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Pathway Description
Naloxone Opioid Antagonist Action Pathway
Homo sapiens
Category:
Metabolite Pathway
Sub-Category:
Drug Action
Created: 2023-06-19
Last Updated: 2023-11-27
Naloxone, also known as Narcan, is a competitive antagonist of mu-type opioid receptors in the central nervous system (CNS). It is used to rapidly reverse an opioid overdose. It is also included in some drug formulations as an abuse-deterrent to prevent injection. Naloxone is currently administered by intramuscular (IM) or subcutaneous (SubQ) injection, nasal spray, or intravenous (IV) injections. When injected intramuscularly (IM), naloxone acts within three to five minutes. The use of this drug has very few side effects. Notably, if injected into a person not currently using opioids, there would be no effects. However, for individuals using opioids or experiencing an overdose, an IM injection of naloxone rapidly reverses opioid effects by competitive binding of the mu-type opioid receptors and can cause the injected individual to immediately experience withdrawal symptoms. Common symptoms of opioid withdrawal include nausea, vomiting, sweating, runny nose, aches, and diarrhea. Naloxone is also available as a nasal spray, sublingual tablet, and oral tablet.
Naloxone inhibits the exchange of GTP for GDP which is required to activate the G-protein complex. This prevents the Gi subunit of the mu opioid receptor from inhibiting adenylate cyclase, which can therefore continue to catalyze ATP into cAMP. cAMP increases the excitability in spinal cord pain transmission neurons which allows the patient to feel pain rather than the analgesic effects of opioids. The inhibition of Mu-type opioid receptors also prevents the Gi subunit of the mu opioid receptor from activating the inwardly rectifying potassium channel increasing K+ conductance which would cause hyperpolarization. Naloxone also prevents the gamma subunit of the mu opioid receptor from inhibiting the N-type calcium channels on the neuron. This allows calcium to enter the neuron and depolarize. The inhibition of mu-opioid receptors prevents hyperpolarization in the neuron, allowing it to fire at a normal rate. The neuron is able to depolarize and the high concentration of calcium releases GABA into the synapse which binds to GABA receptors. GABA receptors inhibits dopamine cell firing in the pain transmission neurons. This prevents the analgesic and depressive effects of opioids, preventing opioid overdose. GABA also inhibits dopamine cell firing in the reward pathway which is the main cause of addiction to opioids and other drugs.
References
Naloxone Opioid Antagonist Pathway References
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