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N-type calcium channel potassium voltage-gated channel subfamily J Adenylate cyclase type 2 GABAA receptor Gamma- aminobutyric acid type B receptor Mu-type opioid receptor γ-Aminobutyric acid Remifentanil cAMP Ca+ Ca+ Na+ Na+ γ-Aminobutyric acid Remifentanil Remifentanil ATP PPi GTP Pain Guanine nucleotide- binding protein G(i) subunit alpha-1 Magnesium Remifentanil inhibits neuron in the brain leading to analgesic and anesthetic effects Less GABA leads to disinhibition of dopamine cell firing in the spinal chord pain transmission neurons. This leads to inhibition of brain signalling Decreased calcium levels lead to decreased neurotransmitter release. Less GABA is released for synaptic vesicles. Remifentanil binds to pre synaptic mu opioid type receptors. The Gi subunit of the mu opioid receptor activates the inwardly rectifying potassium channel increasing K+ conductance. This causes membrane hyperpolarization decreasing the chances of neuronal firing/action potential. Post-Synaptic Neuron Pre-Synaptic Neuron Synapse Cytosol Synaptic Vesicle The mu opioid receptor through the gamma subunit inhibits voltage gated N-type calcium channels stopping the influx of calcium into the neuron. Blood-Brain Barrier Diffusion Remifentanil is taken intravenously With the inhibition of adenylate cyclase, it is unable to synthesize cAMP which further prevents calcium from entering the neuron and depolarization of the neuron
CACNB1 KCNJ9 ADCY2 GABRG2 GABBR1 OPRM1 GNB1 GNG2 γ-Aminobutyric acid Remifentanil cAMP Calcium Calcium Sodium Sodium γ-Aminobutyric acid Remifentanil Remifentanil Adenosine triphosphate Pyrophosphate Guanosine triphosphate Pain GNAI1