| Opioids and endorphins that bind to opiate receptors terminate pain
signals by inhibiting the release of Substance P from pre-synaptic neurons.
The mechanism behind opioid analgesia is complex and only partially understood.
When opioids bind to receptors, a conformational change in the cell inhibits the release of G proteins from the cellular side of the plasma membrane. G proteins are an integral part of the system cells use to transmit signals from receptor sites on their membrane to internal organelles. G protein signals regulate the opening and closing of ion channels. Creating concentration gradients by pumping |
ions through channels is necessary for the propagation of electrical
signals through neurons. Without the proper concentration gradients
for propagation, neurons with activated opiate receptors do not release
Substance P (Leonard, 1992; Besson, 1999).
Opiate receptors are highly concentrated on neurons in the substantia gelatinosa and medial thalamus, but not in the lemniscus system. Therefore, opioids are not effective relievers of sharp pain, such as a pin prick. However, opioids do alleviate dull, prolonged pain, such as that experienced with cancer (Snyder, 1996). |
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Substance P travels across the synapse between neurons to transmit a pain signal. Electrical impulses that travel down the neuron must signal for the release of Substance P. |
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When the opiate receptors on the pre-synaptic neuron are activated, a conformational change prevents to release of Substance P. In this diagram, opiate receptors are activated by endorphins released from a neighboring neuron.. The brain signals for the release of endorphins during unusually traumatic events. Opiate receptors can also be activated by opioids. |
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This site was created during the fall semester of 1999 by Wes
Self, a student at
Davidson College, as part of an assignment in Biology 312 (Animal Physiology). Questions, comments and suggestions are appreciated at weself@davidson.edu |