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Beta-endorphin Mu-type opioid receptor Alpha-1A adrenergic receptor D(1A) dopamine receptor G protein complex Adenylyl cyclase complex GABAA receptor Beta-endorphin Sodium- dependent noradrenaline transporter Sodium- dependent dopamine transporter Glutamate receptor ionotropic Sodium channel Voltage Gated Potassium Channel Nicotinic Acetylcholine Receptor Nicotinic Acetylcholine Receptor Voltage- dependent calcium channel subunit alpha-2/delta-2 Nicotinic Acetylcholine Receptor Pro- opiomelanocortin Neuroendocrine convertase 2 Muscarinic acetylcholine receptor M3 Norepinephrine Dopamine Acetylcholine γ-Aminobutyric acid Anileridine Norepinephrine Na+ Na+ Dopamine Na+ Na+ Ca+ Na+ Na+ K+ Na+ Na+ K+ K+ Na+ Ca+ Ca+ Ca+ Ca+ Acetylcholine Substance P Substance P γ-Aminobutyric acid ATP cAMP PPi Ca+ K+ K+ Pre Synaptic Neuron Postsynaptic Neuron Neuron Membrane Potential (mV) -70 0 +40 Time Action Potential Depolarization Hyperpolarization Peak Action Potential Resting Potential Repolarization Neuron Axon Anileridine is an opioid analgesic that is used for it's relaxing effects and most commonly administered to relieve pains from narcotics. Specifically targeting the CNS to elicits analgesic effects. Anileridine binds to Mu opioid receptors that acts on G coupled proteins that go on to inhibit adenylyl cyclase. Due to this cAMP concentrations are reduced. Reduced cAMP causes a decrease in the influx of calcium into the neuron. Due to the reduction of calcium ions and the elevation of potassium ions into the neuron the cell becomes hyperpolarized. Hyperpolarization increases the threshold level as a result, making it harder for the neuron to be excited. This inhibits neuron activation, reduces pain signals as the threshold level is harder to meet, therefore inhibiting the reception of pain stimulus to the body. The reduction in calcium concentrations inhibits the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and norepinephrine. Without nociceptive substances being released the pain signal is inhibited. The cascade of effects from Anileridine binding to Mu opioid receptor, opens inward rectifying potassium channels and closes calcium channels.