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== Mu Opioid Receptor== | == Mu Opioid Receptor== | ||
<StructureSection load='4n6h' size='340' side='right' caption='Human Delta Opioid 7TM Receptor'scene=''> | <StructureSection load='4n6h' size='340' side='right' caption='Human Delta Opioid 7TM Receptor'scene=''> | ||
Opioid receptors are G-protein coupled receptors (GPCR), which bind endogenous opioid peptide neurotransmitters (such as enkephalins and endorphins) and exogenous synthetic opiate drugs (such as morphine, codeine, and heroin) as ligands to hinder pain-signaling in the brain, peripheral nerves, and digestive tract. μ-opioid receptors are one of the four major classes of opioid receptors, which also includes δ-opioid receptors, κ-opioid receptors, and nociceptin opioid receptors. The μ-opioid receptor MOR-1 is expressed by the gene OPRM1 in vertebrates. <ref>DOI: 10.1124/pr.112.007138</ref> MOR-1 has important implications as a target for pain relievers as well as a treatment for drug abuse. | Opioid receptors are G-protein coupled receptors (GPCR), which bind endogenous opioid peptide neurotransmitters (such as enkephalins and endorphins) and exogenous synthetic opiate drugs (such as morphine, codeine, and heroin) as ligands to hinder pain-signaling in the brain, peripheral nerves, and digestive tract. μ-opioid receptors are one of the four major classes of opioid receptors, which also includes δ-opioid receptors, κ-opioid receptors, and nociceptin opioid receptors. The μ-opioid receptor MOR-1 is expressed by the gene OPRM1 in vertebrates. <ref>DOI: 10.1124/pr.112.007138</ref> MOR-1 has important implications as a target for pain relievers as well as a treatment for drug abuse. | ||
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The biochemistry of opioid addiction points to the ventral tegmental area (VTA) of the brain, the reward center. In this area, there are a high concentration of μ-opioid receptors on the surfaces of neurons. When exogenous opioid agonists are present, they bind to the active site of the μ-opioid receptor. This sends a signal along the axon of the neuron to activate dopaminergic neurons. Upon activation of dopaminergic neurons, dopamine is released into the synapse and binds to post-synaptic receptors. The binding of dopamine results in feelings of euphoria. Exogenous opioids produce larger amounts of dopamine than endogenous opioids. When exogenous opioids are abused, the behavior of abusing them is reinforced by the feelings of pleasure from dopamine. Overtime, an addicted person develops a tolerance and more opioids are needed in order to release the same amount of dopamine as the first use. <ref name= "Article 2" > Contet, Candice, et al. “Mu Opioid Receptor: a Gateway to Drug Addiction.” Current Opinion in Neurobiology, 19 May 2004, pp. 370–378., doi:10.1016/s0959-4388(04)00072-8. </ref>. | The biochemistry of opioid addiction points to the ventral tegmental area (VTA) of the brain, the reward center. In this area, there are a high concentration of μ-opioid receptors on the surfaces of neurons. When exogenous opioid agonists are present, they bind to the active site of the μ-opioid receptor. This sends a signal along the axon of the neuron to activate dopaminergic neurons. Upon activation of dopaminergic neurons, dopamine is released into the synapse and binds to post-synaptic receptors. The binding of dopamine results in feelings of euphoria. Exogenous opioids produce larger amounts of dopamine than endogenous opioids. When exogenous opioids are abused, the behavior of abusing them is reinforced by the feelings of pleasure from dopamine. Overtime, an addicted person develops a tolerance and more opioids are needed in order to release the same amount of dopamine as the first use. <ref name= "Article 2" > Contet, Candice, et al. “Mu Opioid Receptor: a Gateway to Drug Addiction.” Current Opinion in Neurobiology, 19 May 2004, pp. 370–378., doi:10.1016/s0959-4388(04)00072-8. </ref>. | ||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||