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opioid analgesics AND spinal cord
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opioid analgesics mechanism presynaptic calcium channels postsynaptic potassium channels NCBI
The page explains how morphine and other opioids reduce pain transmission in the spinal cord.
At the first pain synapse, a pain-sensing neuron releases chemicals such as glutamate and substance P onto the next spinal neuron. Opioids suppress this process in two ways:
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Presynaptic action: less pain chemical is released
- Morphine binds mainly to mu (μ) opioid receptors on the incoming pain nerve terminal.
- It closes/inhibits voltage-gated Ca²⁺ channels.
- Less calcium enters the nerve terminal.
- Calcium is needed for neurotransmitter vesicles to release their contents, so less glutamate and substance P are released.
- Result: the next neuron receives a much weaker pain signal.
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Postsynaptic action: the next neuron becomes harder to excite
- Morphine binds μ receptors on the postsynaptic neuron.
- It opens K⁺ channels.
- Potassium leaves the cell, making the inside more negative. This is called hyperpolarization.
- A hyperpolarized neuron is less likely to fire an action potential. This produces an inhibitory postsynaptic potential (IPSP).
- Result: pain transmission is inhibited.
Easy memory line
Opioids close calcium channels before the synapse and open potassium channels after the synapse.
- ↓ Ca²⁺ entry presynaptically → ↓ release of pain neurotransmitters
- ↑ K⁺ exit postsynaptically → hyperpolarization → ↓ firing of the pain neuron
Together, these actions reduce ascending pain signals to the brain and cause analgesia. This is the spinal mechanism shown in Katzung's Basic and Clinical Pharmacology, p. 730. The same pre- and postsynaptic mechanism is described in NCBI's opioid analgesics review.
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