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 process is Transcription
It’s the second one!!
and the first answer!!
The nitrogenous bases placed in between the DNA double helix strands, like rungs on a ladder, are positioned there because of the hydrophobic effect and are stabilized by hydrogen bonding. The stability of DNA also relies on the interactions between the hydrogen bonds between bases, hydrogen bonds between bases and surrounding water, and base interaction between neighboring bases.
Hydrogen bonds are able to stabilize the DNA double helix by pairing up with their complementary base pairs (guanine with cytosine and adenine with thymine)
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Because Scientific method is an empirical method of knowledge acquisition, involving careful
