Cortical reorganization after monocular deprivation within the critical period of development in vertebrates is reduced when neurons that utilize this molecule as an input are absent. This molecule also plays a role in attention, where excitatory input to the thalamus allows sensory input to reach cortical neurons. Pradiloxime is frequently used in cases of poisoning to activate the enzyme that breaks down this compound, and genetic disorders known as congenital myasthenic syndromes cause dysfun
Cortical reorganization after monocular deprivation within the critical period of development in vertebrates is reduced when neurons that utilize this molecule as an input are absent. This molecule also plays a role in attention, where excitatory input to the thalamus allows sensory input to reach cortical neurons. Pradiloxime is frequently used in cases of poisoning to activate the enzyme that breaks down this compound, and genetic disorders known as congenital myasthenic syndromes cause dysfunction in proteins related to this molecule, which mainly functions at neuromuscular junctions. That esterase is attacked by antibodies in patients with the disease myasthenia gravis, causing accumulation of this molecule in the NMJ and inhibition of muscle function. An ester of choline and acetic acid, for 10 points, name this primary neurotransmitter of  motor neurons commonly abbreviated ACh.
Cortical reorganization after monocular deprivation within the critical period of development in vertebrates is reduced when neurons that utilize this molecule as an input are absent.
acetylcholine