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Chapter 4

Brain Development, Damage, and Recovery   

 The developing brain starts as a neural tube surrounding a fluid cavity, when the embryo is at about 2 weeks. One end then starts to enlarge and differentiate into the hindbrain, midbrain, and forebrain. The midbrain and hindbrain start out as much larger proportions of the brain, and the forebrain grows and folds the most throughout later stages of embryo/fetus development.

    Neurons mostly form in the first 28 weeks. Immunoglobulins and chemokines are chemicals that guide the neurons and glia when they migrate. After migrating the cell will differentiate into a neuron or glia. Neurons will develop dendrites and an axon. Axons then form synapses onto cells nearby. This process, of forming synapses, is a bit less precise than the migration. But while these synapses develop before birth, connections are strengthened, new ones will be added, and others pruned throughout an individual’s life (though it does slow as we age). Therefore, the connections are honed and become more “precise” over time. 

    New brain neurons can develop after infancy, but it is rare. We do sometimes get new olfactory neurons in the nose, because they are subject to damaging substances from the outside world. The hippocampus and basal ganglia replace about 2% of their neurons each year. But we mostly lose neurons over our lifetime, because we overproduce neurons at first. Each part of the brain includes a period of cell death when many neurons die, which is actually a sign of maturing healthily. As we grow, neurons that are getting less input will die, while neurons that are frequently used will survive and strengthen their connections.

    Most of our brain neurons are irreplaceable, but that does not mean it is not possible to heal from brain damage. Dendrites secrete neurotrophins after they lose contact with an axon, attracting branches from other axons. This is how new synapses form quickly after damage, between dendrites and axons of surviving neurons. Due to denervation supersensitivity, if there are fewer synapses in the brain, the dendrites of the remaining ones will also become more responsive. This compensates for the loss of neurons in many cases, but a side effect is strengthening connections that we might not want to be stronger, like those responsible for pain. Denervation supersensitivity is a frequent cause of chronic pain.

Genetics and Epigenetics

    Some newer discoveries in genetics include that genes don’t each have unique locations. Some genes overlap on their chromosome, and sometimes a single trait  can depend on locations on multiple chromosomes. Some genes don’t encode proteins at all but instead alter the expression of other genes. 
    In addition, many genes are expressed in some cells but not others, and changes in the environment can affect that. So even on the level of genetic expression, the environment already has an influence. Most traits are not determined as simply as by one pair of alleles.
There are sex-limited genes, which are autosomal genes present in both sexes but activated by hormones, so that they are only expressed in one sex or are expressed more in one sex than the other. This includes traits like amount of chest hair or breast size.
    Epigenetics is about changes in gene expression, because not all our genes are expressed all the time in every cell. DNA double helices are usually not in loose strands, even in the nucleus, but wound around proteins called histones. For genes to activate, they need to be a bit unwound from the histones. 
Experiences can alter the chemical environment inside a cell. This can lead to changes in the histones like adding acetyl groups to a histone (loosening its grip), removing acetyl groups (tightening its grip). It can also change DNA when methyl groups are added (turns off) or removed (turns on) from the promoter region at the start of a gene. We know trauma in childhood decreases methylation of brain genes, and this increases risk for depression and PTSD.
    And the “on” or “off” positions can be passed on to later generations. For example, a rat that is malnourished during pregnancy will have offspring whose genes expression is optimized for conserving energy and surviving in a low-resource world. If they end up getting rich, fatty food, though, they have a higher probability of heart disease and obesity.
    Things we know can affect gene expression in later generations in humans: drug addiction, feeling socially isolated or rejected, and malnourishment.

Next Week

    Our upcoming content relates to emotions and cognitive functioning. This includes experiencing stress and panic attacks. Based on this week's reading about epigenetics, we know that stress and emotion can change our gene expression, which affects how we respond to future experiences, and can also be passed down to future generations. I'll be curious to learn about the biological basis for emotions, and how different ones can affect our cell environments.

Comments

  1. I apologize for the delayed feedback. This post actually did not show up at all on my page hence the delayed comment. I am glad I found it because I did not even credited you. The post was a bit lengthy but I really liked what you did with the connection with upcoming chapter. No point deduction.

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