Agonist Spectrum Concept Map

Central Idea: Agonists and antagonists interact with receptors to produce different biological effects.

Main Branches:

• Agonist: Binds to a receptor and initiates a cellular response.
  • Full Agonist: Produces the maximum possible response from the receptor. (e.g., Oxycodone)
    • Mechanism: Mimics the natural ligand, causing a conformational change that activates the G protein signaling pathway.
    • Receptor Target: Varies depending on the agonist (Oxycodone targets mu-opioid receptors)
  • Partial Agonist: Produces a submaximal response compared to a full agonist. (e.g., Brexpiprazole)
    • Mechanism: Binds to the receptor but only partially activates the G protein pathway.
    • Receptor Target: Varies depending on the agonist (Brexpiprazole targets dopamine D2 and serotonin 5-HT1A receptors)
• Antagonist: Binds to a receptor but does not activate it, blocking the effects of agonists. (e.g., Haloperidol)
  • Competitive Antagonist: Competes with the agonist for binding to the receptor. (e.g., Haloperidol)
    • Mechanism: Binds to the receptor without causing a conformational change, preventing agonist binding.
    • Receptor Target: Varies depending on the antagonist (Haloperidol targets dopamine D2 receptors)
  • Noncompetitive Antagonist: Binds to a different site on the receptor, altering its shape and preventing agonist activation. (e.g., Naloxone)
    • Mechanism: Binds allosterically, changing the receptor’s conformation and preventing agonist effect.
    • Receptor Target: Varies depending on the antagonist (Naloxone targets mu-opioid receptors)
• Inverse Agonist: Binds to a receptor and inherently reduces its basal activity below its resting state. (e.g., Pimavanserin) * Mechanism: Binds to the receptor and induces a conformational change that decreases basal activity. * Receptor Target: Varies depending on the inverse agonist (Pimavanserin targets serotonin 5-HT2A receptors)

Medications on the Agonist Spectrum:

• Full Agonist: Oxycodone (mu-opioid receptor agonist – pain medication)
• Partial Agonist: Brexpiprazole (dopamine D2 and serotonin 5-HT1A partial agonist – antipsychotic)
• Competitive Antagonist: Haloperidol (dopamine D2 receptor antagonist – antipsychotic)
• Noncompetitive Antagonist: Naloxone (mu-opioid receptor antagonist – opioid overdose reversal)
• Atypical Antipsychotic (Mechanism not fully understood):
  • Aripiprazole (possibly a partial agonist at dopamine D2 and serotonin 5-HT1A receptors)
  • Risperidone (possibly a partial agonist at dopamine D2 and serotonin 5-HT2A receptors)

Note: The mechanisms of action for Aripiprazole and Risperidone are still being researched and may involve a combination of agonist and antagonist effects at different receptors.

Additional Considerations:

• The specific effects of each medication depend on the receptor it targets and the overall balance of agonist and antagonist activity at that receptor.
• The concept map provides a simplified overview. Real-world interactions between drugs and receptors can be more complex.

Further Research:

• Research the specific mechanisms of action for Aripiprazole and Risperidone.
• Explore the effects of different agonist efficacies (full vs. partial) on cellular signaling pathways.

This concept map provides a framework for understanding how agonists and antagonists interact with receptors to mediate biological activities. You can further explore the specific medications mentioned and their mechanisms of action through additional research.