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Muscarinic acetylcholine receptor M1 Voltage- dependent N-type calcium channel subunit alpha-1B Voltage- dependent calcium channel subunit alpha-2/delta-2 Voltage- dependent L-type calcium channel subunit beta-4 Voltage- dependent L-type calcium channel subunit beta-1 Vesicular acetylcholine transporter High affinity choline transporter 1 Choline O- acetyltransferase Acetylcholinesterase Ca+ Acetylcholine Acetylcholine Trihexyphenidyl Ca+ Acetylcholine Choline Choline Trihexyphenidyl Trihexyphenidyl Acetyl-CoA Choline CoA H2O Acetic acid Efferent Impulses Magnesium Presynaptic neuron Postsynaptic neuron An action potential arrives at the nerve terminal and stimulates the opening of the calcium channel, causing an influx of calcium ions Acetylcholine is synthesized and stored in synaptic vesicles at the nerve terminal Calcium ions stimulates the release of neurotransmitter acetylcholine into the synaptic cleft via exocytosis Acetylcholine in the synaptic cleft activates muscarinic receptors on the post-synaptic membrane Acetylcholine is broken down by acetylcholinesterase into choline and acetyl-coa Choline is taken back up into the nerve terminal and recycled to create more acetylcholine By blocking the activation of the M1 receptor, it causes inhibition of efferent impulses directly - affecting structures innervated by the parasympathetic system and direct central inhibition of cerebral motor centers Trihexyphenidyl is a M1 antagonist, blocking the action of acetylcholine. Synaptic Vesicle Trihexyphenidyl is administered as an oral tablet
CHRM1 CACNA1B CACNA2D2 CACNB4 CACNB1 SLC18A3 SLC5A7 CHAT ACHE Calcium Acetylcholine Acetylcholine Trihexyphenidyl Calcium Acetylcholine Choline Choline Trihexyphenidyl Trihexyphenidyl Acetyl-CoA Choline Coenzyme A Water Acetic acid Efferent Impulses
CHRM1 CACNA1B CACNA2D2 CACNB4 CACNB1 SLC18A3 SLC5A7 CHAT ACHE Ca+ ACh ACh AT Ca+ ACh Choline Choline AT AT Ac-CoA Choline CoA H2O Acoh Eff Imp Mg2+ Presynaptic neuron Postsynaptic neuron An action potential arrives at the nerve terminal and stimulates the opening of the calcium channel, causing an influx of calcium ions Acetylcholine is synthesized and stored in synaptic vesicles at the nerve terminal Calcium ions stimulates the release of neurotransmitter acetylcholine into the synaptic cleft via exocytosis Acetylcholine in the synaptic cleft activates muscarinic receptors on the post-synaptic membrane Acetylcholine is broken down by acetylcholinesterase into choline and acetyl-coa Choline is taken back up into the nerve terminal and recycled to create more acetylcholine By blocking the activation of the M1 receptor, it causes inhibition of efferent impulses directly - affecting structures innervated by the parasympathetic system and direct central inhibition of cerebral motor centers Trihexyphenidyl is a M1 antagonist, blocking the action of acetylcholine. Synaptic Vesicle Trihexyphenidyl is administered as an oral tablet
CHRM1 CACNA1B CACNA2D2 CACNB4 CACNB1 SLC18A3 SLC5A7 CHAT ACHE Ca2+ ACh ACh AT Ca2+ ACh Choline Choline AT AT Ac-CoA Choline CoA H2O Acoh Eff Imp