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Gq protein signaling cascade Phospholipase C Inositol 1,4,5- trisphosphate receptor type 1 Protein kinase C alpha type Voltage- dependent P/Q-type calcium channel subunit alpha-1A Voltage- dependent L-type calcium channel subunit beta-1 Voltage- dependent calcium channel subunit alpha-2/delta-2 Myosin light chain kinase, smooth muscle Muscarinic acetylcholine receptor M3 Acetylcholinesterase Myosin LC-P Myosin light chain 3 Vesicular acetylcholine transporter Calmodulin-1 Myosin light chain phosphatase Choline O- acetyltransferase Calmodulin-1 Inositol 1,4,5-trisphosphate Atropine Acetylcholine Ca+ Ca+ Ca+ Acetylcholine Acetylcholine Atropine Phosphatidylinositol 4,5-bisphosphate Choline Acetylcholine H2O Acetic acid Choline Calcium Ca+ Diacylglycerol Organophosphate Muscle Contraction Muscle Relaxation Magnesium Calcium Manganese Magnesium Sarcoplasmic Reticulum Myosin unbinds from actin causing muscle relaxation Decreased calcium is unable to bind readily to calmodulin so it does not activate myosin light chain kinase Organophosphates and other muscarinic poisons continuously activate muscle contractions. Atropine prevents this, which prevents muscles from seizing. There is an overall decrease in calcium levels in the cytosol caused by the inhibition of the Gq signaling cascade Cytosol Muscle Cell Atropine antagonizes Muscarinic acetylcholine receptors M1-M5 in order to counteract the high concentration of acetylcholine causes by muscarinic poisons. The inhibition of Myosin light chain kinase prevents muscle contraction, leading to muscle relaxation. Organophosphate inhibits acetylcholinesterase which prevents the breakdown of acetylcholine. This leads to a high concentration of acetylcholine which continuously activates muscarinic acetylcholine receptors, causing muscle contractions. Cytosol Presynaptic Neuron Synaptic vesicle Breakdown of acetylcholine can occur in the neuron, or in the extracellular space around neurons and muscles. Actin Myosin Atropine is administered as an intravenous injection
Vacuole GNAQ PLCB1 ITPR1 PRKCA CACNA1A CACNB1 CACNA2D2 MYLK CHRM3 ACHE MYL3 MYL3 SLC18A3 CALM1 PPP1CB CHAT CALM1 Inositol 1,4,5- trisphosphate Atropine Acetylcholine Calcium Calcium Calcium Acetylcholine Acetylcholine Atropine Phosphatidylinositol 4,5- bisphosphate Choline Acetylcholine Water Acetic acid Choline Calcium Diacylglycerol Organophosphate Muscle Contraction Muscle Relaxation
GNAQ PLCB1 ITPR1 PRKCA CACNA1A CACNB1 CACNA2D2 MYLK CHRM3 ACHE MYL3 MYL3 SLC18A3 CALM1 PPP1CB CHAT CALM1 Inotp Atropin ACh Ca+ Ca+ Ca+ ACh ACh Atropin P45P Choline ACh H2O Acoh Choline Ca2+ Ca+ Diacylg Organ Mus Con Mus Rel Mg2+ Ca2+ Mn2+ Mg2+ Sarcoplasmic Reticulum Myosin unbinds from actin causing muscle relaxation Decreased calcium is unable to bind readily to calmodulin so it does not activate myosin light chain kinase Organophosphates and other muscarinic poisons continuously activate muscle contractions. Atropine prevents this, which prevents muscles from seizing. There is an overall decrease in calcium levels in the cytosol caused by the inhibition of the Gq signaling cascade Cytosol Muscle Cell Atropine antagonizes Muscarinic acetylcholine receptors M1-M5 in order to counteract the high concentration of acetylcholine causes by muscarinic poisons. The inhibition of Myosin light chain kinase prevents muscle contraction, leading to muscle relaxation. Organophosphate inhibits acetylcholinesterase which prevents the breakdown of acetylcholine. This leads to a high concentration of acetylcholine which continuously activates muscarinic acetylcholine receptors, causing muscle contractions. Cytosol Presynaptic Neuron Synaptic vesicle Breakdown of acetylcholine can occur in the neuron, or in the extracellular space around neurons and muscles. Actin Myosin Atropine is administered as an intravenous injection
Vacuole GNAQ PLCB1 ITPR1 PRKCA CACNA1A CACNB1 CACNA2D2 MYLK CHRM3 ACHE MYL3 MYL3 SLC18A3 CALM1 PPP1CB CHAT CALM1 Inotp Atropin ACh Ca2+ Ca2+ Ca2+ ACh ACh Atropin P45P Choline ACh H2O Acoh Choline Ca2+ Diacylg Organ Mus Con Mus Rel