<span>d.involves accumulation of rhodopsin</span>
Answer:
Muscle contraction function.
Explanation:
The nerve endings possess synaptic acetylcholine vesicles ready to be released. The action potential depolarizes the presynaptic terminal and increases the concentration of axoplasmic calcium; Acetylcholine molecules are thus released, so that the concentration of the neurotransmitter at postsynaptic (nicotinic) receptors is temporarily increased. This is followed by post-synaptic membrane depolarization, muscle membrane action potential with increased rnioplasmic calcium concentration, and finally muscle contraction. Acetylcholine is hydrolyzed by acetylcholinesterase and resynaptic at the presynaptic level by cholinecetyltransferase. The etiopathogenesis of myasthenia gravis is autoimmune and there are antibodies against acetylcholine receptors that circulate in the blood, as well as a decrease in the number of receptors on the motor plates, that is, it is produced by the postsynaptic blockage of the myoneural plaque, that generates fatigue and localized or generalized muscle weakness that is characterized by the worsening of the contractile force of the muscle.
The ribosome is the location of translation, while transcription always takes place in the nucleus.
