reserpine. Pharmacology: Most often used to treat mild to moderate hypertension. Rarely used as an antipsychotic. Mode of action: Reserpine works by irreversibly blocking the vesicular monoamine transporter (VMAT). This transporter normally transports dopamine (DA), 5-HT (serotonin), and norepinephrine (NE) from the cytoplasm to the vesicle in the presynaptic neuron. Because these neurotransmitters are not packaged, they are degraded quickly by monoamine oxidases (MAOs). 4. Inhibition of synthesis of the neurotransmitter. Drug: p-chlorophenylalanine (PCPA).

Pharmacology: Indirect serotonin antagonist. Primarily used in research. Mode of action: PCPA acts as an inhibitor to tryptophan hydroxylase, which is an essential, rate-limiting enzyme in the biosynthesis of serotonin. Therefore, PCPA acts as an inhibitor to neurotransmitter synthesis. 5. Reduced reuptake of the neurotransmitter from the synapse. Drug: Amphetamines Pharmacology: Low doses of amphetamine salts (such as Adderall) are used to treat ADHD. Mode of action: Amphetamine binds to the dopamine transporter (DAT) and blocks the transporter’s ability to clear DA from the synapse.

6: Reduced degradation of the neurotransmitter in the synapse. Drug: Sarin Gas (Nerve Gas) Pharmacology: Lethal poison. Classified as weapon of mass destruction. Mode of action: Sarin gas works by forming a covalent bond with a serine residue in cholinesterase. Cholinesterase is an enzyme primarily responsible for degraded acetylcholine in the synapse. This bond causes a structural change in cholinesterase that renders it inactive, causing ACh to build up in the synapse. ACh accumulation causes the muscle or organ to be unable to relax, and death will occur as a result of asphyxiation.

7. Agonists (evoke same response as neurotransmitter) or antagonists (block response to neurotransmitter) can occupy the receptors. Drug: Scopolamine Pharmacology: Used to prevent motion sickness. Mode of action: Scopolamine acts as an muscarinic antagonist/anticholinergic drug. Although its mechanism is not completely understood, it is believed that scopolamine blocks communication between the nerves of the vestibule in the ear and the vomiting center in the brain by blocking the action of acetylcholine. Scopolamine may also work directly on the vomiting center. 8.

Reduced biochemical response inside the dendrite. Drug: Morphine Pharmacology: Opioid Mode of action: Morphine, unlike most opioids, does not promote endocytosis of ? -opioid receptors because it fails to cause phosphorylation of them by activation of G-protein-coupled receptor kinases (GRKs). Instead, morphine uses a novel pathway that is not fully understood. Overall, chronic treatment with morphine results in a decrease in ? -opioid receptor sensitivity, an increase in acute desensitization, and a reduction in the recovery from acute desensitization in locus ceruleus neurons.

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