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Beta-endorphin Adenylate cyclase type 2 Serine/threonine- protein phosphatase PP1-beta catalytic subunit Voltage- dependent L-type calcium channel subunit beta-1 G protein- activated inward rectifier potassium channel 3 Myosin light chain 3 Myosin light chain 3 Mu-type opioid receptor Neuronal acetylcholine receptor subunit beta-2 NO Acetylcholine Methylnaltrexone Na+ NO NO Acetylcholine Na+ Ca+ Ca+ Na+ Na+ ATP cAMP PPi Methylnaltrexone GTP Neuronal acetylcholine receptor subunit alpha-4 Muscle Relaxation nAchR Smooth Muscle Contraction Guanine nucleotide- binding protein G(i) subunit alpha-1 Magnesium Manganese More ACh leads to stimule all three types of contractions of the smooth muscle cells of the GI tract. Neuromuscular Junction Increased calcium levels lead to increased neurotransmitter release. NO is released by synaptic vesicles in inhibitory motorneurones. NO relaxes the smooth muscle cells of the GI tract. The rythmic action of the neurotransmitters creates the peristalsis and the good GI transit. Smooth Muscle Myocyte Increased calcium levels lead to increased neurotransmitter release. Acetylcholine is released by synaptic vesicles. Methylnaltrexone 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-type opioid receptors prevents the Gi subunit of the mu opioid receptor from activating the outward rectifying sodium channel. This prevents hyperpolarization Pre-Synaptic Neuron Cytosol Synaptic Vesicle With the mu opioid receptor unable to inhibit adenylate cyclase, it is able to synthesize cAMP which increases the excitability of the neuron leading to neurotransmitter release Synaptic Vesicle
Unknown ADCY2 PPP1CB CACNB1 KCNJ9 MYL3 MYL3 OPRM1 GNB1 GNG2 Unknown Nitric oxide Acetylcholine Methylnaltrexone Sodium Nitric oxide Nitric oxide Acetylcholine Sodium Calcium Calcium Sodium Sodium Adenosine triphosphate cAMP Pyrophosphate Methylnaltrexone Guanosine triphosphate Unknown Muscle Relaxation nAchR Smooth Muscle Contraction GNAI1
ADCY2 PPP1CB CACNB1 KCNJ9 MYL3 MYL3 OPRM1 GNB1 GNG2 NO ACh Methy Na+ NO NO ACh Na+ Ca+ Ca+ Na+ Na+ ATP cAMP PPi Methy GTP Mus Rel PW128245 GNAI1 Mg2+ Mn2+ More ACh leads to stimule all three types of contractions of the smooth muscle cells of the GI tract. Neuromuscular Junction Increased calcium levels lead to increased neurotransmitter release. NO is released by synaptic vesicles in inhibitory motorneurones. NO relaxes the smooth muscle cells of the GI tract. The rythmic action of the neurotransmitters creates the peristalsis and the good GI transit. Smooth Muscle Myocyte Increased calcium levels lead to increased neurotransmitter release. Acetylcholine is released by synaptic vesicles. Methylnaltrexone 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-type opioid receptors prevents the Gi subunit of the mu opioid receptor from activating the outward rectifying sodium channel. This prevents hyperpolarization Pre-Synaptic Neuron Cytosol Synaptic Vesicle With the mu opioid receptor unable to inhibit adenylate cyclase, it is able to synthesize cAMP which increases the excitability of the neuron leading to neurotransmitter release Synaptic Vesicle
ADCY2 PPP1CB CACNB1 KCNJ9 MYL3 MYL3 OPRM1 GNB1 GNG2 NO ACh Methy Na+ NO NO ACh Na+ Ca2+ Ca2+ Na+ Na+ ATP cAMP Ppi Methy GTP Mus Rel PW128245 GNAI1