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Jlenok [28]
4 years ago
10

The speed of neurotransmission in the frontal lobe increases during adolescence due to the growth of

Biology
2 answers:
ollegr [7]4 years ago
8 0

<u>Answer:</u>

The speed of neurotransmission in the frontal lobe increases during adolescence due to the growth of Myelin

<u>Explanation:</u>

Myelin is a fatty material, rich in lipids, which coats nerve cell axons to separate them and increases the rate of data transmission along the axon. The myelinated nerve cell axon can be associated with an electrical wire, i.e, axon covered by insulating material called myelin. Due to this action people will be more active, enthusiastic as the transmission of signals are very fast.

In other words, Myelin can significantly increase the speed of neurotransmission as it separates the axon and assembles voltage-gated sodium channel clusters at discrete nodes along its length. The growth in myelin results in the increase of speed of transmission of electrical impulse along the nerve cell or the axon

Marizza181 [45]4 years ago
4 0

Answer: Myelin

Explanation:

The speed of the neurotransmission increases as we grow. The behavior of the teenager is quite different from the behavior of the adolescents.

They are more active, heroic and wants to take risk. This is because their brains are not completely developed till they reach the age of 25.

As they grow and reach the late 20s the white mater in the brain increases as the frontal lobe is the last part of the brain development.

Due to the development of the myelin in the frontal lobe the transmission of the signal increases at adolescence.

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Answer:

Normal Strand: alanine - methionine - histidine
Mutated Strand: glutamine - cysteine - no third amino acid.

Explanation:

<h3>mRNA Structure</h3>

Messenger ribonucleic acid (mRNA) is the RNA that is used in cells for protein synthesis. It has a single strand made by the transcription of DNA by RNA polymerase. It contains four nucleotides: Adenine (A), Guanine (G), Cytosine (C), and Uracil (U).

<h3>DNA Replication</h3>

Before transcribing, we need to create the complementary strand of the DNA. We're going to write out the nucleotides of the complementary strand by matching the nucleotides in these pairs: (A & T) and (C & G).

              Normal Strand: GCA ATG CAC
Complementary Strand: CGT TAC GTG

Next, we can transcribe this to find our mRNA. We're going to do the same thing to the complementary DNA strand, but with Uracils instead of Thymines. So our pairs are: (A & U) and (C & G)

Complementary DNA Strand: CGT TAC GTG
                        mRNA Strand: GCA AUG CAC

You'll notice that the mRNA strand is almost exactly like the new mRNA strand, but with Uracil instead of Thymine.

<h3>Reading Codons</h3>

Each set of three nucleotides is known as a codon, which encodes the amino acids that ribosomes make into proteins. To read the codons, you need to have a chart like the one I attached. Start in the middle and work your way to the edge of the circle. Some amino acids have multiple codons. There are also "stop" and "start" codons that signify the beginning and ends of proteins.

mRNA Strand: GCA AUG CAC
Amino Acids:   Ala   Met   His

Our sequence is alanine, methionine, and histidine.

<h3>Frameshift Mutations</h3>

A frameshift mutation occurs when a nucleotide is either added or removed from the DNA. It causes your reading frame to shift and will mess up every codon past where the mutation was. This is different than a point mutation, where a nucleotide is <em>swapped</em> because that will only mess up the one codon that it happened in. Frameshift mutations are usually more detrimental than point mutations because they cause wider spread damage.

<h3>Mutated Strand</h3>

Let's repeat what we did earlier on the mutated strand to see what changed.

              Mutated Strand: CAA TGC AC
Complementary Strand: GTT ACG TG
---
Complementary DNA Strand: GTT ACG TG
                        mRNA Strand: CAA UGC AC
---
mRNA Strand: CAA UGC AC
Amino Acids:   Glu   Cys   X
---
Our amino acid sequence is glutamine, cysteine, and no third amino acid.

As you can see, removing the first nucleotide of the strand caused every codon to change. The last codon is now incomplete and won't be read at all. If this happened in a cell, the protein that was created from this mutated strand would be incorrect and may not function completely or at all.

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