Quantitative metabolomics services for biomarker discovery and validation.
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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 ABC transporter, substrate- binding lipoprotein ATP-binding cassette sub-family C member 3 Cytochrome P450 2D6 Mu-type opioid receptor Gβ Gγ γ-Aminobutyric acid Morphine cAMP Ca+ Ca+ Na+ Na+ γ-Aminobutyric acid Ethylmorphine Ethylmorphine Morphine Morphine Morphine ATP PPi Heme GTP Pain Guanine nucleotide- binding protein G(i) subunit alpha-1 Magnesium Morphine depresses neurons in the cough centre of the brainstem Less GABA leads to disinhibition of dopamine cell firing in the spinal chord pain transmission neurons. This leads to the suppression of the cough centre of the brain Decreased calcium levels lead to decreased neurotransmitter release. Less GABA is released for synaptic vesicles. Morphine 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 Morphine diffuses across the blood-brain barrier 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 Hepatocyte Liver Diffusion Ethylmorphine is taken orally
CACNB1 KCNJ9 ADCY2 GABRG2 GABBR1 CDR20291_0805 ABCC3 CYP2D6 OPRM1 GNB1 GNG2 γ-Aminobutyric acid Morphine cAMP Calcium Calcium Sodium Sodium γ-Aminobutyric acid Ethylmorphine Ethylmorphine Morphine Morphine Morphine Adenosine triphosphate Pyrophosphate Guanosine triphosphate Pain GNAI1